Immune relapsing-inflammation layer (IBD relapse hysteresis, induction/maintenance asymmetry, colitis→cancer bridge)

Inflammatory bowel disease is the R19 switch with a self-sustaining flare basin: the relapsing-remitting course is a hysteresis (the flip-to-flare drive exceeds the return-to-remission drive, so a flare persists as the trigger recedes), which forces the induction-vs-maintenance asymmetry — the same dose holds remission but cannot break a flare. Cumulative burden lowers the same §7 barrier scale, so colitis-cancer risk rises to the cited anchor and collapses on remission.

The first Tier-3 primitive: a relapsing mucosal inflammation is the §2 R19 switch ds/dt = g·s − s³ + h whose active-inflammation basin self-sustains (vendored single-source as flare_state / flare_burden / inflammatory_barrier_scale in the substrate). Inflammatory bowel disease shows the defining relapsing-remitting HYSTERESIS — ramping the antigenic drive up flips to a flare past the induction spinodal, but ramping down regains remission only at a markedly lower drive, so the flare persists as the original trigger recedes. That hysteresis forces the therapeutic asymmetry: breaking an established flare (induction) needs suppression past antigen + spinodal, but a far lower maintenance dose then holds it — the SAME mid-dose has two opposite outcomes by history (it holds a patient in remission but cannot break a patient in flare), which is induction-then-taper as the substrate's own logic. The second reading bridges to the §7 carcinogen kernel: cumulative inflammatory burden lowers the IDENTICAL barrier scale g_eff = g_barrier − κ·burden the §10 kernel uses for chronic H. pylori, so colitis-associated colorectal cancer is the same barrier step under a different sustained injury — one bisection locks κ to the cited UC colorectal-cancer anchor (RR≈2.4, Jess 2012), the risk rises monotonically with burden, and because the driver is a barrier-SCALE reduction the kernel's reversibility applies (sustained remission / mucosal healing restores g_eff and collapses the excess risk toward baseline). This closes the §21 out-of-kernel small-bowel-adenocarcinoma boundary on the inflammation route. The same element in its antigen-DEPENDENT regime reads the immune enteropathies — celiac (and microscopic / eosinophilic / autoimmune) flares on the antigen (gluten) and remits on its removal, with the barrier and the villous surface recovering — the distinct operating regime where driver removal alone suffices. The relapsing hysteresis, the induction/maintenance asymmetry and the burden→barrier→cancer continuity are [V], the spinodal thresholds exact [F], the colitis-CRC RR a cited anchor [L]; the absolute remission and cancer-incidence rates, the celiac absorptive magnitude (needs an absorption layer), and the felt / affective component (mind, behind the firewall) are [O] with stated obstacles.

Inflammatory bowel disease — Crohn's disease and ulcerative colitis — needs one element none of the motility, secretory, gate, reservoir or afferent modules contain: a relapsing mucosal inflammation that flares and remits on its own clock and, over years, raises cancer risk. This is the first Tier-3 primitive, and like the gate and the reservoir it is not new dynamics: a relapsing inflammation is the §2 R19 switch ds/dt = g·s − s³ + h whose active-inflammation basin self-sustains once entered, with the antigenic drive as the bias. Nothing is fitted; the one anchor (the colitis-cancer slope) is a single bisection.

The defining clinical feature is the relapsing-remitting course with hysteresis. Ramping the antigenic drive UP, the mucosa holds in remission and then flips discontinuously into a flare past the induction spinodal; ramping back DOWN, it does not return at the same point — the flare basin self-sustains, so remission is regained only at a markedly lower drive. The flip-up and the flip-down thresholds differ: that gap is the relapse hysteresis, and it is exactly why a flare, once established, persists even as the original trigger recedes.

That hysteresis forces the central therapeutic asymmetry. Breaking an established flare — induction — needs a suppression drive past the upper threshold antigen + spinodal (here 0.885); but once remission is regained, a far lower maintenance dose (threshold 0.115) holds it, because the remission basin is now self-sustaining. The model makes the point sharply: the same mid-strength dose has two opposite outcomes by history — it holds a patient already in remission but cannot break a patient in flare. Induction-then-taper-to-maintenance is the substrate's own logic, not a dosing convention.

The second reading bridges this layer to the §7 carcinogen kernel and closes a boundary the §21 kernel left open. Cumulative inflammatory burden lowers the same R19 barrier scale g_eff = g_barrier − κ·burden that the §10 kernel uses for chronic H. pylori — so colitis-associated colorectal cancer is not a separate mechanism but the same barrier step driven by a different sustained injury. One bisection locks κ to the cited ulcerative-colitis colorectal-cancer anchor (RR ≈ 2.4, Jess 2012); the risk then rises monotonically with accumulated burden:

Because the driver is a barrier-scale reduction, the kernel's signature reversibility applies: sustained suppression (mucosal healing) restores g_eff and collapses the excess risk back toward baseline — which is exactly why durable remission, not just symptom control, is the surveillance-and-cancer-prevention goal.

This closes the §21 out-of-kernel small-bowel adenocarcinoma boundary on the inflammation route: the kernel deferred it for want of a barrier-lowering driver, and the relapsing-inflammation primitive now supplies exactly that (closes_small_bowel_boundary = True) — chronic small-bowel Crohn's lowers the same scale, the same way.

The same element, in its antigen-dependent regime, also reads the immune enteropathies. Where IBD needs active suppression to escape the self-sustaining flare, celiac disease (and microscopic / eosinophilic / autoimmune enteropathy) is driven directly by an identified antigen: present the driver (gluten) and the element flares; remove it and the element returns to remission with the barrier — and, for celiac, the villous surface — recovering. Driver removal alone suffices, the distinct operating regime of the same primitive.

Treatment (model reading). IBD -- SUPPRESS the inflammatory drive: an immunosuppressant / biologic raises the suppression term past the induction threshold (antigen + spinodal) to flip an active flare back to remission, then a LOWER maintenance dose holds it (the model's induction-vs-maintenance asymmetry). Sustained remission restores the section-7 barrier scale, so the model frames dysplasia surveillance and cancer risk on the SAME barrier step -- mucosal healing lowers the crossing RR back toward baseline. For celiac / microscopic / eosinophilic / autoimmune the lever is removing the antigen / eosinophil / immune driver (the barrier and, for celiac, the villous surface recover). Target directions [V]; absolute remission rates, cancer incidence, and the celiac absorptive magnitude [O].

The relapsing-remitting hysteresis, the induction-vs-maintenance asymmetry, and the burden→barrier→cancer continuity (closing the §21 small-bowel boundary) are forced by the substrate [V], with the induction and maintenance thresholds exact spinodal identities [F] and the colitis-cancer RR a cited anchor [L]. What stays open [O], each with its obstacle: the absolute remission and cancer-incidence rates (clinical-cohort calibration), the celiac absorptive (villous-surface) magnitude (needs an absorption layer), and — the firewall — the felt / affective component, which is mind's; this section moves only the inflammatory-drive term, never the felt interpretation.