The Itaconate Shunt within the GLA Framework — Diagram Series
Conceptual diagrams examining how immune–metabolic constraint described by the itaconate shunt
may interact with system-level control and recovery processes in the GLA framework.
Figure A1 — Placement of the Itaconate Shunt within the GLA Architecture
The itaconate shunt is positioned as an immune-metabolic mechanism operating within the broader GLA control
architecture, potentially amplifying energy limitation when upstream buffering and recovery systems fail to
resolve post-infectious stress.
Design note: Downward arrows only to avoid implying a single causal loop; the itaconate shunt is emphasized as a
contained immune-metabolic sub-layer rather than a primary system-level driver. :contentReference[oaicite:1]{index=1}
Figure A2 — Phenotype-Dependent Relevance of the Itaconate Shunt
The contribution of immune-metabolic suppression varies by GLA amplifier phenotype, aligning most strongly with
metabolic-dominant (M1) presentations and acting as a secondary lock-in mechanism in vascular-dominant (M2) disease.
Caption: The contribution of immune-metabolic suppression varies by GLA amplifier phenotype, aligning most strongly
with metabolic-dominant (M1) presentations and acting as a secondary lock-in mechanism in vascular-dominant (M2) disease. :contentReference[oaicite:1]{index=1}
Figure A3 — Phase Dependence: When the Itaconate Shunt Matters Most
Immune-metabolic suppression may emerge as a secondary stabilizing response early in disease but becomes most
impactful as a lock-in amplifier once baseline recovery capacity erodes.
Caption: Immune-metabolic suppression may emerge as a secondary stabilizing response early in disease but becomes
most impactful as a lock-in amplifier once baseline recovery capacity erodes. :contentReference[oaicite:1]{index=1}
Figure B1 — Different Questions, Different Layers
The itaconate shunt focuses on intracellular metabolic state, whereas GLA addresses system-level regulation of load,
recovery, and buffering.
Caption: The itaconate shunt focuses on intracellular metabolic state, whereas GLA addresses system-level regulation
of load, recovery, and buffering. :contentReference[oaicite:1]{index=1}
Figure B2 — Two Explanations of PEM (Side-by-Side)
Distinct mechanistic paths can converge on similar post-exertional symptom amplification.
Caption: Distinct mechanistic paths can converge on similar post-exertional symptom amplification. :contentReference[oaicite:1]{index=1}
Figure B3 — Treatment Risk Visualization (Control vs Capacity)
Interventions targeting metabolic throughput may be stabilizing or destabilizing depending on underlying control state.
Caption: Interventions targeting metabolic throughput may be stabilizing or destabilizing depending on underlying control state. :contentReference[oaicite:1]{index=1}