Type 2 diabetes: a crossed glucose setpoint

Type 2 diabetes is the glucose homeostat with its loop gain dropped (insulin resistance) while a chronic caloric/adiposity forcing pushes disposal down. With the barrier shrunk and the crossing threshold lowered, the state CROSSES the euglycemic basin to the hyperglycemic one (crossed = True). It is an attractor-shift, not a tuning error.

INSR node (γ 1.4956). A loop-gain drop of 0.4500 gives g_eff 0.8226 and residual spinodal 0.2872; the chronic forcing exceeds it, so the loop crosses to the disease basin. Shape [V]; RR vs cited BMI/HbA1c cohorts [L]; absolute incidence [O].

Mechanism

insulin resistance lowers glucose-loop gain (shallower euglycemic basin) while a chronic caloric/adiposity forcing pushes disposal down; past the reduced spinodal the state crosses to the hyperglycemic basin.

The numbers

Healthy spinodal 0.7040 drops to residual 0.2872 under the gain loss; the chronic forcing 0.6200 exceeds it, so the euglycemic basin is crossed. The pathological state settles at -1.1641 (the hyperglycemic branch).

Why this matters for treatment

If the disease is a CROSSING, simply reducing the forcing may not return the state once it has crossed -- restoring loop gain (re-sensitisation) is needed to re-open the euglycemic basin. That is the falsifiable claim the restoration chapters build on.

RR vs cohort risk is [L] cited; the attractor-shift SHAPE is [V]; absolute incidence is [O] -- the obstacle is calibrating the model forcing axis to clinical units.