Mecanotransducción Interoceptiva Subumbilical: Validación Paramétrica del Protocolo Neumohidráulico IC-H para la Síntesis de Serotonina, GABA Entérico y Desactivación de la Red de Relevancia (Salience Network)

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Background: Neuro-mecanobiology and gastroenterology demonstrate that physical deformation of deep visceral and fascial abdominal layers regulates central emotional processing and autonomic tones. Objective: This short communication provides a reverse-engineering validation of the sub-umbilical biomechanical Cognitive Engineering (IC-H) protocol, optimized for mechanical neurotransmitter translocation and central Salience Network (SN) modulation using a unified forces baseline. Methods: The algorithm utilizes an ionic-protonic-lipidic priming phase (500 mL H2O + 1.5 g NaCl + H+ ions from citric acid + 10 mL Extra Virgin Olive Oil [EVOO]). After 20 minutes, a deep, sustained pneumohydraulic compression (35 s percussion @ 2.1 Hz, 4 respiratory cycles, and 10 s terminal static compression) is applied to the sub-umbilical region maintaining a unified force threshold of 1.0–1.5 N over the transversalis fascia, the linea alba, and preperitoneal sliding planes under active core contraction. Results: Molecular models validate that ionic priming establishes a non-compressible hydrostatic cushion (nu ≈ 0.499) within the hyaluronic acid matrix, preventing force dissipation. Protons (H^+) act as allosteric modulators, reducing the mechanical gating threshold of Piezo2 channels. The local tensional torque of 1.0–1.5 N triggers the opening of Piezo2 channels expressed on mucosal enterochromaffin (EC) cells and fascial mast cells. The resulting intracellular Ca²⁺ influx drives the exocytosis of Serotonin (5-HT) into the lamina propria, binding to 5-HT3 receptors on vagal afferent terminals and driving an orthodromic sensory signal toward the Nucleus of the Tract Solitary (NTS), which upregulates central serotonergic tone at the dorsal raphe nucleus. Concurrently, mechanical loading stimulates Gamma-Aminobutyric Acid (GABA) release from synaptic vesicles of enteric interneurons via GAD activation. Interstitial GABA binds to ionotropic GABA-A receptors, inducing a Cl^--mediated hyperpolarization that blocks mast cell degranulation and silences visceral sympathetic drive. Centrally, this dual homeostatic de-escalation results in a transitory functional deactivation of the Anterior Insula and the amygdala, crashing the physiological basis of cognitive distress. Conclusion: This parametric sub-umbilical window acts as a non-pharmacological biomechanical switch to downregulate central interoceptive threat networks.