MJB ADHD · Static reading view · Interactive version
Status: sourced-draft · Content checked 2026-10-06
Precursor supply, reuptake inhibition, transmitter release and receptor activation are different interventions. Compare the indication and evidence as well as the mechanism.
“Acts on dopamine” does not identify one treatment class or one shared disease. The same shorthand can describe medicines doing substantially different jobs. Start with what is being treated and how benefit is measured.

Separate: guanfacine is an alpha-2A adrenergic agonist, not a dopamine-receptor agonist. F6, W1.
Ask beside each: indication, outcome, preparation, monitoring. No potency or safety ladder. US labels are not UK availability. Illicit stimulants are not a treatment ladder.
| Intervention | Main distinction | Evidence and context |
|---|---|---|
| Levodopa | Dopamine precursor; commonly paired with carbidopa or benserazide | Established Parkinson symptom treatment; specialist use for specific movement disorders F12N7 |
| Methylphenidate | Dopamine/noradrenaline reuptake inhibition | ADHD treatment; individual response and formulation matter W1 |
| Dexamfetamine | Catecholamine release and transporter effects | ADHD treatment; differs from a dopamine precursor R8W1 |
| Lisdexamfetamine | Prodrug converted to dexamfetamine | Conversion changes exposure timing; it is not levodopa R10 |
| Adderall | Mixed amphetamine salts | US ADHD product; not identical to dexamfetamine-only medicine F7 |
| Atomoxetine | Noradrenaline-transporter inhibition | ADHD treatment with its own evidence and response profile F5W1 |
| Guanfacine | Alpha-2A adrenergic receptor agonist | Receptor target differs from a dopamine agonist; adult UK use needs tertiary-service advice under NG87 F6W1 |
| Dopamine agonists | Activate dopamine receptors | Parkinson options with specific benefits and impulse-control risks F9 |
| Saffron | Human ADHD evidence exists; therapeutic mechanism remains unresolved | Preliminary studies do not establish equivalence to a selective dopamine reuptake inhibitor F1 |
| Mucuna | Contains levodopa | Parkinson studies require attention to preparation and population F3F4 |
Ask what symptom or impairment an option is meant to improve; which population was studied; what monitoring is needed; and why this option fits your clinical assessment. An inadequate response should lead to a review of the plan and alternatives.
Cocaine blocks dopamine reuptake; exposure and effects also depend on delivery. Crack is a smokeable form of cocaine. Shared stimulant mechanisms do not make different substances or preparations therapeutically interchangeable.
F8Methamphetamine has a US prescription ADHD product label. That does not establish the safety, quality or clinical equivalence of illicit methamphetamine, or current UK prescribing availability.
F13This is a pharmacology comparison. Cocaine/crack are not established ADHD treatments. No evidence reviewed here supports using them as substitutes for a prescribed treatment plan. Regulated formulation, delivery, evidence, interactions and monitoring are substantive parts of treatment.
Calling every non-stimulant a general stabiliser overlooks that atomoxetine is an ADHD treatment and guanfacine has a specific receptor target. Calling every “agonist” a dopamine agonist confuses different receptor families.
NICE recommends atomoxetine for adults unable to tolerate, or inadequately responding to, specified stimulant trials. Adults with persistent non-response after stimulant and non-stimulant treatment warrant specialist escalation.
W1See How ADHD medicines act, What treatment trials show and Saffron and Mucuna: what the evidence actually says. Mechanism, regulatory label and clinical comparative evidence answer different questions. This page does not supply a safest-to-most-dangerous league table: a defensible comparison needs a particular patient group, preparation and outcome.
This targeted map is not a complete interaction review or a head-to-head comparison of every listed option. “More dopamine” is not a general measure of better function, and symptom response does not measure a person's dopamine concentration.