Disease as setpoint, clock and sense-organ failure
Mineral, acid-base and electrolyte diseases are failures of defended setpoints on the same R19 substrate. Six modes are derived and demonstrated; major diseases (osteoporosis, hyperparathyroidism, acidosis/alkalosis, electrolyte disorders, stones, ADH1, BPPV) map onto them, with rare/monogenic forms cited from the disease volume.
Disease in this system is a failure of a defended setpoint, a clock, or a sense organ on the same R19 substrate — not a local lesion. Six failure modes follow from the substrate: loop-gain drop, setpoint drift, reservoir depletion, buffer-arm failure, threshold crossing, instrument failure.
The derived failure modes
The substrate yields the failure laws directly: a loop-gain drop blows up the setpoint variance (Var=σ²/2k) and slows correction; a comparator reset makes the loop defend a pathological value; a hard solubility/precipitation threshold is crossed discontinuously (the spinodal). All three are demonstrated (True).
| major disease | failure mode |
|---|---|
| osteoporosis | reservoir depletion (+ loop-gain drop with estrogen loss/aging_senescence) |
| primary hyperparathyroidism | setpoint drift (PTH set-point reset UP) |
| metabolic acidosis / alkalosis | buffer-arm failure (renal or respiratory arm gain drops) |
| common electrolyte disorders | loop-gain drop / setpoint deviation (Na/K) |
| nephrolithiasis (calcium stones) | threshold/spinodal crossing (supersaturation) |
| autosomal dominant hypocalcemia type 1 (ADH1) | instrument failure (CaSR gain-of-fn -> setpoint reset DOWN) |
| BPPV (benign paroxysmal positional vertigo) | mineral-reservoir + instrument failure (otoconia) |
Rare and monogenic forms (MEN1, FHH, RTA transporters, Liddle, primary hyperoxaluria, ADH1 CaSR) are owned by the disease volume and enter here as a cited parameter (a setpoint shift or arm-gain change); the systemic trajectory is computed here.