This paper proposes the Cobalt Preservation Hypothesis: that cobalamin (“vitamin B12”) evolved primarily as a redox-preserving delivery, protection, and reuse system for cobalt, rather than as a conventional dietary vitamin. This paper argues that the extraordinary molecular complexity of the cobalamin system—including intrinsic factor, receptor-mediated absorption, dedicated transport proteins, and intracellular chaperones—reflects an evolutionary necessity: cobalt, while catalytically essential, is uniquely vulnerable to oxidative inactivation in oxygen-rich biological systems. Additionally, this paper proposes that differential outcomes between injectable and oral supplementation in patients lacking intrinsic factor may be explained by oxidative damage to the cobalt atom during unprotected transit through portal circulation. Finally, it is observed that current nomenclature obscures cobalt’s biological essentiality, disconnecting health conversations from emerging resource sustainability concerns. This expanded version integrates recent 2025–2026 research on cobalamin trafficking, epigenetic implications of cobalt status, and environmental health risks from cobalt scarcity. New sections address links to methylation and epigenetics, structural insights into cobalt-sulfur coordination, known pharmacological disruptors of the cobalt preservation system, diagnostic limitations of standard testing, a clinical advisory on nitrous oxide (N₂O) exposure, and testable predictions for clinical and biochemical validation. The hypothesis remains focused on functional medicine applications, emphasizing overlooked patterns in B12 metabolism that may explain “normal labs but persistent symptoms.” The novel contributions are: (1) framing cobalamin as a cobalt-preservation architecture; (2) the Cobalt Damage Hypothesis for absorption disparities; (3) epigenetic links to cobalt-dependent methylation; (4) identification of pharmacological agents that compromise the preservation system; and (5) forward-looking integration of biological and sustainability contexts. Keywords: cobalamin, cobalt, vitamin B12, methylation, epigenetics, redox preservation, functional medicine, oxidative damage, nitrous oxide, metformin, proton pump inhibitors, sustainability, hypothesis.