Additional Tier-1 perturbations (dumping, reflux, insulinoma, FD, SIBO)

Five further Tier-1 disorders perturb already-built modules: dumping drives a faster, higher glucose peak plus a biphasic reactive-hypoglycaemia crossing on the §5 loop; reflux oesophagitis reuses the §13 erosion kernel; insulinoma mirrors type-1 diabetes; functional dyspepsia is a mild point on the §11 ICC axis; SIBO stasis rises as the §4 sweep weakens. Mechanisms [V], dumping magnitude [O].

Five scattered Tier-1 disorders, each one moved parameter of a module from §2–§14 (group A, no new primitive). Dumping's early/late metabolic features emerge on the §5 homeostat (the mechanical rapid-emptying magnitude is an honest [O]); reflux-oesophagitis erosion reuses the §13 Kramers kernel; insulinoma is the mirror of §12 type 1, with reactive hypoglycaemia sharing the late-dumping undershoot; functional dyspepsia is the mild end of the §11 ICC axis; SIBO stasis rises as the §4 propulsive sweep weakens. Mechanisms [V]; anchors [L]; the dumping magnitude/nadir, SIBO bacterial load and FD felt component are [O] with stated obstacles.

Five further Tier-1 disorders are grouped here because each is one perturbed parameter of a module already built in §2–§14, adding no new substrate primitive (this is group A). The discipline is unchanged: a single knob is moved, the phenotype is read off, and where the substrate genuinely cannot express a feature it is recorded open [O] with its obstacle, never tuned into agreement.

Dumping syndrome — a metabolic reading on the §5 homeostat

Dumping's defining features are metabolic, and they emerge cleanly on the glucose loop. Early dumping: the same carbohydrate load delivered faster (a sharper meal pulse) drives a monotonically higher glucose peak — from 6.052 mM at slow delivery to 9.103 mM at the fastest — because the loop's finite insulin response cannot keep pace with the steepened input.

Late dumping is the same delivery speed coupled to an exaggerated incretin-driven insulin response: the curve becomes biphasic — an early hyperglycaemic peak followed by a reactive nadir that crosses the cited 3.9 mM hypoglycaemia threshold, deepening with delivery speed. This ties late dumping to insulinoma and reactive hypoglycaemia below through the shared §5 reactive undershoot.

The mechanical rapid-emptying magnitude is the honest negative. The §4 transporter is a conserved-bolus hard occlusion wave whose displacement saturates at the tube end, so it cannot express emptying faster than normal (0.006% overshoot at the fastest observable) — the slow side reduces correctly, but the rapid side is geometrically pinned. The true lesion is loss of the gastric accommodation reservoir and pyloric brake, a Tier-2 element (group B); this magnitude is open [O].

Treatment (model reading). The target is the inverse of the prokinetic goal of §11/§14: slow gastric emptying and carbohydrate delivery. Smaller, more frequent, lower-glycaemic meals broaden the delivery pulse and flatten the peak; surgically, restoring the reservoir / pyloric brake is the mechanical target. The direction is forced [V]; absolute efficacy and the absolute nadir are open [O].

Reflux oesophagitis — the §13 barrier kernel on the oesophageal mucosa

The mucosal-injury part of reflux oesophagitis needs no new model: oesophageal acid exposure is a sustained bias h that lowers the mucosal-integrity barrier, read on the identical exact-barrier Kramers kernel as §13. Erosion relative risk rises monotone and convex in acid-exposure dose with the same calibrated slope (κ = 0.060544) as the gastritis curve — no new anchor, no shape fit.

Treatment (model reading). Lower the acid-exposure bias h — acid suppression (proton-pump inhibitors) moves the system back down the convex erosion curve. Eliminating the reflux source (lower-oesophageal-sphincter incompetence) needs the Tier-2 sphincter gate (group B); this section owns only the acid-injury crossing. The target direction is forced [V]; absolute efficacy and incidence are open [O].

Insulinoma and reactive hypoglycaemia — the mirror of type 1 on the §5 loop

Insulinoma is an autonomous, unregulated insulin source on the validated glucose loop: it pulls the fasting fixed point below the 5 mM setpoint and below the cited 3.9 mM threshold, deepening monotonically with source strength — the exact mirror of §12 type-1 capacity loss, where a missing insulin arm instead raised glucose past 7 mM. Removing the source returns the loop to setpoint (4.819 mM), the resection prediction.

Reactive hypoglycaemia is a meal followed by an exaggerated, delayed insulin response that drives a reactive undershoot below baseline, deepening with the overshoot — the same §5 mechanism behind late dumping, a distinct aetiology with the same loop signature.

Treatment (model reading). Insulinoma — remove the autonomous source (surgical resection / limit the unregulated secretion term); the model shows the loop returns to setpoint once the source is gone. Reactive hypoglycaemia — blunt the post-prandial insulin spike (slower carbohydrate, smaller meals). Target direction is forced [V]; absolute glucose and efficacy are open [O].

Functional dyspepsia (motility component) — the mild end of the §11 ICC axis

A mild reduction of gastric contraction amplitude (a mild §11 ICC lesion) produces a mild emptying-rate delay — present and monotone, but far short of the severe-gastroparesis collapse. The functional-dyspepsia operating point (98.1% of normal emptying) is clearly distinct from severe gastroparesis on the same axis (20.6%); the delay is resolved only on a short emptying-rate window, before completion saturates it.

Treatment (model reading). Prokinetics raise the effective gastric contraction (as in §11) and restore the emptying rate. The post-prandial-distress / early-satiation (felt) component is the Tier-2 accommodation reservoir (fundic-relaxing agents) plus afferent gain (neuromodulators), with the felt interpretation living in the mind volume behind the firewall. The motility target is [V] partial; the felt component is open [O].

SIBO (motility component) — stasis from a weakened §4 sweep

Small-intestinal bacterial overgrowth's motility predisposition is loss of the strong periodic housekeeping propulsion: reducing the propulsive drive on the §4 transporter produces stasis, read as a rising retained proximal fraction, with a collapse mirroring the colonic-inertia threshold of §14. The lumen clears at normal drive (0.0 retained) and holds most of the bolus at low drive (0.978 retained).

Treatment (model reading). Restore the periodic propulsive sweep — prokinetics / motilin-class agents reinstate clearance and lower the retained fraction. The bacterial overgrowth load itself is out of model (it needs a microbial layer), and the explicit migrating-motor-complex periodic sweep is deferred to Tier-2 (group B) under the No-Tuning rule. The motility target is [V]; the bacterial load is open [O].

Across all five: the metabolic, erosion and stasis mechanisms are forced by the substrate [V]; the hypoglycaemia and NSAID anchors are cited [L]; and four features stay honestly open [O] with stated obstacles — the dumping mechanical magnitude and absolute nadir, the SIBO bacterial load, and the functional-dyspepsia felt component — each pointing at a Tier-2 element rather than a fitted coefficient.