PH003 — Emotional Regulation
Capacity to modulate emotional responses and maintain affective stability.
How well emotional responses can be modulated so mood and reactivity stay within a workable range.
Therapeutic areas: TA001 ★TA002TA003TA004TA006
Provenance: Core Version 1 ADHD registry phenome. Benchmarked against RDoC Negative Valence and Arousal/Regulatory Systems; distinct from Apprehensive Worry (PH016), Stress Reactivity (PH015), and Social Engagement (PH018). (origin: BRAIN)
Related phenomes: PH015 — Stress Reactivity, PH016 — Apprehensive Worry / Perseverative Thought, PH018 — Social Engagement Capacity
External framework cross-references
RDoC domains
- Negative Valence Systems — sustained affect / affective regulation
- Arousal and Regulatory Systems — affective regulation
DSM / ICD context
- Attention-deficit/hyperactivity disorder — emotional dysregulation
- Major depressive disorder
- Generalised anxiety disorder
Foundational Evidence
Evidence Confidence: Low–Medium
Registry-level score for this phenome's foundational evidence stack — not Biology → Phenome Confidence on individual mechanism pages.
Construct and inhibitory-balance biology are strong; registry nutrition layer draws on mood/anxiety intervention reviews — not direct emotional-regulation phenome trials.
Registry-level foundational evidence for this phenome. Mechanism pages link to phenome IDs and carry relationship-specific evidence — not duplicated here.
Construct landmark papers
- Oades et al. (2010) — Reviews dopamine and serotonin roles in motivation, affect, and ADHD-related emotional function.
- Edden et al. (2012) — GABA deficits in ADHD cohorts — construct validation for excitation–inhibition and affective control.
Biology → phenome landmark papers
- Fernstrom (2013) — Serotonergic precursor biology intersects affective modulation pathways.
- Briguglio et al. (2018) — Dietary neurotransmitter biology review spanning mood and anxiety-relevant serotonergic context.
Nutrition → biology landmark papers
- Kiecolt-Glaser et al. (2011) — Omega-3 lowered anxiety and inflammatory markers in stressed adults — upstream affective biology.
- Jackson et al. (2021) — Saffron RCT reported mood improvements — adjacent human nutrition→affective biology support.
Connected mechanisms
BRS-X(ECS)
- BRS-X(ECS-PM1) — NAPE → NAE Biosynthesis Capacity (modulates · low)
- BRS-X(ECS-PM2) — Omega-3-Derived Endocannabinoidome Signalling (modulates · low)
- BRS-X(ECS-PM3) — FAAH-Mediated Endocannabinoid Preservation (modulates · low)
- BRS-X(ECS-PM5) — Endocannabinoid Stress-Buffering Capacity (modulates · low-medium)
BRS-X(Hormones)
- BRS-X(Hormones-PM1) — Oestrogen Signalling Stability (modulates · low-medium)
- BRS-X(Hormones-PM2) — Estrobolome Regulation (modulates · low-medium)
- BRS-X(Hormones-PM3) — Progesterone-Supportive Microbial Metabolism (modulates · low)
- BRS-X(Hormones-PM4) — Metabolic-Reproductive Hormone Integration (indirect · low)
- BRS-X(Hormones-PM5) — Testosterone Signalling Stability (modulates · low)
- BRS-X(Hormones-PM6) — Androgen-Microbiome Regulation (indirect · low)
BRS1
- BRS1-FM1-PM1 — Amino-Acid Availability & Prioritisation (modulates · low)
- BRS1-FM1-PM2 — LAT1 Competitive Transport Modulation (modulates · low)
- BRS1-FM1-PM4 — Serotonergic Signalling Regulation (supports · high)
- BRS1-FM3-PM6 — Neuronal Membrane DHA Incorporation (modulates · medium)
- BRS1-FM4-PM7 — GABA–Glutamate Neurotransmission Balance (modulates · medium)
- BRS1-FM4-PM8 — GABA Synthesis Capacity (modulates · medium)
- BRS2-FM1-PM3 — SAMe Synthesis (indirect · low-medium)
BRS3
- BRS3-FM1-PM1 — NF-kB Signalling Regulation (modulates · low)
- BRS3-FM1-PM2 — Gut-Derived Inflammatory Signalling (modulates · low)
- BRS3-FM2-PM4 — ROS Generation vs Clearance Balance (modulates · low)
- BRS3-FM2-PM5 — Lipid Peroxidation Control (modulates · low)
- BRS3-FM2-PM6 — Antioxidant Network Recycling (modulates · low)
- BRS3-FM3-PM7 — Cytokine Network Modulation (modulates · low-medium)
- BRS3-FM3-PM8 — Eicosanoid / SPM Balance (modulates · low-medium)