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 consistency (code) outputs (relative rates depend on the noise scale D); 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 (its values depend on the chosen noise scale D; the code uses D_ref = 0.25·B0). Presbycusis is the special case of the Hopf amplifier pushed off criticality, collapsing the F^(1/3) gain. Shapes are consistency (code); 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. The relative crossing-rate column below (2.14×–52.46×) depends on the chosen noise scale D (the code uses D_ref = 0.25·B0, so rate_rel = exp(4·(1−(1−d)²))), not only the absolute rate; only the barrier-fraction column (1−d)² is D-free.
| loop-gain drop d | barrier fraction | relative crossing rate (D_ref = 0.25·B0) |
|---|---|---|
| 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) | interpretation/[L] |
| myopia | emmetropization / defocus | growth-control loop fails → axial elongation → myopia via the classical 2.69 D/mm | interpretation/[L] |
| presbycusis / NIHL | cochlear amplifier / Hopf µ | hair-cell + prestin loss pushes µ off criticality → the F^(1/3) gain collapses → threshold shift | interpretation/[L] |
| cataract | lens solubility / chaperone | oxidative damage → crystallins cross the aggregation spinodal → insoluble scatter (near-irreversible) | interpretation/[L] |
| AMD (geographic atrophy) | complement regulation | lost regulation raises the inflammatory loop gain → chronic activation → RPE/photoreceptor atrophy | interpretation/[L] |
| diabetic retinopathy | retinal microvasculature | chronic hyperglycemia → ischemia → VEGF-driven neovascular attractor (seam to metabolism) | interpretation/[L] |
| BPPV / vertigo | instrument fault | otoconia dislodge into a canal → false angular-velocity signal | interpretation/[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.