ABSTRACT Medical physiology traditionally models intestinal peristalsis as a sequential hydraulic pump. While recent discoveries involving mechanoreceptors (Piezo channels) and pacemaker cells (Cajal) explain the biochemical triggers, current models overlook a fundamental thermodynamic constraint: the strict incompressibility of dense luminal fluids (ΔV = 0). Pushing such an incompressible mass via purely linear dynamics would cause a structural frontal collision, triggering the Law of Toxic Geometry and dissipating mechanical energy into localized, damaging Tensorial Heat (Q). In this study, we propose a paradigm shift based on Macroscopic Tensorial Mechanics 1. We hypothesize the intestine functions as a topological metamaterial—a crossed double logarithmic spiral network engineered according to the Law of Tensorial Economy. Under this framework, peristalsis is governed by the Tensorial Elastic Derivative (Ξ), which mathematically couples radial and axial velocities (vR/vL) to act as a continuous spatial dipole (a "Traveling CET"). By synchronizing an active rolling phase (Tensorial Systole) with a simultaneous, adjacent unrolling phase (Tensorial Diastole), the system converts linear input into pure spatiotemporal Torsion (τ). This coupled double-flow advances the incompressible mass while preserving total volumetric invariance and minimizing thermodynamic friction. Applying this biomechanical framework, Crohn's Disease "skip lesions" can be reinterpreted as focal topological collapses. A localized structural alteration of the spiral's constant angle (α) breaks the continuous dipole, forcing the segment to revert to linear hydraulic dynamics. This failure triggers localized thermodynamic dissipation (Q → MAX), presenting a mechanical explanation for the alternation between remission and relapse, and suggesting that inflammatory exacerbation partly represents a physiological response to contain a highly localized spatiotemporal burn.
Salvatore Leonardi (Sun,) studied this question.
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