Ghost in the Chronos: The Natural Criticality Hypothesis of Subjective Time — An Action-Readiness Density Model via TRP Channels, Glial Axis, and Second-Person Integration (Version 4)

Subjective time is reformulated not as a representation of experience but as a density of action-readiness that fluctuates with body–brain coupling. The framework approximates subjective time as the inverse of action-readiness density and introduces TRP channel families as the interface with the lower boundary of the nervous system. Centrally expressed TRP channels in astrocytes may help maintain self-organized criticality and 1/f fluctuations via glial–neuronal calcium dynamics. A decline in the coupling parameter not only reduces action-readiness density but also impairs its 1/f temporal structure. Second-person interaction is proposed as a mechanistic pillar: inter-brain synchrony shows that bidirectional social exchange sustains action-readiness oscillations that isolated exposure cannot, so degradation of coupling narrows the social surface through which action-readiness can be jointly elevated.

Study at a glance

Abstract

A unified neurological principle of subjective time has yet to be established. Recent advances in neurophenomenology have sought to mathematically connect first-person experience with third-person measurement, increasingly treating subjective time as a formalizable object. Da Costa and colleagues have related phenomenology to belief dynamics and offered mathematical hypotheses regarding metabolic cost and subjective time. Against this background, the present paper reformulates subjective time not as a representational form of experiential content, but as a problem of action-readiness density—a quantity that fluctuates under body–brain coupling. Specifically, we retain the existing framework that approximates subjective time ts(t) as the inverse of action-readiness density r(t), while introducing TRP channel families as the interface with the lower boundary of the nervous system. We further propose that centrally expressed TRP channels in astrocytes may contribute to the maintenance of self-organised criticality (SOC) and 1/f fluctuations via glial– neuronal Ca2+ dynamics. A decline in b(t) may not only attenuate the magnitude of r(t) but also impair its 1/f temporal structure. We further propose that second- person interaction constitutes not merely an intervention surface but a mechanistic pillar of the framework: inter-brain synchrony research demonstrates that contingent, bidirectional social exchange sustains r(t) oscillations that isolated exposure cannot replicate, such that b(t) degradation directly narrows the social surface through which r(t) can be jointly elevated.