Arts Engagement, Active Inference, and Allostatic Regulation: A Neurobiological Framework for Understanding the Health Effects of Aesthetic Experience

A growing body of evidence indicates that arts engagement produces measurable effects on mental and physical health, yet a mechanistic account linking aesthetic experience to physiological regulation remains lacking. This review proposes a neurobiological framework grounded in two convergent theoretical traditions: the active inference formulation of brain function and the allostatic model of physiological regulation. Both frameworks describe organisms as anticipatory systems that maintain viability through model-based predictive control. When active inference chronically fails as in sustained stress, trauma, or learned helplessness, the resulting allostatic load produces systemic metabolic dysregulation and disease vulnerability. This review argues that arts engagement provides contexts optimally suited to restoring effective active inference across sensorimotor, cognitive, affective, and social timescales, thereby recalibrating allostatic regulation. Arts engagement is positioned not as the only activity capable of producing such effects, but as a distinctive and potentially major instance of structured agentic experience, distinguished by its simultaneous engagement of multiple levels of the predictive hierarchy, its intrinsic epistemic motivation, and its capacity to sustain graded uncertainty without pragmatic consequence. A schematic computational specification of the framework is provided, identifying the generative model structure, precision parameters, and expected free energy decomposition relevant to arts-mediated allostatic recalibration. The framework is systematically compared with six alternative accounts of arts-health effects, showing where predictions converge and diverge. Developmental and lifespan perspectives are elaborated, with specific predictions for critical-period effects. The framework generates directional hypotheses for metabolomic, neuroendocrine, and neuroimaging studies, including predictions that distinguish the proposed mechanism from generic stress reduction.