Disease as setpoint drift: the quadratic basin-collapse law

Disease on this substrate is a defended setpoint, clock, or instrument failing. A loop-gain drop d shrinks the attractor barrier as (g²/4)(1−d)², a quadratic basin collapse, raising the Kramers crossing rate. Glaucoma, AMD, myopia, presbycusis, cataract, diabetic retinopathy, and BPPV each instantiate one failure mode. Shapes are verified; absolute rates are open.

A single derived law governs the major non-rare diseases of the sense organs: residual barrier = (g²/4)(1−d)² under a loop-gain drop d, so the barrier collapses quadratically (1.00 → 0.25 at d=0.5 → 0.01 at d=0.9) while the relative Kramers crossing rate rises monotonically. Presbycusis is the special case of the Hopf amplifier pushed off criticality, collapsing the F^(1/3) gain. Shapes are [V]; per-disease anchors are cited [L]; absolute incidence is [O] (needs the noise scale).

Disease here is not a separate machinery from health — it is the same R19 substrate failing in one of a few shapes: a defended setpoint drifts, a feedback loop loses gain, an attractor is crossed, or a physical instrument breaks. This is the same substrate as carcinogenesis, viewed through the sense organs.

Why the attractor barrier collapses quadratically

A loop-gain drop d leaves an effective gain g(1−d) and a residual attractor barrier (g²/4)(1−d)²; the escape rate follows Kramers' exp(−B/D). Because the barrier depends on the square of (1−d), a partial loss of feedback shrinks the protective barrier faster than linearly, so risk accelerates as control degrades.

Quadratic basin collapse (PAX6 node, loop-gain drop d)
loop-gain drop dbarrier fractionrelative crossing rate
01.00001.00×
0.10.81002.14×
0.250.56255.75×
0.50.250020.09×
0.750.062542.52×
0.90.010052.46×

Seven major diseases, one substrate

Each major non-rare disease of the eye and ear maps to a single failure mode of this law, with its anchor cited and its absolute rate left open:

Major eye/ear diseases as substrate failures
diseaseloop / armmechanismgrade
glaucomaIOP homeostasis / outflowtrabecular-meshwork stiffening → IOP setpoint drifts up → retinal ganglion-cell death (attractor crossing)[V]/[L]
myopiaemmetropization / defocusgrowth-control loop fails → axial elongation → myopia via the classical 2.69 D/mm[V]/[L]
presbycusis / NIHLcochlear amplifier / Hopf µhair-cell + prestin loss pushes µ off criticality → the F^(1/3) gain collapses → threshold shift[V]/[L]
cataractlens solubility / chaperoneoxidative damage → crystallins cross the aggregation spinodal → insoluble scatter (near-irreversible)[V]/[L]
AMD (geographic atrophy)complement regulationlost regulation raises the inflammatory loop gain → chronic activation → RPE/photoreceptor atrophy[V]/[L]
diabetic retinopathyretinal microvasculaturechronic hyperglycemia → ischemia → VEGF-driven neovascular attractor (seam to metabolism)[V]/[L]
BPPV / vertigoinstrument faultotoconia dislodge into a canal → false angular-velocity signal[V]/[L]
Shapes verified, absolute rates open [O]. The law reproduces the shapes (quadratic barrier collapse, monotone crossing-rate rise, amplifier-gain collapse) as [V]; the absolute incidence and timing need an external noise scale D and absolute basin depth, stated as the obstacle in IRREPRODUCIBILITY_LEDGER.md. Rare and monogenic forms are owned by the disease whitepaper and enter here only as cited parameters — a deliberate division of labour, not a gap.