PH002 — Motivation / Drive
Capacity to initiate effort, pursue goals, and maintain goal-directed behaviour.
How readily a person starts effort, pursues goals, and stays engaged with what matters to them.
Therapeutic areas: TA001 ★TA003TA004TA007
Provenance: Core Version 1 ADHD registry phenome. Benchmarked against RDoC Positive Valence Systems (motivation, reward learning) and kept distinct from Behavioural Activation (PH010) and Reward Regulation (PH009). (origin: BRAIN)
Related phenomes: PH009 — Reward Regulation, PH010 — Behavioural Activation
External framework cross-references
RDoC domains
- Positive Valence Systems — reward learning
- Positive Valence Systems — motivation / effort
DSM / ICD context
- Attention-deficit/hyperactivity disorder
- Major depressive disorder — motivational symptoms
Foundational Evidence
Evidence Confidence: Low–Medium
Registry-level score for this phenome's foundational evidence stack — not Biology → Phenome Confidence on individual mechanism pages.
Dopaminergic and endocannabinoid motivation biology are review-supported; open-label tyrosine and dietary precursor evidence is mechanistic or adjunct — not definitive motivation-intervention efficacy.
Registry-level foundational evidence for this phenome. Mechanism pages link to phenome IDs and carry relationship-specific evidence — not duplicated here.
Construct landmark papers
- MacDonald et al. (2024) — Reviews dopamine signalling in motivation and goal-directed behaviour.
- Aquili (2020) — Catecholaminergic neurotransmission framing for effort and drive biology.
Biology → phenome landmark papers
- Fernstrom (2013) — Precursor transport and tyrosine availability upstream of catecholaminergic drive circuits.
- Garani et al. (2021) — Endocannabinoid system modulation of motivation and stress-related behavioural states.
Nutrition → biology landmark papers
- Wurtman et al. (2003) — Dietary tyrosine and precursor manipulation affects catecholamine synthesis biology.
- Reimherr et al. (1987) — Open-label tyrosine supplementation in ADHD — early human adjunct evidence for drive/activation biology.
Connected mechanisms
BRS-X(ECS)
- BRS-X(ECS-PM1) — NAPE → NAE Biosynthesis Capacity (supports · low-medium)
- BRS-X(ECS-PM4) — Endocannabinoid–Dopamine Neuromodulation (supports · low-medium)
BRS-X(Hormones)
- BRS-X(Hormones-PM5) — Testosterone Signalling Stability (supports · medium)
- BRS-X(Hormones-PM6) — Androgen-Microbiome Regulation (indirect · low)
BRS1
- BRS1-FM1-PM1 — Amino-Acid Availability & Prioritisation (modulates · low-medium)
- BRS1-FM1-PM2 — LAT1 Competitive Transport Modulation (modulates · low-medium)
- BRS1-FM1-PM3 — Noradrenergic Signalling (modulates · medium)