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Good article Methamphetamine has been listed as one of the Natural sciences good articles under the good article criteria. If you can improve it further, please do so. If it no longer meets these criteria, you can reassess it.
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Amendment to the first sentence[edit]

Hi, I think the first sentence should instead read like: "Methamphetamine[note 1] (pronunciation: /mɛθæmˈfɛtəmin/; contracted from N-methyl-alpha-methylphenethylamine) is a neurotoxin and potent psychostimulant of the phenethylamine and amphetamine classes, that is used medically, in some countries, to treat resistant cases of attention deficit hyperactivity disorder (ADHD) and obesity, but is better known for its role as an infamous drug of abuse."

Note: I have ignored much of the formatting in this sentence, the bolding and hyperlinking of the words and letters I think is fine the way it is.

Now my reasoning for this suggested change is that most people don't know it's used to treat ADHD or obesity, even there it's only used in some countries (mostly North American countries) and even then only in resistant cases, hence it might be more helpful to mention this and the fact it is well-known drug of abuse. I would just edit it myself, but I felt as this is a good article a consensus should be reached on something as important as the first sentence. Thoughts and opinions will be welcome by anyone. Even people I tend to ruffle the feathers of as I do still value their opinions as Wikipedia is still a democracy. Brenton (contribs · email · talk · uploads) 14:29, 20 July 2014 (UTC)

Seems a bit long. How's this? Seppi333 (Insert  | Maintained) 19:28, 20 July 2014 (UTC)
Sure, I think that's better than my suggestion due to my lack of concision. Face-smile.svg Brenton (contribs · email · talk · uploads) 19:41, 20 July 2014 (UTC)


I like how it says that meethamphetamine is much more toxic than ritalin and amphetamine. This makes no sense. At low doses toxicity would be absolutely the same. I am not even saying that it compares meth additcs to schoolers on ritaline by 18mg. Higher toxicity is achievable only at large doses due to more powerful output capabilities of meth. Extreemator (talk) 06:45, 31 July 2014 (UTC)

The article states that meth is neurotoxic even at low doses in humans – and amphetamine and methylphenidate are not – because that's what the citations say. The article compares the neuroplastic effect of high dose meth to those of low dose amph because that's as much as could be said from neuroimaging reviews wrt those drugs in humans.
I'd suggest reading the sources if you want an explanation about a statement. Seppi333 (Insert  | Maintained) 00:06, 2 August 2014 (UTC)

Levmetamfetamine as a USAN[edit]

@Fuse809: I'm fairly certain that levomethamphetamine doesn't have a USAN, since it has never been a pharmaceutical drug in the United States. I've read elsewhere that manufacturers (e.g., Vicks) use the INN on their packaging primarily to avoid the stigma associated with the term "methamphetamine". In any event, I'd normally just remove a clause I find dubious, but I figured I'd ask first: do you have a ref for the levmetamfetamine USAN? Nevermind, it's apparently in the very same ref I used to cite the INN... I'm clearly very perceptive. >.> Seppi333 (Insert  | Maintained) 23:45, 6 October 2014 (UTC)

Clarity on freebase vs salts[edit]

It's obvious to me why the melting point is listed as 3*C but that's likely to seem very weird for the majority of the population. Should it be made clearer that many of the chemical properties are referring to the freebase oil and not the more commonly seen hydrochloride salt?

Semi-protected edit request on 27 December 2014[edit]

"Unlike amphetamine, methamphetamine is directly neurotoxic to dopamine neurons.[39]" Source 39 is bogus, the authors do not cite any research to support this statement, it seems to be no more than an opinion. "Methamphetamine also inhibits VMAT1, has agonist activity at all alpha-2 adrenergic receptor and sigma receptor subtypes, and is directly toxic to dopamine neurons in humans, whereas there is no evidence of acute amphetamine toxicity in humans.[39][44][57][63]" None of the cited sources support the statement that there is no amphetamine toxicity in humans. That statement should be removed or supported by valid sources. (talk) 00:47, 27 December 2014 (UTC)

See WP:MEDRS for what constitutes a valid medical source. Seppi333 (Insert  | Maintained) 01:00, 27 December 2014 (UTC)

Off-label use of prescription methamphetamine?[edit]

Is there any off-label medical uses for prescription methamphetamine other than ADHD and obesity? Probably narcolepsy, idiopathic hypersomnia and depression but without sources this is just a guess. Clr324 (say hi) 08:24, 19 February 2015 (UTC)

I imagine all of those are, but I doubt I can find a source that says that. Seppi333 (Insert  | Maintained) 01:55, 20 February 2015 (UTC)
That just sucks. :( I'll look for sources anyways just in case there is any. Edit: Easier than I thought. Clr324 (say hi) 03:55, 20 February 2015 (UTC)

New image[edit]

@Boghog: Hey, hope it's not too muxh to ask, but can you draw a new structure diagram for this article as well when you get a chance? I'd like to keep the Dbox images consistent across articles. Seppi333 (Insert  | Maintained) 02:51, 4 April 2015 (UTC)

No problem. I have updated the structure so that it is consistent with the one used in amphetamine. Boghog (talk) 09:28, 4 April 2015 (UTC)

Require sources[edit]

Recreationally, methamphetamine is used to increase sexual desire, lift the mood, and increase energy, allowing some users to engage in sexual activity continuously for several days straight.

Done although the entire recreational use section needs expansion. Sizeofint (talk) 16:21, 15 April 2015 (UTC)
The current ref for this sentence in the lead par is San Francisco Meth Zombies (TV documentary). National Geographic Channel. August 2013. ASIN B00EHAOBAO. Is this is an adequate source?? I know the sentence is prefixed with "Recreationally", but the inference is that meth enables continuous bonking for several days straight. So first qn is: is it true? 2nd qn: my body can be aroused that long much without any drugs (it can get to the state that the more we have sex, the more we want to have sex; my girlfriend's tendency to orgasm remains roughly constant, my frequency of ejaculation reduces with time and my refractory period grows), but we would not be capable of staying awake that long or being so obsessed for so long without drugs - this suggests to me that the most pertinent factor is not so much that meth enables extended sexual performance, but that it enables extreme wakefulness and obsession; is clarification along these lines appropriate? — Preceding unsigned comment added by (talk) 12:51, 10 May 2015 (UTC)
Yes, this should be clarified. This section needs additional information and sources so everything is not based off a National Geographic documentary. Sizeofint (talk) 21:22, 10 May 2015 (UTC)
  1. Yes. It is a reliable source.
  2. No. You aren't a reliable source. Seppi333 (Insert ) 22:55, 10 May 2015 (UTC)
I agree that the section needs expansion though. Seppi333 (Insert ) 02:23, 15 May 2015 (UTC)


LOL, who edited that one? Amphetamine of even garden variety is technically necrotic to neuron integrity DEPENDENT UPON MULTI-FACTORIAL CRITERIA - the statement "UNLIKE AMPHETAMINE..." simply stupidly fails to delve into these, unhelpfully and the simplism is brutal. As if your kid's Ritalin or Adderall was a magically different compound than Desoxyn... Someone state the facts more subtly and wisely here, rephrase things... Makes Wikipedia look retarded. Genetic polymorphisms of individuals and a million other factors determine whether amphetamine shall prove neurologically damaging, but the reality of its capacity above all these contingent factors, to obliterate Homo Sapiens axon-dendrite-ETC. connections necessary for cephalic functionality, is just a brute factum. — Preceding unsigned comment added by 2602:304:B34B:A940:F051:AB0F:3A76:DE48 (talk) 04:34, 19 June 2015 (UTC)

The reference for that statement is reliable but is somewhat on the old side. If you have a newer WP:MEDRS compliant source feel free to provide it and we can update this section. Sizeofint (talk) 05:11, 19 June 2015 (UTC)
Lol. There's a link to the sections in the body right after that statement... the superscripted [i] and [iii], which explains one significant pharmacodynamic and associated toxicodynamic difference that has been identified between methamphetamine and amphetamine. Did you bother clicking that link before ranting here? A single methyl group is the difference between phenethylamine and amphetamine as well, so maybe the brain produces its own necrosis-inducing neurotoxins? Seppi333 (Insert ) 07:25, 19 June 2015 (UTC)

Neurotoxicity update[edit]

CC-by-2.5 neurodegeneration image from this ref.[1]

Reviews to add (at some point)...

  1. [2] - includes coverage of human low-dose methamphetamine-induced neurotoxicity
  2. [3] - 2nd human neurotoxicity review

Seppi333 (Insert ) 03:45, 13 July 2015 (UTC)

Updated: Seppi333 (Insert ) 17:50, 18 July 2015 (UTC)


  1. ^ a b Beardsley PM, Hauser KF (2014). "Glial modulators as potential treatments of psychostimulant abuse". Adv. Pharmacol. 69: 1–69. doi:10.1016/B978-0-12-420118-7.00001-9. PMC 4103010. PMID 24484974. 
  2. ^ Yu S, Zhu L, Shen Q, Bai X, Di X (March 2015). "Recent advances in methamphetamine neurotoxicity mechanisms and its molecular pathophysiology". Behav. Neurol. 2015: 103969. doi:10.1155/2015/103969. PMC 4377385. PMID 25861156. 
  3. ^ Salamanca SA, Sorrentino EE, Nosanchuk JD, Martinez LR (January 2015). "Impact of methamphetamine on infection and immunity". Front. Neurosci. 8: 445. doi:10.3389/fnins.2014.00445. PMC 4290678. PMID 25628526. 
  4. ^ Saha K, Sambo D, Richardson BD, Lin LM, Butler B, Villarroel L et al. (August 2014). "Intracellular methamphetamine prevents the dopamine-induced enhancement of neuronal firing". J. Biol. Chem. 289 (32): 22246–22257. doi:10.1074/jbc.M114.563056. PMID 24962577. The primary target of psychostimulants such as amphetamine and methamphetamine is the dopamine transporter (DAT), the major regulator of extracellular dopamine levels in the brain. However, the behavioral and neurophysiological correlates of methamphetamine and amphetamine administration are unique from one another, thereby suggesting these two compounds impact dopaminergic neurotransmission differentially. ... The intracellular application of methamphetamine, but not amphetamine, prevented the dopamine-induced increase in the spontaneous firing of dopaminergic neurons and the corresponding DAT-mediated inward current. The results reveal a new mechanism for methamphetamine-induced dysregulation of dopaminergic neurons. 
  5. ^ Steinkellner T, Freissmuth M, Sitte HH, Montgomery T (2011). "The ugly side of amphetamines: short- and long-term toxicity of 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy'), methamphetamine and D-amphetamine". Biol. Chem. 392 (1-2): 103–15. doi:10.1515/BC.2011.016. PMC 4497800. PMID 21194370. d-AMPH and METH vary considerably in their toxic and addictive effects. Although d-AMPH has a higher affinity for DAT than METH (Howell and Kimmel, 2008), the latter is a more potent and also more perilous stimulant than d-AMPH. This could be as a result of their differing effects on cellular targets such as MAOs, mitochondrial electron transport chain complexes and their interactions with different signal transduction pathways. METH is more lipophilic than d-AMPH. Therefore, it readily enters the cell via diffusion in addition to DAT-dependent uptake. Furthermore, METH has been shown to release more DA and intracellular Ca2+ than d-AMPH at physiologic membrane potentials. These effects can be blocked by DAT inhibitors (Goodwin et al., 2009). This increased DA release perhaps provides an explanation for the enhanced abuse potential and the strong euphoric effects of acute METH exposure in humans. Chronic METH abuse leads to the degeneration of monoaminergic terminals (Davidson et al., 2001; Krasnova and Cadet, 2009) and reduced DAT and DA levels in the striatum of mice, rats and monkeys (Anderson and Itzhak, 2006; Graham et al., 2008; Melega et al., 2008). Similar effects have been reported in people subjected to positron emission tomography (PET) (Volkow et al., 2001). In contrast to MDMA, the metabolism of d-AMPH/METH does not appear to be significant in the manifestation of drug neurotoxicity. However, increases in DA metabolism following d-AMPH/METH-induced DA release have been implicated in the expression of amphetamine neurotoxicity, primarily through the production of oxidative stress (Krasnova and Cadet, 2009). 
  6. ^ Matsumoto RR, Nguyen L, Kaushal N, Robson MJ (2014). "Sigma (σ) receptors as potential therapeutic targets to mitigate psychostimulant effects". Adv. Pharmacol. 69: 323–386. doi:10.1016/B978-0-12-420118-7.00009-3. PMID 24484982. 
  7. ^ Kaushal N, Matsumoto RR (March 2011). "Role of sigma receptors in methamphetamine-induced neurotoxicity". Curr Neuropharmacol 9 (1): 54–57. doi:10.2174/157015911795016930. PMC 3137201. PMID 21886562. 
  8. ^ Rodvelt KR, Miller DK (September 2010). "Could sigma receptor ligands be a treatment for methamphetamine addiction?". Curr Drug Abuse Rev 3 (3): 156–162. doi:10.2174/1874473711003030156. PMID 21054260. 
  9. ^ Friend DM, Fricks-Gleason AN, Keefe KA (2014). "Is there a role for nitric oxide in methamphetamine-induced dopamine terminal degeneration?". Neurotox Res 25 (2): 153–60. doi:10.1007/s12640-013-9415-2. PMC 3880644. PMID 23918001.