The Central Homeorhetic Principle: Lipid-Organized Boundary Systems as Constraints on Cellular State Realization

Sequence information can specify molecular components, but specification is not equivalent to cellular state realization. A gene product contributes to living function only when the cell occupies a physical state in which gradients persist, compartments remain intact, diffusion and phase organization remain compatible with execution, and perturbations can be recovered without loss of viability. This gap defines a state-realization problem: what physical architecture constrains the feasible state space within which molecular programs can be executed, stabilized, reversed, or transformed? From this problem, I derive a set of substrate requirements: self-bounded aqueous interfaces, selective permeability, electrochemical asymmetry, tunable continuous physical variables, cross-scale coupling, recursive interaction with protein and information-memory systems, and measurable recovery dynamics. Lipid-organized boundary systems satisfy these requirements in an exceptionally integrated way in modern aqueous cellular life. I therefore propose the Central Homeorhetic Principle (CHP): cellular identity, robustness, and fate transitions are constrained by a distributed homeorhetic state architecture, with lipid-organized boundary systems occupying a privileged but nonexclusive substrate position. CHP is not a rejection of the Central Dogma, nor a claim that lipids alone determine phenotype. It is a complementary constraint framework that asks how molecular information becomes physically executable and dynamically sustainable. The proposed mechanism is a distributed constraint-sensing-enactment loop in which boundary-state variables are sensed, evaluated through thresholds, converted into regulatory responses, and recursively remodeled by execution and memory systems. The framework yields testable predictions concerning temporal precedence of boundary-state shifts, threshold-like fate transitions, recovery kinetics, state degeneracy, protocell persistence, and state-trajectory restoration. It is falsifiable if boundary-state variables consistently follow rather than precede commitment, fail to alter fate thresholds under controlled perturbation, or add no predictive power beyond molecular profiles.