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Aging is increasingly understood as a systems-level process that reorganizes biological dynamics across molecular, cellular, tissue and physiological scales. Evidence from single-cell biology, epigenomics, mitochondrial research, circadian regulation, resilience science and network physiology shows that aging involves both expanding heterogeneity of biological states and weakening coordination among interacting subsystems. Here we introduce a new theoretical–conceptual framework that interprets early aging as a multiscale transition shaped by rising regulatory dispersion and declining systemic coherence. Regulatory dispersion, represented through entropy-based measures, reflects the breadth and accessibility of biological configurations, whereas systemic coherence captures statistical dependency, shared regulatory information and coordinated constraint across scales. We clarify how these constructs can be estimated in practice using contemporary omics and physiological datasets, and how hierarchical, fractal and scale-free architectures propagate dispersion–coherence dynamics throughout biological organization. The framework generates testable predictions regarding resilience loss, early-warning signals, biological age heterogeneity and responsiveness to interventions that restore coherence or constrain maladaptive dispersion. Rather than replacing mechanistic theories, this conceptual lens integrates diverse hallmarks of aging within a unified dynamical architecture, offering new opportunities for early detection and targeted modulation of destabilizing trajectories.
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Correia et al. (2026) studied this question.
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