PH001 — Focus / Attention Stability
Capacity to sustain, shift, and regulate attention across changing cognitive demands.
How steadily a person can hold, shift, and return attention when tasks or distractions change.
Therapeutic areas: TA001 ★TA002TA004TA005TA006TA007
Provenance: Core Version 1 ADHD registry phenome (pre-v3). Benchmarked against RDoC Cognitive Systems (attention, cognitive control) and distinguished from Cognitive Clarity (PH011) as sustained/shifted attention versus processing clarity. (origin: BRAIN)
Related phenomes: PH002 — Motivation / Drive, PH011 — Cognitive Clarity
External framework cross-references
RDoC domains
- Cognitive Systems — attention
- Cognitive Systems — cognitive control
DSM / ICD context
- Attention-deficit/hyperactivity disorder
Foundational Evidence
Registry-level Phenome Evidence Confidence (below) is independent of Biology → Phenome Confidence and Evidence Confidence on individual mechanism pages. Use the scoring guide for definitions of all three scores.
These are three independent scores. They are not combined or averaged. A phenome can have Medium registry evidence while individual mechanism rows show different Biology → Phenome and Evidence scores.
1. Phenome Evidence Confidence (Phenome Registry only)
Question: How convincing is the foundational evidence that this phenome is a valid, well-defined functional construct — and that diet-relevant biology can plausibly connect to it?
Not a roll-up of Biology → Phenome Confidence or Evidence Confidence from Primary Mechanism page rows. Those are scored per mechanism; this score is assigned once per phenome at registry level.
Derived from foundational landmark evidence organised in up to three layers: construct validation, biology→phenome linkage, and nutrition→biology modulation. Each layer may include one or many landmark papers depending on registry review.
2. Biology → Phenome Confidence (Primary Mechanism page §3 rows)
Question: If this PM/FM biology were substantially impaired in isolation, how directly would that phenome be expected to suffer — within BRAIN architecture?
How it is derived: Reviewers read the PM/FM definition and biological function first — initially ignoring attached references and whether dietary intervention studies exist. References are reviewed only when scoring Evidence Confidence (below).
Score levels (the value shown on each row as Biology → Phenome Confidence):
- High — primary biological determinant (e.g. noradrenergic signalling → attention; GABA synthesis → calming tone)
- Medium — major contributory determinant, not the sole driver
- Low–Medium — established but indirect, modulatory, or one integrative step removed
- Low — distal, conditional, or weak biological coupling
“Not dietary treatment efficacy” means this score does not ask whether a diet or supplement treats the phenome. It asks whether the biology itself is architecturally relevant. Limited dietary RCT evidence belongs in Evidence Confidence, not here.
3. Evidence Confidence (Primary Mechanism page §3 rows)
Question: How convincing are the attached Key References on that specific row that this biology actually relates to this phenome?
How it is derived: Assigned after Biology → Phenome Confidence, by reviewing only the references on that PM/FM row. Judges whether refs support the relationship — not just mechanism or phenome in isolation.
- High — strong convergent human evidence directly linking mechanism biology to phenome variation
- Medium — multiple human lines supporting the relationship; may include one bridge study with an inferential step
- Low–Medium — convergent translational stack without direct mechanism↔phenome measurement on the row
- Low — mechanistic or preclinical only; mechanism and phenome supported separately but not bridged
Often equal to or lower than Biology → Phenome Confidence. Can occasionally be higher when outcome evidence is stronger than the mechanism's contributory role.
Phenome Evidence Confidence: Low–Medium
ADHD-focused construct and precursor-transport biology are well represented; human dietary attention-outcome evidence on the registry stack is indirect (omega-3 cognition trials) — not dietary ADHD treatment efficacy.
Construct landmark papers
- Millichap & Yee (2012) — Reviews diet and nutritional factors in ADHD — foundational construct framing for attention phenotypes.
- Aquili (2020) — Reviews catecholaminergic neurotransmission and attentional function relevant to ADHD biology.
Biology → phenome landmark papers
- Fernstrom (2013) — Large neutral amino acid transport and precursor availability intersect monoaminergic attention pathways.
- Derbyshire & Maes (2023) — Links oxidative stress and neuroinflammation biology to ADHD symptom domains including attention.
Nutrition → biology landmark papers
- Wang et al. (2019) — Dietary patterns and amino-acid context modulate neurotransmitter precursor biology upstream of attention.
- Oulhaj et al. (2016) — Omega-3 supplementation associated with cognitive performance improvements in ageing — adjacent human nutrition→cognition support.
Connected mechanisms
- BRS-X(Hormones-PM1) — Oestrogen Signalling Stability (indirect · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
BRS1
- BRS1-FM1-PM1 — Amino-Acid Availability & Prioritisation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS1-FM1-PM2 — LAT1 Competitive Transport Modulation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS1-FM1-PM3 — Noradrenergic Signalling (modulates · Biology → Phenome: High · Evidence: Low–Medium)
- BRS1-FM2-PM5 — Acetylcholine Synthesis Support (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS1-FM3-PM6 — Neuronal Membrane DHA Incorporation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS1-FM4-PM7 — GABA–Glutamate Neurotransmission Balance (modulates · Biology → Phenome: High · Evidence: Low–Medium)
- BRS1-FM4-PM9 — Glutamate Clearance & Recycling (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
BRS2
- BRS2-FM1-PM1 — Folate/B12-Dependent Homocysteine Remethylation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS2-FM1-PM2 — Betaine/BHMT Remethylation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS2-FM1-PM4 — Methionine Cycle Flux (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS2-FM3-PM7 — Phosphatidylcholine Formation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
BRS3
- BRS3-FM1-PM1 — NF-kB Signalling Regulation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM1-PM2 — Gut-Derived Inflammatory Signalling (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM2-PM3 — Nrf2-ARE Antioxidant Activation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM2-PM4 — ROS Generation vs Clearance Balance (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM2-PM5 — Lipid Peroxidation Control (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM3-PM7 — Cytokine Network Modulation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS3-FM3-PM8 — Eicosanoid / SPM Balance (modulates · Biology → Phenome: Low · Evidence: Low)
BRS4
- BRS4-FM1-PM1 — Electron Transport Chain Function (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS4-FM3-PM6 — Carnitine-Mediated Fat Transport (modulates · Biology → Phenome: Medium · Evidence: Medium)
BRS5
- BRS5-FM1-PM1 — Gut Barrier / Tight Junction Integrity (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS5-FM1-PM2 — LPS / Endotoxin Containment (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS5-FM1-PM3 — Keystone Taxa Support (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS5-FM2-PM4 — Microbial Ecological Turnover & Competitive Selection (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS5-FM2-PM5 — SCFA Production & Signalling (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS5-FM3-PM8 — Neurotransmitter Precursor Biotransformation & Availability (modulates · Biology → Phenome: Low–Medium · Evidence: Low)
BRS6
- BRS6-FM1-PM1 — Glucose Appearance Kinetics (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)
- BRS6-FM1-PM2 — Glycaemic Variability Regulation (modulates · Biology → Phenome: Low–Medium · Evidence: Low–Medium)