Dimensional Constraints in the Etiology of Neurosis (A Biophysically Constrained Thermodynamic Model)

Abstract Previous formulations of the Etiology of Neurosis framework proposed a causal relationship between SRGAP2C-induced synaptic expansion and thermodynamic instability through heuristic equivalences between information entropy and energetic cost. While conceptually useful, such formulations lacked dimensional homogeneity. Here, we formalize a framework wherein information entropy (H) is reconceptualized not as a direct energetic driver, but as a structural constraint coupled to metabolic expenditure via a phenomenological conversion coefficient (α). Integrating Karl Friston’s Free Energy Principle (FEP), we propose that neurosis is not a deterministic consequence of genetic expansion, but a dynamic instability emerging when regulatory control mechanisms—particularly Default Mode Network (DMN) suppression efficiency—fail to manage a high-dimensional neural state space. Finally, we utilize the asymptotic regulatory ideal of Minimum Entropy Production (MEP), aligning the framework with non-equilibrium thermodynamics constraints. This establishes a dimensionally consistent and falsifiable biophysical model linking evolutionary neurogenetics, metabolic efficiency, and large-scale network regulation.