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.
| loop-gain drop d | barrier fraction | relative crossing rate |
|---|---|---|
| 0 | 1.0000 | 1.00× |
| 0.1 | 0.8100 | 2.14× |
| 0.25 | 0.5625 | 5.75× |
| 0.5 | 0.2500 | 20.09× |
| 0.75 | 0.0625 | 42.52× |
| 0.9 | 0.0100 | 52.46× |
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:
| disease | loop / arm | mechanism | grade |
|---|---|---|---|
| glaucoma | IOP homeostasis / outflow | trabecular-meshwork stiffening → IOP setpoint drifts up → retinal ganglion-cell death (attractor crossing) | [V]/[L] |
| myopia | emmetropization / defocus | growth-control loop fails → axial elongation → myopia via the classical 2.69 D/mm | [V]/[L] |
| presbycusis / NIHL | cochlear amplifier / Hopf µ | hair-cell + prestin loss pushes µ off criticality → the F^(1/3) gain collapses → threshold shift | [V]/[L] |
| cataract | lens solubility / chaperone | oxidative damage → crystallins cross the aggregation spinodal → insoluble scatter (near-irreversible) | [V]/[L] |
| AMD (geographic atrophy) | complement regulation | lost regulation raises the inflammatory loop gain → chronic activation → RPE/photoreceptor atrophy | [V]/[L] |
| diabetic retinopathy | retinal microvasculature | chronic hyperglycemia → ischemia → VEGF-driven neovascular attractor (seam to metabolism) | [V]/[L] |
| BPPV / vertigo | instrument fault | otoconia dislodge into a canal → false angular-velocity signal | [V]/[L] |
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.