Life as Counterfactual Geometry: An Adversarial Theory of Biological Function

Living systems exhibit anticipation, adaptability, and resilience that cannot be fully explained by stimulus–response models, static homeostasis, or convergence-based optimization. This work addresses this gap by proposing a theoretical framework in which a central aspect of biological function is understood through the geometry and stability of distributions over unrealized but accessible future trajectories. We formalize these distributions as a counterfactual manifold, defined as a probabilistically supported subset of path space induced by a system’s effective internal dynamics. Using tools from information geometry and dynamical systems theory, we analyze adaptive systems that modify the laws governing their own future trajectories and construct explicit dual-channel adversarial dynamics that couple processes expanding future possibilities with antagonistic processes enforcing feasibility constraints. We show that adaptive systems of this kind are generically unstable, tending toward either collapse of accessible futures or unbounded sensitivity to perturbation. Constructive adversarial dynamics are sufficient to stabilize counterfactual geometry without requiring convergence to a fixed point. A minimal adversarial model reveals three generic regimes: collapse, runaway sensitivity, and bounded non-convergent regulation. The framework yields operational, falsifiable predictions through measurable proxies based on response diversity, perturbation sensitivity, recovery geometry, and boundary residence, allowing these regimes to be discriminated using finite observations without reconstructing underlying state-space dynamics. Interpreting disease as instability of counterfactual geometry provides a unifying language for understanding rigidity, volatility, and context dependence across biological domains. Rather than replacing mechanistic models, the proposed framework offers a higher-level geometric and dynamical perspective in which such models can be embedded and compared, shifting attention from component-level dysfunction to the stability of biological futures and establishing a principled foundation for analyzing disease, intervention, and adaptability across scales.