Gastric accommodation reservoir (functional dyspepsia, post-prandial distress)

The post-prandial-distress component of functional dyspepsia rides a new Tier-2 primitive: a reservoir, the R19 wall relaxed toward yield. Impaired fundic accommodation stiffens the wall, so a fixed meal raises intra-gastric pressure prematurely — early satiation and post-prandial distress — and restoring accommodation lowers it. The maximal-compliance yield point is exactly the R19 spinodal.

The second Tier-2 primitive is a reservoir: the §2 R19 switch ds/dt = g·s − s³ + h resting contracted at s = −√g, which a vagal accommodation drive relaxes toward its yield point. The wall stiffness is the R19 restoring curvature k = 3s² − g, the compliance C = 1/k, and a fixed meal raises pressure P = V·k — nothing fitted. Functional dyspepsia (post-prandial distress) is impaired accommodation: as accommodation falls the wall stiffens, compliance falls (early satiation) and the fixed-meal pressure rises monotonically toward the stiff unaccommodated baseline. This is the post-prandial-distress axis that §15 (FD-motility) left open; together they cover the two functional-dyspepsia axes. The maximal-compliance yield point is exactly the R19 spinodal (an algebraic identity). Treatment raises the compliance term to lower the meal pressure. Mechanism [V] partial; the felt distress (B3 afferent gain + mind firewall) and the absolute meal-volume / pressure scale [O] with stated obstacles.

The post-prandial-distress component of functional dyspepsia needs one element the transport, homeostat and gate modules do not contain: a reservoir — a fundic compliance that absorbs a meal volume without a pressure spike. This is the second Tier-2 primitive, and like the gate it is not new dynamics: the fundic wall is the §2 R19 switch ds/dt = g·s − s³ + h resting contracted at s = −√g, which a vagal accommodation drive relaxes toward its yield point. The wall stiffness is the R19 restoring curvature k = 3s² − g, the compliance its inverse C = 1/k, and a fixed meal raises pressure P = V·k; nothing is fitted.

Functional dyspepsia (post-prandial distress) is impaired fundic accommodation: as accommodation falls the operating point retreats toward the contracted rest, the wall stiffens, and the same meal raises intra-gastric pressure prematurely. Sweeping accommodation as a fraction of the yield drive (so the knob is tied to the substrate, never tuned), the compliance falls from 1.793 to 0.515 — early satiation, less meal tolerated per unit satiation pressure — while the fixed-meal pressure climbs from 28% to 97% of the stiff unaccommodated baseline. A normal fundus absorbs the meal (28% of baseline); impaired accommodation is premature pressure (91%).

This is the post-prandial-distress axis that the §15 functional-dyspepsia-motility reader explicitly left open. §15 owns the mild emptying delay (the epigastric-pain / motility side); this section owns the accommodation / early-satiation side; and together they cover the two recognised functional-dyspepsia axes. They are distinct lesions of distinct modules — a mild §11 ICC reduction versus a stiff fundic reservoir — which is why a patient may have either or both.

The reservoir's maximal-compliance limit is not a fitted bound: the yield point, where the wall stiffness vanishes and the compliance diverges, is exactly the R19 spinodal. At s = −√(g/3) the stiffness 3s² − g is identically zero (k = 1e-16), and that point is where the contracted fixed point merges with the unstable one at the spinodal drive — an algebraic property of the double well, not a tuned ceiling. Readings operate strictly below it, since the marginal saddle-node has critical slowing.

Treatment (model reading). functional dyspepsia (post-prandial distress) -- RESTORE fundic accommodation: a fundic-relaxing agent raises the compliance term, sliding the reservoir wall back toward its yield point so a fixed meal is absorbed without the premature pressure rise (the model lowers the meal pressure monotonically as accommodation is restored). The motility/emptying component is the s15 prokinetic target; this reader owns the accommodation/early-satiation axis. The FELT distress itself is afferent-gain (B3) with the felt interpretation in `mind` (firewall). Target direction [V]; absolute efficacy and the felt symptom mapping [O].

The premature-pressure / early-satiation mechanism is forced by the substrate [V] — partial, because the post-prandial-distress axis is what §15 left open while the motility axis lives there. What stays open [O], each with its obstacle: the felt post-prandial-distress symptom itself, which is the group B3 visceral afferent-gain term with the felt interpretation in mind behind the firewall (the lever that raises that peripheral afferent's firing threshold — and the drug class it points to — is mapped in §28); and the absolute meal-volume and intra-gastric-pressure scale, a model unit needing barostat / manometry calibration.