Methamphetamine
N-methylamphetamine
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Methamphetamine — meth, ice, crystal — is a synthetic stimulant of the phenethylamine class. It is the N-methylated derivative of amphetamine, distinguished by greater potency and longer duration. Methamphetamine is a monoamine releasing agent with predominantly dopaminergic and noradrenergic activity,[1] producing its effects through reverse transport of neurotransmitters into the synapse.[2]
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amphetamine, cocaine, methylphenidate +1 moreamphetamine, cocaine, methylphenidate, MDMA show less
Synthesized by Nagayoshi Nagai in 1893 and first crystallized by Akira Ogata in 1919, methamphetamine emerged from research on ephedrine derivatives.[3] Military forces distributed it as a wakefulness agent during World War II; postwar surplus triggered Japan's first major stimulant epidemic.[4] It remains Schedule II in the United States — marketed as Desoxyn for ADHD — while illicit crystal methamphetamine is among the most widely used stimulants globally.[5]
Subjective effects include intense euphoria, wakefulness, appetite suppression, cognitive stimulation, and cardiovascular activation. The experience is characteristically driven and focused — a hard-edged dopaminergic stimulation without the empathogenic warmth of entactogens, where productivity dominates at lower doses and compulsive restlessness emerges at higher ones. Anxiety, paranoia, bruxism, and stereotyped repetitive behavior are common unsought effects.
Methamphetamine carries extremely high addiction liability and produces cardiovascular toxicity — including stroke and heart muscle damage — as its primary organ-system risk.[6] Behavioral sensitization, not simple tolerance, underlies relapse vulnerability; chronic use creates lasting susceptibility to paranoid psychosis retriggerable by small doses or stress long after abstinence.[7] Decades of clinical, neuroimaging, and epidemiological research underpin the current understanding, though no approved pharmacotherapy for methamphetamine use disorder exists.[8]
History[edit]
Discovery
Nagayoshi Nagai, a Japanese pharmacist at Tokyo Imperial University, first synthesized methamphetamine from ephedrine in 1893.[3] Akira Ogata achieved the first crystallization in 1919, using reduction of ephedrine with red phosphorus and iodine — a synthetic route that remains the chemical basis for clandestine production today.[3]
Military and pharmaceutical era
Marketed as Pervitin in Germany and Philopon in Japan during the 1930s, methamphetamine was distributed to military personnel on both sides of World War II as a wakefulness and performance-enhancing agent. The war's end released massive surplus stocks onto the Japanese civilian market, producing the country's first major methamphetamine epidemic — a crisis that became a driving force behind international drug control efforts.[4] Desoxyn (d-methamphetamine hydrochloride) remains one of very few approved pharmaceutical preparations, FDA-authorized for ADHD and short-term obesity management.
Regulation and modern crisis
The 1971 United Nations Convention on Psychotropic Substances placed methamphetamine on Schedule II, acknowledging both high abuse potential and accepted therapeutic use.[4] Illicit crystal methamphetamine expanded from production centers in Southeast Asia and the Pacific during the 1990s to become a global public health crisis, with clandestine manufacturing shifting from small domestic laboratories to industrial-scale operations in Mexico and Southeast Asia.[5]
The name "methamphetamine" derives from its chemical structure: methyl-alpha-methyl-phenyl-ethyl-amine. Street names reflect form and geography — "ice" and "crystal" refer to the translucent crystalline hydrochloride salt; "speed" overlaps with amphetamine; "Tina" emerged from chemsex communities. The compound occupies an unusual cultural position: simultaneously a legally prescribed medication, a wartime performance enhancer distributed across multiple armies, and one of the most stigmatized illicit drugs in public discourse.
Chemistry[edit]
Structural class
Methamphetamine belongs to the substituted phenethylamine family. The core structure consists of a phenyl ring attached to an ethylamine side chain, with an α-methyl group (the amphetamine scaffold) and an additional N-methyl substituent. This N-methylation increases the molecule's fat solubility relative to Amphetamine, enabling faster passage across the blood-brain barrier and contributing to methamphetamine's greater CNS potency.[3]
Molecular properties
| Molecular formula | C₁₀H₁₅N |
| Molecular weight | 149.23 g/mol |
Stereochemistry
The molecule contains a single chirality center, producing two mirror-image forms with markedly different pharmacological profiles. The d-enantiomer (d-methamphetamine or dextromethamphetamine) is the active CNS stimulant responsible for psychoactive, reinforcing, and neurotoxic effects. The l-enantiomer (l-methamphetamine) retains peripheral cardiovascular effects but has minimal activity in the brain,[9] and is used in some over-the-counter nasal decongestants.
Illicit methamphetamine consists predominantly of the d-enantiomer, typically as the hydrochloride salt. The racemic mixture may be encountered depending on synthetic route.
Physical properties
Methamphetamine free base is a colorless, volatile liquid with a characteristic amine odor. The hydrochloride salt forms clear to white crystals or crystalline powder — the "crystal" or "ice" form refers to large translucent crystals produced by recrystallization.citation needed The compound is highly fat-soluble, distributing widely throughout body tissues including the brain.[10]
Pharmacology[edit]
Mechanism of action
Methamphetamine enters nerve terminals through the same transporters that normally recycle dopamine, norepinephrine, and serotonin back into cells. Once inside, it forces these transporters to run in reverse, pumping monoamines out of the neuron and into the synapse in a process called reverse transport.[11][2] The effect is strongest for norepinephrine and dopamine, with comparatively weak serotonin release — a profile that distinguishes methamphetamine from serotonin-preferring compounds like MDMA.[1]
A second mechanism amplifies this effect. Methamphetamine also enters dopamine storage vesicles inside the neuron (via VMAT2), disrupting their contents and spilling dopamine into the cell body. This extra dopamine then becomes available for reverse transport out through DAT, producing extracellular dopamine concentrations far beyond what transporter reversal alone would achieve.[2][12]
Additional targets include TAAR1, a receptor that normally acts as a brake on dopamine signaling,[13] and β2-adrenergic receptors.[14] Methamphetamine also weakly inhibits the enzyme monoamine oxidase, though this contributes only marginally to its effects at typical doses.[15]
Pharmacokinetics
Methamphetamine reaches the brain efficiently regardless of route: bioavailability is approximately 90% when smoked and 67% when taken orally.[10] Smoked and intravenous routes produce near-instantaneous onset (peak plasma levels within seconds); oral onset requires 15–30 minutes. The half-life of 10–12 hours supports the prolonged duration of effects.[10]
The liver metabolizes methamphetamine through two main pathways: one produces an inactive metabolite (p-hydroxymethamphetamine), the other yields amphetamine as an active metabolite.[3] A substantial fraction (37–45%) is excreted unchanged in urine.[10][3] Urine acidity strongly influences elimination speed: acidic urine accelerates excretion, while alkaline urine prolongs the drug's presence in the body.
Neuroscience[edit]
Reward pathway and cognitive effects
Methamphetamine's defining neural action is a massive surge of dopamine in the brain's reward circuit — projections from the ventral tegmental area to the nucleus accumbens. The non-exocytotic dopamine flood overwhelms normal signaling, producing supra-physiological stimulation that drives the intense reinforcement and compulsive drug-seeking characteristic of methamphetamine use disorder.[5]
At low doses, dopamine enhancement in the prefrontal cortex can improve attention and working memory — but only in individuals with depressed baseline performance,[16] consistent with an inverted-U relationship between dopamine levels and cognitive function.
Neurotoxicity and sensitization
Chronic use produces progressive damage to dopamine and serotonin nerve terminals through converging mechanisms: excess cytosolic dopamine generates reactive oxygen species, mitochondrial function deteriorates, and sustained neuroinflammation amplifies the damage.[17][18] Neuroimaging confirms persistent DAT reductions of 23–25% in the striatum after years of abstinence,[7] alongside gray-matter loss in limbic cortex and reduced hippocampal volume correlated with memory suppression.[19]
Rather than simple tolerance, methamphetamine produces behavioral sensitization — a progressive and enduring enhancement of response to the drug with repeated exposure.[20] The brain becomes more reactive, not less, to methamphetamine's rewarding effects over time, creating escalating vulnerability to relapse. Sensitization also extends to psychosis: chronic users develop lasting susceptibility to paranoid episodes triggered by small doses or non-drug stressors even after years of abstinence.[21]
Selective TAAR1 agonists may offer a new treatment approach for methamphetamine addiction by reducing drug-seeking without the side effects of dopamine blockers — the structural basis for this interaction is now characterized,[13] but clinical translation remains untested.
Subjective Effects[edit]
Methamphetamine produces a characteristically driven, focused stimulation dominated by dopamine and norepinephrine activity. At lower oral doses, the experience centers on wakefulness, mental clarity, and purposeful energy; as dose increases, the focused drive gives way to compulsive restlessness, anxiety, and stereotyped repetitive behavior. Route of administration is the strongest modifier — smoked and intravenous routes deliver an intense, sharply delineated rush absent from oral dosing, partly explaining the higher addiction liability of non-oral routes.[10]
Compared to amphetamine, methamphetamine's effects are qualitatively similar but subjectively more intense and longer-lasting, owing to faster brain penetration. The experience lacks the serotonin-mediated empathogenic warmth of MDMA — where MDMA dissolves boundaries between self and others, methamphetamine sharpens them, producing a hard-edged, inward-directed focus that registers as either productive concentration or anxious hypervigilance depending on set and setting.
Effect Grid
At common doses (10–25 mg oral), the full stimulant experience is present: pronounced euphoria, significant energy and wakefulness, marked appetite suppression, and increased sociability. Thought acceleration is prominent — ideas come rapidly and may feel unusually clear or important. Motivation and confidence increase substantially. Some users report enhanced empathy and talkativeness at the lower end of this range.
Cardiovascular effects become significant: elevated heart rate (10–20 bpm above baseline), increased blood pressure, and peripheral vasoconstriction. Bruxism, dry mouth, and urinary retention are common. Body temperature may rise slightly. Sweating increases.
Sleep is impossible for 6–10 hours after oral dosing at this range. Appetite is profoundly suppressed. Functional activities requiring focus may feel enhanced, though complex decision-making can be impaired by overconfidence.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Sound sensitivity · Auditory enhancement · Visual haze / noise · Brightness alteration · Auditory misinterpretation · Peripheral misidentification · Visual drifting · Auditory distortion · Spatial disorientation · Auditory hallucinations · External hallucinations · Shadow people · Olfactory hallucination · Object transformations · Internal hallucinations · Persisting hallucinations
Auditory misinterpretation · Peripheral misidentification · Visual drifting · Auditory distortion · Spatial disorientation · Auditory hallucinations · External hallucinations · Shadow people · Olfactory hallucination · Object transformations · Internal hallucinations · Persisting hallucinations
Wakefulness · Dry mouth · Insomnia · Dehydration sensation · Excessive sweating · Muscle tension · Body high · Heart rate perception changes · Physical fatigue · Restlessness · Respiratory stimulation · Spontaneous body sensations · Temperature dysregulation · Bruxism · Sexual arousal enhancement · Constipation · Tactile euphoria · Tingling / electric sensations · Sexual arousal suppression · Headache · Nausea · Trembling · Vibrations / buzzing · Involuntary body movements · Seizure threshold reduction · Dizziness · Motor control impairment · Motor control enhancement · Vomiting · Tactile hallucination
Dehydration sensation · Excessive sweating · Muscle tension · Body high · Heart rate perception changes · Physical fatigue · Restlessness · Respiratory stimulation · Spontaneous body sensations · Bruxism · Sexual arousal enhancement · Constipation · Tactile euphoria · Tingling / electric sensations · Sexual arousal suppression · Headache · Nausea · Trembling · Vibrations / buzzing · Involuntary body movements · Seizure threshold reduction · Dizziness · Motor control impairment · Motor control enhancement · Vomiting · Tactile hallucination
Focus enhancement · Motivation enhancement · Motivation suppression · Cognitive dysphoria · Information processing enhancement · Cognitive impairment · Immersion enhancement · Aesthetic enhancement · Analysis enhancement · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Thought loops · Thought organization · Creativity enhancement · Language enhancement · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought disorganization · Memory enhancement · Humor enhancement · Confusion · Delusions of sobriety · Information processing suppression · Memory fragmentation · Memory suppression · Suggestibility enhancement · Thought deceleration · Delusions · Delirium
Cognitive dysphoria · Information processing enhancement · Cognitive impairment · Immersion enhancement · Aesthetic enhancement · Analysis enhancement · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Thought loops · Thought organization · Creativity enhancement · Language enhancement · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought disorganization · Memory enhancement · Humor enhancement · Confusion · Information processing suppression · Memory fragmentation · Memory suppression · Suggestibility enhancement · Thought deceleration · Delusions · Delirium
Anxiety · Dysphoria · Emotional enhancement · Emotional lability · Empathy enhancement · Suicidal ideation · Empathy suppression · Mania
Emotional lability · Empathy enhancement · Empathy suppression · Mania
Communication enhancement · Flow state · Sociability enhancement · Automaticity · Emotional susceptibility · Sociability suppression · Social connection · Social disconnection · Communication suppression · Trust enhancement · Self-control enhancement · Depersonalization · Derealization
Emotional susceptibility · Sociability suppression · Social connection · Social disconnection · Communication suppression · Trust enhancement · Self-control enhancement · Depersonalization · Derealization
Timeline
First alerts appear 15–30 minutes after ingestion: a subtle brightening of mood, mild increase in alertness, and faint body warmth. Effects are barely distinguishable from placebo at this stage.
Stimulation builds steadily over 30–90 minutes. Euphoria, increased energy, and appetite suppression become clearly perceptible. Heart rate rises.
Full stimulant intensity is sustained for 2–4 hours. Pronounced euphoria, wakefulness, thought acceleration, and sociability dominate. Cardiovascular activation is significant.
Effects gradually diminish but remain clearly present for 2–3 hours. Stimulation persists without the euphoric peak. Focus may narrow or become compulsive.
The comedown spans 1–2 hours. Fatigue, irritability, and mild depressed mood emerge as stimulant effects recede. Appetite begins to return.
Residual effects persist for 6–24 hours: mild fatigue, low mood, impaired concentration, and disturbed sleep architecture. Some individuals experience rebound hypersomnia and hyperphagia.
⚠ Do not drive or operate machinery during the comedown and afterglow period; stimulant-related fatigue and impaired reaction time persist well beyond the subjective experience.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- High
- Withdrawal
- Moderate
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- Moderate
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- High
- Cross-tol.
- amphetamine · cocaine · methylphenidate
Toxicity
Acute toxicity
Acute methamphetamine toxicity presents as a stimulant overdose syndrome: dangerously elevated body temperature, severe high blood pressure, rapid heart rate, agitation, and seizures.[3] In one emergency department series, methamphetamine was implicated in 72% of agitated patient presentations.[22] No human lethal dose has been established — individual sensitivity varies enormously, and deaths have occurred at doses far below predictions from animal data.safety citation needed
Heart and circulation
Cardiovascular complications are the second leading cause of death in methamphetamine users.[6] These include severe high blood pressure from norepinephrine release, heart muscle damage (methamphetamine-associated cardiomyopathy, partially reversible with abstinence), pulmonary arterial hypertension with severity comparable to the idiopathic form,[23] heart attacks, aortic tears, and abnormal heart rhythms.
Reduced carboxylesterase 1 activity may contribute to blood vessel damage through oxidative stress.[24]
Stroke
Methamphetamine is a significant cause of stroke in adults under 45.[25] Yen et al. documented 7 consecutive cases of stroke following methamphetamine inhalation (mean age 32): 5 hemorrhagic and 2 ischemic, all within 3 days of use.[26] Mechanisms include acute blood pressure spikes, blood vessel spasm, and drug-induced vessel inflammation.
Brain damage
Chronic use produces persistent reductions in DAT density (23–25% in key motor regions by brain imaging),[7] gray-matter loss in emotional regulation areas (11.3%), hippocampal shrinkage (7.8%), and white-matter changes (7.0%).[19] These deficits persist years into abstinence and correlate with memory suppression.
Reproductive toxicity
Prenatal methamphetamine exposure produces developmental delay, growth restriction, and sensorimotor deficits in animal models. Adverse outcomes have been documented in neonates born to methamphetamine-using mothers.[27]
Psychological risks
Methamphetamine-induced psychosis — paranoid delusions, auditory and visual hallucinations, and persecutory ideation — occurs at high doses or after prolonged use. Acute episodes are typically self-limiting.[28]
The critical long-term risk is sensitization to psychosis. Chronic use produces lasting vulnerability: even after prolonged abstinence, small methamphetamine doses — or non-drug stressors including sleep deprivation and psychological stress — can reliably trigger acute psychotic recurrence indistinguishable from the initial episode.[21][29] This sensitization has no established time limit for resolution.
Persistent psychosis is associated with more severe cognitive impairment, suggesting that psychosis vulnerability may serve as a marker for underlying brain damage.[30]
Tolerance & dependence
Methamphetamine carries extremely high addiction liability, producing among the strongest behavioral sensitization of any drug of abuse.[5] Tolerance develops through downregulation, with neuroimaging confirming persistent dopamine transporter reductions after years of abstinence[7] — reflecting structural nerve terminal loss rather than reversible adaptation.
Simultaneously, behavioral sensitization to rewarding effects develops, creating the paradox of increasing response to some drug effects while tolerance develops to others. Cross-tolerance within the dopaminergic stimulant class is established.
Withdrawal is characterized by depression, fatigue, excessive sleep, appetite enhancement, anhedonia, and cognitive impairment. No FDA-approved medication exists for methamphetamine use disorder.[8][31] The evidence base for withdrawal treatment remains poor,[32] though mirtazapine, naltrexone, and bupropion show potential.[33] The combination of extended-release naltrexone and bupropion has the strongest trial evidence to date.[34]
Drug interactions
Monoamine oxidase inhibitors
The combination of methamphetamine with any MAOI — irreversible (phenelzine, tranylcypromine), reversible (moclobemide), or dietary (Syrian rue) — is among the most dangerous drug combinations in pharmacology. It can produce fatal blood pressure crisis, serotonin syndrome, and brain hemorrhage.[35] This combination is absolutely contraindicated.
Serotonergic agents
Methamphetamine's serotonin-releasing activity, while weak relative to its dopamine effects, becomes clinically significant when combined with serotonin reuptake inhibitors (SSRIs, SNRIs), tramadol, or other serotonergic drugs. The combined serotonergic burden creates risk for serotonin syndrome — a potentially fatal condition presenting as dangerously elevated body temperature, muscle rigidity, and cardiovascular instability.[36] Tramadol compounds this risk by additionally lowering the seizure threshold.safety citation needed
CYP2D6 inhibitors
Fluoxetine, paroxetine, bupropion, and quinidine inhibit methamphetamine's primary metabolic pathway, increasing systemic exposure and elevating cardiovascular and CNS toxicity risk.[3] This metabolic interaction compounds the serotonergic risk of SSRIs.
Other stimulants
Combination with MDMA, amphetamine, or cocaine produces additive cardiovascular strain — high blood pressure, rapid heart rate, elevated body temperature — and amplified neurotoxicity risk. Methamphetamine combined with MDMA carries particular concern for serotonin syndrome through combined serotonin release.
CNS depressants
Alcohol, GHB/GBL, and benzodiazepines may mask methamphetamine intoxication severity, creating risk for delayed recognition of either stimulant toxicity or depressant overdose. GHB combined with methamphetamine is common in chemsex contexts; the stimulant effect may mask respiratory depression risk if GHB dosing is escalated.
Contraindications
Absolute
- Concurrent MAOI use: Fatal blood pressure crisis, serotonin toxicity, and brain hemorrhage are documented consequences[35]
- Severe heart or blood vessel disease: Including uncontrolled high blood pressure, heart muscle damage, recent heart attack, and aortic aneurysm[3]
- Overactive thyroid: Stimulant effects compound thyroid-mediated cardiovascular stress
- History of drug-induced psychosis: Sensitization produces lasting vulnerability to psychotic recurrence[21]
- Glaucoma: pupil dilation and stimulant effects raise eye pressure
Relative
- History of abnormal heart rhythm or heart muscle damage: Noradrenergic effects worsen cardiac conduction problems
- Concurrent serotonergic medications: SSRIs, SNRIs, tramadol — serotonin syndrome risk[36]
- History of seizures: Methamphetamine lowers seizure threshold
- Pregnancy: Prenatal exposure associated with adverse outcomes[27]
- Bipolar disorder: Stimulant exposure may trigger manic episodes
Harm Reduction[edit]
Forms & Identification
Crystal methamphetamine's appearance — translucent shards or white crystalline powder — provides no reliable information about purity, potency, or adulterant content. Industrial-scale production has increased average purity in many markets, but this also means dose estimation by eye or weight carries less margin for error than when street product was more adulterated.
Reagent testing confirms the presence of a methamphetamine-type compound but cannot distinguish d-methamphetamine from the inactive l-enantiomer or detect dangerous cutting agents at low concentrations. Fentanyl test strips are strongly recommended in any market where opioid contamination of stimulant supply has been documented, as even trace fentanyl contamination can be fatal in users without opioid tolerance.
Guidelines
- Test every batch with reagent kits and fentanyl test strips before use
- Start with the lowest effective dose and wait for full onset before redosing — oral onset requires 15–30 minutes
- Set a firm time limit for the session; methamphetamine's long duration makes it easy to extend use into multiple days
- Stay hydrated with water or electrolyte drinks — aim for regular sips rather than large volumes
- Eat before and during use; appetite suppression masks caloric need
- Avoid redosing to chase the initial rush — this is the pattern most associated with binge use and escalating toxicity
- Monitor body temperature; if you feel overheated, cool down actively with cold water and air circulation
- Have a trusted person aware of your use who can check in
Set & Setting
Route of administration is the single most important risk modifier. Oral use produces gradual onset and manageable intensity; smoked and injected routes deliver a rapid, intense rush that substantially increases addiction liability and cardiovascular strain. Choosing oral administration over non-oral routes is the single most effective harm reduction decision for this substance.
Environment matters. A controlled, familiar setting with trusted people present reduces the likelihood of anxiety escalation and paranoid ideation. Sleep deprivation, dehydration, and high ambient temperature amplify both cardiovascular risk and psychological distress.
Aftercare & integration. The methamphetamine comedown is dominated by dopamine depletion: expect low mood, fatigue, appetite enhancement, and difficulty concentrating for 1–3 days after use, potentially longer after extended binges. Sleep is the most important recovery tool — prioritize it above all else, and do not use more methamphetamine to counteract the crash.
Eat nutrient-dense meals even when appetite is low; protein and complex carbohydrates support neurotransmitter recovery. Hydrate consistently. Avoid making significant decisions during the acute comedown, as anhedonia and cognitive fog distort judgment. If low mood persists beyond a week, or if paranoid thinking does not resolve fully, seek professional evaluation — these can be early signs of a more sustained withdrawal.
Recovery & Support
Methamphetamine use disorder is among the most difficult substance addictions to treat, but recovery is achievable. No FDA-approved medication currently exists for methamphetamine dependence,[8] though the combination of extended-release naltrexone and bupropion shows the strongest clinical trial evidence to date.[34]
Behavioral therapies remain the primary evidence-based treatment: contingency management (incentive-based programs rewarding abstinence) and cognitive-behavioral therapy have the most consistent support. Peer support through groups such as Crystal Meth Anonymous provides community structure during recovery.
Anyone experiencing persistent psychotic symptoms, sustained depression, or inability to stop use despite wanting to should seek professional help. The sensitization to psychosis that develops with chronic use means that any return to methamphetamine — even at small doses — carries risk of acute psychotic recurrence, potentially for life.[21]
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: chest pain, seizure, loss of consciousness, body temperature hot enough to feel through clothing, severe confusion, or psychotic behavior (threatening self or others) all require immediate medical attention. An uncomfortable but manageable stimulant experience — anxiety, restlessness, rapid heartbeat — becomes an emergency when these signs appear.
Immediate steps:
- 1. Call emergency services if anyone shows the above signs
- 2. Move the person to a cool, quiet environment
- 3. Remove excess clothing and apply cool water to skin if overheated
- 4. Do not physically restrain unless there is immediate danger of self-harm or harm to others
- 5. If the person is unconscious, place in the recovery position (on their side) and monitor breathing
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (methamphetamine), estimated amount and time of use, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
Methamphetamine is internationally controlled under the 1971 United Nations Convention on Psychotropic Substances (Schedule II), acknowledging therapeutic utility under strict controls while classifying the substance as having high abuse potential.[4] It occupies an unusual regulatory position: one of few Schedule II substances for which a pharmaceutical preparation (Desoxyn) remains approved and marketed, while simultaneously ranking among the most widely manufactured illicit drugs globally.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule II (Controlled Substances Act) | High abuse potential with accepted medical use. Desoxyn FDA-approved for ADHD and short-term obesity. Severe federal penalties for non-medical manufacture, distribution, and possession.[37] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Highest restriction tier. Maximum penalties: life imprisonment for supply/production; 7 years for possession.[37] |
| Canada | Schedule I (CDSA) | No authorized pharmaceutical use. Maximum criminal penalties for trafficking, production, and import/export.[38] |
| Australia | Schedule 8 (SUSMP) | Controlled medicine requiring prescription with strict prescribing and dispensing requirements.[37] |
| European Union | Varies by member state | Member states implement the 1971 Convention individually. Not approved for medical use in EU. Classification generally equivalent to Schedule I or Class A. |
| International | Schedule II (1971 UN Convention) | Permits medical use under national control with international manufacturing and trade restrictions.[4] |
references
- [1]
- [2] ^abcSulzer D, Chen TK, Lau YY, Kristensen H, Rayport S, Ewing A (1995) Amphetamine redistributes dopamine from synaptic vesicles to the cytosol and promotes reverse transport — Journal of Neuroscience PMID:7751968
- [3]
- [4]
- [5] ^abcdCourtney KE, Ray LA (2014) Methamphetamine: an update on epidemiology, pharmacology, clinical phenomenology, and treatment literature — Drug and alcohol dependence doi:10.1016/j.drugalcdep.2014.08.003
- [6] ^abParatz ED, Cunningham NJ, MacIsaac AI (2016) The Cardiac Complications of Methamphetamines — Heart, Lung and Circulation doi:10.1016/j.hlc.2015.10.019