BRS6 → BRS4 — Neuroendocrine Control of Bioenergetic Recovery
Glucocorticoid signalling and glucose handling from BRS6 can constrain mitochondrial capacity in BRS4.
Dependency
BRS6 allocates cortisol rhythm, autonomic tone and glycaemic supply. Those mediators reach mitochondria as substrate, glucocorticoid signalling and redox pressure. BRS4 then determines whether ATP generation and recovery keep pace.
Principal Routes
| Route | Contribution to BRS4 | Relationship |
|---|---|---|
| Glucocorticoid signalling | Can induce mitochondrial allostatic load | Direct |
| Glucose / insulin instability | Alters mitochondrial fuel supply and glucotoxicity risk | Direct |
Network Interpretation
This is a primary stress-to-energy bridge. Downstream inflammatory and transmitter effects may continue as BRS6 → BRS4 → BRS3 → BRS1 (see BRS6 → BRS1). Gut metabolites are not part of this page.
Boundary and Evidence Status
Mitochondrial allostatic load is a reviewed mechanistic model, not a demonstrated ADHD pathway. The dependency does not establish that changing cortisol or meal pattern restores mitochondrial function or clinical outcomes.
Supporting Evidence
- Picard, Juster and McEwen, 2014 — Proposes mitochondrial allostatic load as a route by which glucocorticoids, glucose imbalance and chronic stress damage bioenergetic capacity.
- McEwen, 2006 — Reviews protective and damaging effects of stress mediators, including metabolic allocation under sustained demand.