Mechanical Agitation as a Dissipative Engine for Protocell Growth: Modeling Critical Slowing Down and Szostak's Cannibalism

Abstract

Classical in vitro experiments in abiogenesis frequently encounter the limitations of static, closed-test-tube environments. This paper presents a theoretical model of protocellular evolution, conceptualizing the early Earth as an open nonlinear system driven by persistent mechanical agitation (tidal forces, geothermal shearing). We bridge the colloid chemistry of fatty acid vesicles with Prigogine’s thermodynamics of dissipative structures far from equilibrium. Using Python-based simulations, we model the phenomenon of Critical Slowing Down (CSD) at the membrane interface. Our results demonstrate that repeated mechanical stress leads to material fatigue, expanding the relaxation time (beyond 10 seconds) and driving a sharp increase in lag-1 autocorrelation from 0.75 to 0.96, signaling proximity to a bifurcation point. We formulate an epistemological limit: in the CSD state, the system’s energy landscape flattens, making it impossible to precisely measure the true equilibrium state within a finite observation time. Crucially, we demonstrate that this accumulated mechanical tension in the unstable CSD state acts as a dissipative engine. It overcomes the chemical activation barrier to trigger the kinetics of Szostak's cannibalism—assimilating free amphiphiles from the environment. This process relaxes membrane tension and re-stabilizes the vesicle into a new stable state with a higher level of organization. Thus, the mechanical turmoil of the early Earth was not a destructive agent, but the primary evolutionary partner of protocells.