Aging as Signal Desynchronization: A Falsifiable Framework Centered on ECAR-0
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Current aging paradigms focus primarily on the accumulation of molecular and cellular damage. We propose an alternative, falsifiable framework: aging as a progressive desynchronization from organism-level timing signals, culminating in a quantifiable metabolic state we term ECAR-0. This state is defined by a high basal extracellular acidification rate (ECAR, indicating glycolytic flux) with a blunted oxygen consumption rate (OCR, indicating mitochondrial respiration) response to circadian hormonal cues (e.g., melatonin). We hypothesize that ECAR-0 represents cellular "deafness" to systemic timing information, leading to a failure of tissue-level coordination that precedes and drives phenotypic decline. This framework generates five specific, falsifiable predictions that directly contradict expectations from pure damage-accumulation models. We provide explicit experimental protocols to decisively test between desynchronization and damage-centric paradigms. IP Framework & Rights Assertion: 1. Text Layer (Open Access): This manuscript is licensed under a Creative Commons Attribution 4.0 International (CC BY 4.0) license. 2. Pattern Layer (Sovereign IP): All underlying methodological frameworks—including but not limited to the Signal Desynchronization Model, the ECAR-0 operational definition, and the structure of the falsifiable prediction matrix—are asserted as sovereign intellectual property under emerging Pattern Rights principles. These patterns are not covered by the CC BY license. 3. Defense Layer (Controlled): Any application, derivation, or implementation of this work with potential national security or defense implications is subject to the DFARS 252.227-7013 "Rights in Technical Data—Noncommercial Items" clause and related U.S. export control regulations (EAR/ITAR). Commercial or defense-related inquiries must be directed to the corresponding author with appropriate disclosures.



