Epigenetic Rejuvenation, Longevity, and Identity-Preserving Restoration: A TCGS--SEQUENTION Theory of Ageing as Canalization Drift and Loss of Morphostatic Jurisdiction

Ageing biology increasingly describes biological age as a measurable and partially reversible state rather than as the biological content of elapsed duration. DNA-methylation and multi-omic clocks, transient OSK/OSKM expression, maturation-phase reprogramming, chemical rejuvenation, targeted chromatin editing, and spatially resolved ageing maps jointly show that aged cells and tissues can move toward younger molecular and functional configurations while, within bounded intervention windows, retaining lineage identity. A complementary evolutionary Neural Cellular Automaton study shows that a controller selected to construct a multicellular morphology can later exhibit ageing-like anatomical deterioration without an explicit age variable or programmed degenerative sequence; imposed defects in differentiation, cellular competency, communication, or encoded control accelerate the decline; information associated with lost structures can remain spatially detectable; and sparse, boundary-aware interventions can reactivate restoration \cite{PioLopez2025}. The paper's principal methodological contribution is a geometry of four coupled restoration coordinates that refuses to collapse biological age, lineage identity, malignancy, and post-challenge recovery into one scalar. For lineage $\ell$, $\Aage$ measures multi-map biological-age displacement, $\Mmal$ measures malignancy or tissue-level misalignment, and $\Dlin$ is the operational distance to a preregistered lineage-identity equivalence class. Morphostatic performance is setpoint-aware: $\Goffset$ measures the pre-challenge offset in assay geometry $a$ from the validated target basin, whereas $\Gmor=(\Gcomp,\Gspeed)$ separates homeostatic return completeness from durable recovery speed under a named perturbation $c$. The combined profile is $\Gprofile=(\Goffset,\Gcomp,\Gspeed)$. The load-bearing non-entailment is conditional on the empirical existence of one discordant within-lineage witness pair: \[ \Aage(q_1)<\Aage(q_2)\not\Rightarrow\Mmal(q_1)<\Mmal(q_2), \qquad \Mmal(q_1)<\Mmal(q_2)\not\Rightarrow\Aage(q_1)<\Aage(q_2). \] Consequently, a clock reduction is not evidence of oncological safety, and cancer reversion need not rejuvenate the reverted carrier. Identity-preserving rejuvenation requires lower $\Aage$, membership in the intended lineage class, bounded $\Mmal$, an admissible target-basin offset, and adequate joint recovery under every preregistered challenge. Complete reprogramming, dysplasia, teratoma formation, organ dysfunction, and oncogenic partial reprogramming are classified as corridor overshoot rather than successful age reversal. The paper replaces a non-identifiable scalar notion of morphostatic gain with three separately typed quantities: target-setpoint location, homeostatic return completeness, and durable recovery speed. Completeness and speed are estimated jointly by trajectory-level bootstrap because they share the same terminal and initial deviations. Recovering, nonrecovering, and worsening trajectories are declared before analysis; speed is undefined by design in the worsening region. The window-dependent recovery integral is retained only as a secondary burden summary, and an exponential rate constant is reported only when the locked model passes its diagnostics. Boundary integrity, intercellular communication, and niche organization are measured before challenge and tested first as predictors of the three-category outcome and then, conditionally among identifiable recoverers, under competing additive and gated models. Biological identity is class-valued, whereas $\Dlin$ is its tolerance-bearing empirical proxy. These corrections make post-withdrawal challenge testing, rather than endpoint clocks alone, the decisive discriminator between durable restoration and continuous forcing. Within TCGS--SEQUENTION, four-dimensional Countersp