A Control-Theoretic Model of Damage Accumulation and Boundedness in Biological Aging
Fuente:
arXiv
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| Natura: | Preprint |
| Pubblicazione: |
2026
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| _version_ | 1866914376167981056 |
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| author | Barkman, Tristan |
| author_facet | Barkman, Tristan |
| contents | Aging interventions frequently improve function and healthspan without arresting long-term deterioration, indicating that existing frameworks do not fully specify the control conditions required for bounded organismal aging. A compact control-theoretic formulation is developed in which total organismal burden is decomposed into two lesion classes with distinct controllability properties: regulatable damage, whose accumulation and clearance are modulated by endogenous systemic repair, and information-limited damage, whose detection or correction is inaccessible to physiological control. Under mild dynamical assumptions, a sufficiency theorem is established: sustained boundedness of total damage is achieved if and only if endogenous repair persistently exceeds production of regulatable damage and information-limited damage is actively bounded or removed by engineered interventions. Deterministic phase diagrams identify distinct bounded, drifting, and runaway regimes separated by a nontrivial control boundary. A global Latin-hypercube sensitivity analysis with partial rank correlations shows that production of information-limited lesions dominates the asymptotic aging rate, whereas increases in physiological repair capacity have weak marginal influence beyond saturation. Stochastic extensions reveal threshold and sequencing effects relevant to oncogenic risk. The framework yields testable predictions and operational guidance for intervention ordering, biomarker selection, and experimental design in aging research. All conclusions are statements about the dynamical model defined here; biological translation requires empirical identification of observables corresponding to the model variables. |
| format | Preprint |
| id |
arxiv_https___arxiv_org_abs_2603_06657 |
| institution | arXiv |
| publishDate | 2026 |
| record_format | arxiv |
| spellingShingle | A Control-Theoretic Model of Damage Accumulation and Boundedness in Biological Aging Barkman, Tristan Other Quantitative Biology Aging interventions frequently improve function and healthspan without arresting long-term deterioration, indicating that existing frameworks do not fully specify the control conditions required for bounded organismal aging. A compact control-theoretic formulation is developed in which total organismal burden is decomposed into two lesion classes with distinct controllability properties: regulatable damage, whose accumulation and clearance are modulated by endogenous systemic repair, and information-limited damage, whose detection or correction is inaccessible to physiological control. Under mild dynamical assumptions, a sufficiency theorem is established: sustained boundedness of total damage is achieved if and only if endogenous repair persistently exceeds production of regulatable damage and information-limited damage is actively bounded or removed by engineered interventions. Deterministic phase diagrams identify distinct bounded, drifting, and runaway regimes separated by a nontrivial control boundary. A global Latin-hypercube sensitivity analysis with partial rank correlations shows that production of information-limited lesions dominates the asymptotic aging rate, whereas increases in physiological repair capacity have weak marginal influence beyond saturation. Stochastic extensions reveal threshold and sequencing effects relevant to oncogenic risk. The framework yields testable predictions and operational guidance for intervention ordering, biomarker selection, and experimental design in aging research. All conclusions are statements about the dynamical model defined here; biological translation requires empirical identification of observables corresponding to the model variables. |
| title | A Control-Theoretic Model of Damage Accumulation and Boundedness in Biological Aging |
| topic | Other Quantitative Biology |
| url | https://arxiv.org/abs/2603.06657 |