← Harm reduction

Amphetamine Pharmacokinetics

The long half-life (~10–11h) is the central harm reduction message. Set the time axis to 36h and see exactly what is still in your system the next morning, afternoon, and evening.

Test your substance. Speed sold in Europe varies enormously in purity (often 5–30% amphetamine sulfate). Cutting agents include caffeine, paracetamol, and increasingly cathinones. Reagent test kits confirm amphetamine presence.
Population-average PK. Amphetamine elimination is pH-dependent — individual diet, kidney function, and urinary pH all affect duration substantially.

Compound

kg

Vitamin C acidifies urine and speeds amphetamine elimination by ~50% (methamphetamine elimination by ~20%). The blue dashed line shows the curve with vitamin C supplementation. This is a documented harm reduction strategy — it does not eliminate risk but reduces duration.

Dose schedule

First dose
50mg
10mg200mg
Total: 50mg(0.71 mg/kg)
SHOW36h
020 Sub-threshold2060 Mild stimulant effects60150 Active effects150300 Strong — CV strain begins300600 High CV risk / hyperthermia
The next morning problem: With t½ ~11h, a dose taken at 10pm Saturday still has 53% of its peak concentration at 8am Sunday and 25% at 8am Monday. Set the time axis to 48h and take a dose at t=0 to see exactly what is in your system when Monday morning lectures start.

pH-dependent elimination: Amphetamine is a weak base (pKa 9.9). In acidic urine, more is in the ionised form and cannot be reabsorbed — elimination rate increases substantially. Vitamin C (ascorbic acid) acidifies urine and can reduce t½ by ~30–50%. Alkaline urine (baking soda, antacids) does the opposite — extending duration and increasing plasma levels. The blue dashed curve shows the vitamin C effect.

Methamphetamine vs amphetamine: Similar t½ but meth produces roughly 3× more dopamine release per unit plasma concentration and has greater CNS penetration. This means greater euphoria, greater cardiovascular strain, and greater neurotoxicity risk at equivalent plasma levels. The effect zones are scaled accordingly.

Dangerous combinations

MAOIsLETHAL

Hypertensive crisis and serotonin syndrome. Amphetamines cause massive monoamine release — MAOIs prevent their breakdown. Can be fatal within minutes. Never combine under any circumstances. Includes some antidepressants and linezolid.

Other stimulants (cocaine, MDMA, caffeine at high dose)SEVERE

Additive and potentially synergistic cardiovascular strain. Combined tachycardia, hypertension, and hyperthermia. Substantially increases risk of cardiac events and stroke.

LithiumSEVERE

Unpredictable interaction. Lithium can reduce stimulant effects (leading to dose escalation) but also increases serotonergic effects. Serious toxicity risk.

AlcoholMODERATE–HIGH

Amphetamine masks alcohol intoxication — people drink far more than they realise. The stimulant effect wears off before the alcohol does, causing sudden severe intoxication. Cardiovascular strain from both substances.

KetamineMODERATE

Combined cardiovascular strain from stimulant + anaesthetic. Amphetamine can mask ketamine sedation, leading to redosing. Disorientation and inability to assess own condition significantly increased.

CannabisMODERATE

Increased anxiety and paranoia. Cannabis used to "take the edge off" stimulant effects can unpredictably amplify anxiety instead. Cardiovascular effects additive.

Acidifying agents (vitamin C / ascorbic acid)INTERACTION — USEFUL

Acidic urine significantly speeds amphetamine elimination. Vitamin C supplementation is used as a harm reduction strategy to reduce duration and help comedown. Toggle the "Vitamin C" option to see the effect modelled.

Concerned about stimulant use? Jellinek.nl and Trimbos.nl offer free, confidential support.