Allergic (acquired) smell loss
Allergic rhinitis is an immune disease, so its mechanism is cited to immune §11, not re-derived. The volume owns only the consequence: conductive loss is a reversible drive suppression on intact switches (recovers at κ = 1), sensorineural loss a persistent organ degradation — told apart by restoring the drive.
The allergy mechanism is consumed from immune §11 (cited, not re-derived). Conductive loss is a reversible drive suppression (baseline h₀ = 0.65881; recovers to 7/7 at κ = 1); sensorineural loss is a persistent organ degradation (0/7 at full drive).
The honest framing — the most common nose disease is an immune disease
Allergic rhinitis is not primarily an olfactory disease; it is a Type-2 immune hypersensitivity. So its mechanism — sensitization, the latch, controlled desensitization — is consumed from the immune volume's §11, cited and never re-derived here. This volume owns only the olfactory consequence: how allergy takes your smell.
It takes smell two ways, told apart by a single move — restoring the drive. The split between conductive and sensorineural loss falls out of which substrate layer moved.
Conductive loss — a drive suppression on intact switches (reversible)
Mucosal swelling reduces odorant flux, attenuating the per-receptor drive to κ·h₀ with the baseline odour drive h₀ = 0.65881. γ is untouched — no switch defect — so the panel flips off in spinodal order as κ falls.
| κ (conductive) | percept (# OR on) |
|---|---|
| 1.00 | 7 |
| 0.95 | 7 |
| 0.90 | 7 |
| 0.86 | 5 |
| 0.82 | 3 |
| 0.60 | 0 |
| 0.30 | 0 |
| 0.00 | 0 |
Because nothing structural changed, restoring κ → 1 returns the percept to 7 of 7 exactly. Conductive smell loss is reversible: the frozen flip and measured γ are intact; only the drive moved.
Sensorineural loss — an organ degradation (persistent)
Chronic Type-2 inflammation can drop the OSN compartment's master cis-drive below its γ-set presence threshold — the same R19 organ-formation failure as congenital anosmia (§4), reached by inflammation rather than a mutation. With the organ gone, no drive can rescue it.
| organiser | γ | h* = presence | healthy | damaged |
|---|---|---|---|---|
| EBF1 | 1.4097 | 0.64423 | present | absent |
| EMX2 | 1.4574 | 0.67720 | present | absent |
| LHX2 | 1.5172 | 0.71930 | present | absent |
At full conductive drive κ = 1 with the organ damaged the percept is 0 of 7 — anosmia. Sensorineural loss is persistent because it is an organ failure, not a drive failure.
The discriminator and the firewall in action
One move separates them. Under a partial conductive block (κ = 0.82) the percept is 3 of 7; restoring the drive returns it to 7 of 7. The sensorineural percept stays 0 of 7 under the same move. The substrate expresses the clinical conductive-vs-sensorineural distinction as drive (§1/§2) versus organ (§2/§3).
The direction-only levers are sign only: conductive → restore odorant access (κ↑), with the upstream immune cause cited to §11 desensitization; sensorineural → act on the organ, recovery not guaranteed. No dose, molecule, or efficacy. The volume adds no gene — the measured atlas is untouched — and κ and the organ degradation are abstract structural representations, never fitted.