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Published July 18, 2026 | Version 9

THE ARCHITECTURE OF IMPEDANCE: Unifying Synaptic Proteins, Nyquist-Shannon Sampling, and P-FIT Bus Resistance in the Autism Spectrum Phenotype

  • 1. Independent Researcher

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ABSTRACT

Current psychiatric paradigms primarily characterize Autism Spectrum Disorder (ASD) through behavioral observation, resulting in a dualistic gap between molecular genetics and systemic cognitive output. We propose a paradigm shift utilizing the High Entropy Predictive Organization Efficiency (HEPOE) framework to suggest that ASD is not fundamentally a behavioral or developmental deficit, but rather can be conceptualized as an Architecture of Impedance, generating a state of Compulsory Thermodynamic Inefficiency. By integrating the structural decay of post-synaptic density proteins (e.g., SHANK3) with the Nyquist-Shannon sampling theorem, we hypothesize that the core of the ASD phenotype is the inability to compress data at the sensory entry gate (Ωsensory). This uncompressed, high-volume data load is proposed to force the predictive architecture to push raw information through high-resistance white matter pathways defined by the Parieto-Frontal Integration Theory (P-FIT), generating massive network friction (Ωnetwork). We introduce the comprehensive Systemic Friction equation. This framework redefines the varying Support Levels of ASD (Levels 1, 2, and 3) not as static psychological traits, but as the mathematical rate of Predictive Solvency (S(t)) decay. The so-called "social deficits" and rigid routines are thereby reframed as autonomous Entropic Damping protocols, emergent homeostatic attractor states representing the path of least thermodynamic resistance to prevent thermal and metabolic exhaustion in a high-friction neural hardware.

Keywords: Autism Spectrum Disorder (ASD). HEPOE Theory. Predictive Solvency. Nyquist-Shannon Sampling. Systemic Friction. P-FIT Bus Resistance. Systemic Impedance. Entropic Damping.

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https://originalmy.com/bitregistro/22430ab07b8029e4d5b857c88b231a7ed9158b81f0faa983c003967a86d486e0
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INPI BR 10 2026 003794 0
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INPI BR 51 2026 000122 6
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INPI BR 51 2026 001253 8

Related works

References
Preprint: 10.5281/ZENODO.18284802 (DOI)

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