Taurine, Chloride Signaling, and Circadian Hydration: A Systems Hypothesis Linking Osmolyte Regulation, Bile Acid Signaling, and Renal Electrolyte Interpretation, Lantern of Sulfur, Vertical Terrain Axis, Concept A, Version 12 (March 2026)

This hypothesis preprint explores the potential role of taurine as a stabilizing osmolyte within chloride-dominant regulatory physiology, integrating mechanisms from neuroscience, metabolism, renal physiology, and cardiovascular regulation. Taurine is a sulfur-containing amino acid derivative that functions as a cellular osmolyte, bile acid conjugation substrate, mitochondrial stabilizer, and neuromodulatory molecule. These properties position taurine at several physiological interfaces relevant to hydration sensing, renal electrolyte interpretation, and systemic metabolic signaling. The paper proposes a systems framework linking circadian hydration timing, metabolic load, bile acid signaling, nitric oxide regulation, and renal chloride transport mechanisms. Within this cascade, renal ion execution layers involving NKCC2 sodium-potassium-chloride transport and pendrin-mediated chloride–bicarbonate exchange may contribute to chloride-dominant acid–base patterns such as hyperchloremic non-anion-gap metabolic acidosis (NAGMA). Within this model, taurine may function as a modulatory node intersecting multiple regulatory layers, including: • hypothalamic osmotic sensing• bile acid conjugation and FXR signaling• endothelial nitric oxide regulation• mitochondrial stabilization• renal tubular osmotic balance These interactions suggest that taurine may participate in the broader physiological processes governing fluid interpretation, electrolyte signaling, and systemic regulatory adaptation to hydration and metabolic stress. The framework is presented as a hypothesis-generating integration of existing physiological systems rather than a causal claim. A series of testable predictions are proposed involving osmolyte profiles, bile acid signaling, nitric oxide regulation, circadian hydration timing, and renal chloride transporter activity. This work emerges from the broader Lantern of Sulfur systems physiology framework, which examines chloride-dominant acid–base patterns as potential signals of regulatory imbalance across hydration signaling, metabolic timing systems, and renal electrolyte interpretation. Related framework work:Hyperchloremia as a Terrain Signal — https://zenodo.org/records/18986769