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I propose and operationalize a testable hypothesis: a relatively highly receptive neurofunctional architecture (hereafter supersensory system) precedes and conditions the developmental trajectory of complex cognition. In this framework, sensitivity is defined not as a personality trait but as a measurable multimodal construct (Sensitivity Index, SI) derived from peripheral and central nervous system properties, including quantitative sensory thresholds, autonomic reactivity, EEG/fMRI signatures, and diffusion MRI microstructure.
I further posit a functional threshold (Sensitivity Breakpoint, SB): when SI exceeds SB under sufficiently enriched and secure environmental conditions, neuroplastic mechanisms are activated in ways that increase the probability of accelerated cognitive crystallization and the emergence of high intellectual ability.
The hypothesis integrates evolutionary and embryological evidence that nervous tissue predates centralized encephalic structures (Garlick, 2002; Boyce & Ellis, 2005), and it positions plasticity as the mediating process between initial sensory receptivity and later cognitive outcomes.
I specify falsifiable predictions, including longitudinal SI → connectivity change mappings, differential outcomes under enrichment and deprivation, and separable effects of SI subcomponents (e.g., sensory-perceptual vs. affective reactivity) on cognitive performance. An operational roadmap for measuring SI and estimating SB is provided, with recommendations for cohort, twin, and intervention designs to evaluate causality.
The aim is to shift focus from brain-centric models toward a body–brain systems approach to the functional origins of human cognitive variability.
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Title Sensitivity as the Functional Origin of Intelligence
I propose and operationalize a testable hypothesis: a relatively highly receptive neurofunctional architecture (hereafter supersensory system) precedes and conditions the developmental trajectory of complex cognition. In this framework, sensitivity is defined not as a personality trait but as a measurable multimodal construct (Sensitivity Index, SI) derived from peripheral and central nervous system properties, including quantitative sensory thresholds, autonomic reactivity, EEG/fMRI signatures, and diffusion MRI microstructure.
I further posit a functional threshold (Sensitivity Breakpoint, SB): when SI exceeds SB under sufficiently enriched and secure environmental conditions, neuroplastic mechanisms are activated in ways that increase the probability of accelerated cognitive crystallization and the emergence of high intellectual ability.
The hypothesis integrates evolutionary and embryological evidence that nervous tissue predates centralized encephalic structures (Garlick, 2002; Boyce & Ellis, 2005), and it positions plasticity as the mediating process between initial sensory receptivity and later cognitive outcomes.
I specify falsifiable predictions, including longitudinal SI → connectivity change mappings, differential outcomes under enrichment and deprivation, and separable effects of SI subcomponents (e.g., sensory-perceptual vs. affective reactivity) on cognitive performance. An operational roadmap for measuring SI and estimating SB is provided, with recommendations for cohort, twin, and intervention designs to evaluate causality.
The aim is to shift focus from brain-centric models toward a body–brain systems approach to the functional origins of human cognitive variability.
Work type Technical
Tags inteligencia, soberanía de datos, educacion, sistema nervioso, desarrollo cognitivo, neurología, blockchain, altas capacidades, aprender, empatía, ix, alphauser, supersistema nervioso, \innovacion ux ético, neurodivergencia, examenes, neuroevolución, arquitectura cognitiva, intelligence trace, alta sensibilidad
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Identifier 2509233143143
Entry date Sep 23, 2025, 6:49 PM UTC
License Creative Commons Attribution-NonCommercial-NoDerivatives 4.0
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Author 100.00 %. Holder Sílvia Barroso. Date Sep 23, 2025.
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