Table 3.
Hypotheses of the allostatic triage model of psychopathology (ATP Model).
| H1. | Preexisting peripheral (AL) and/or CNS metabolic inefficiency (MAL), and increases in biological energy demand such as acute inflammation will increase the experience of negative affect during stress |
| H2. | Affect will closely represent biological metabolic efficiency in healthy organisms, likely within the biological systems and CNS networks implicated in expected future behaviors |
| H3. | Allostatic Triage: when stress-induced energy demand exceeds the energy production capacity of the CNS, energy will be triaged to the least expensive regions and networks expected to ensure short-term survival, and away from more expensive regions and networks that may produce better long-term outcomes |
| H4. | Affect-Driven Prioritization: Affective intensity predicts the degree of stress-induced triage of CNS network functional connectivity (e.g., highly negatively valanced states will produce greater triage compared to less negatively valanced states) |
| H5. | In psychopathology and chronic disease states, affect will become less associated with biological metabolic efficiency (reduced allostatic metabolic inefficiency), but will continue to predict allostatic triage in the CNS |
| H6. | Triage-Driven Canalization: Persistent allostatic triage from one network or circuit to another will predict the persistent changes in CNS functional connectivity that develop over time in the process of psychopathogenesis (i.e., allostatic triage predicts which networks are canalized) |
AL: Allostatic Load, CNS: Central Nervous System, MAL: Mitochondrial Allostatic Load.