The twelve hallmarks of aging describe heterogeneous molecular, cellular, tissue, and systemic changes but do not by themselves explain how they become an organism-level loss of repair capacity. Aging is represented as a cost-constrained, stochastic loss of autopoietic repair closure. Hallmark processes are organized as coupled local-to-global constraint layers on a finite biological complex: global sections represent compatible repair modes, while a connecting morphism measures when coherent regulatory states generate material-repair incompatibilities. The principal accounting identity states that coupled repair reserve equals material-repair closure plus regulatory-interface closure minus cross-hallmark obstruction rank. The identity follows from standard exact-sequence and rank-nullity arguments; its biological content lies in the construction of the coupled aging object and the interpretation of obstruction rank as cross-hallmark repair incompatibility. A dynamical extension places repair under finite, fallible control, stochastic perturbation, delayed feedforward dependence, and an explicit viability domain, allowing additional surveillance to reduce global repair when coupling costs exceed local gains. A reproducible two-compartment example specifies stalk variables, restriction maps, coboundary matrices, H0, H1, connecting-map rank, and an approximate persistence interval. Published epigenetic-clock, skeletal-muscle regeneration, and senolytic results are literature-anchored mappings rather than empirical validation. The proposed invariants therefore target one structural dimension of aging: loss of achievable, globally compatible repair under finite biological control.
