Surprise! Using Physiological Stress for Allostatic Regulation Under the Active Inference Framework
Allostasis proposes that long-term viability of a living system is achieved through anticipatory adjustments of its physiology and behaviour: emphasising physiological and affective stress as an adaptive state that minimises long-term prediction errors. More recently, the active inference framework (AIF) has also sought to explain action and long-term adaptation through the minimisation of future errors (free energy), through the learning of statistical contingencies of the world, offering a formalism for allostatic regulation. We suggest that framing prediction errors through the lens of biological hormonal dynamics proposed by allostasis offers a way to integrate these two models together in a biologically-plausible manner. In this paper, we describe our initial work in developing a model that grounds prediction errors (surprisal) into the secretion of a physiological stress hormone (cortisol) acting as an adaptive mediator on a homeostatically-controlled physiology. We evaluate this using a computational model in simulations using an active inference agent endowed with an artificial physiology, regulated through homeostatic and allostatic control in a stochastic environment. Our results find that allostatic functions of cortisol (stress), secreted as a function of prediction errors, provide adaptive advantages to the agent's long-term physiological regulation. We argue that the coupling of information-theoretic prediction errors to low-level, biological hormonal dynamics of stress can provide a computationally efficient model to long-term regulation for embodied intelligent systems.
Authors
- Robert Lowe (ORCID: https://orcid.org/0000-0002-1525-0745)
- Imran Khan (ORCID: https://orcid.org/0000-0002-8483-2896)
Institutions
- University of Gothenburg (SE)
Publication Details
- Published
- 2024-09-15
- DOI
- https://doi.org/10.1109/acii63134.2024.00024
- Primary Topic
- Mental Health Research Topics
- Type
- article
- Field-Weighted Citation Impact
- 0.00