The pilosebaceous duct is a channel that jams shut when its net occlusion drive crosses a spinodal. Putting a newly measured PRDM1 γ on the same R19 switch yields a hysteretic comedo with no fitted constant; acne and hidradenitis suppurativa then follow as that one jam at two depths, the deep tract rupturing irreversibly.
The pilosebaceous duct — a follicular channel that occludes into a comedo — is reproduced as a hysteretic two-state jam on the same R19 switch as the barrier and wound, running on a newly measured PRDM1/Blimp1 γ carried through the identical promoter-ΔG pipeline that reproduces MITF and EDAR byte-for-byte. The duct snaps shut discontinuously at an upper spinodal and reopens only at a lower one [V] Simulation-verified; the occlusion set-points are forced regime scales [F] Forced (substrate) and absolute lesion counts stay open [O] Open (obstacle stated). Acne vulgaris (reversible comedo, cleared by a combined regimen) and hidradenitis suppurativa (a deeper jam whose ruptured sinus tract resists drive reduction and needs surgery) follow as the one jam at two depths, passing an intervention-reversal battery and a three-way opposite-mode discriminant, the layer adding no constant while the core-battery hash stays fixed.
The pilosebaceous duct is a channel that can jam shut — the package's own physical class
The integumentary class is jamming: a barrier or channel driven past a spinodal by an external insult. The pilosebaceous duct is a textbook member the earlier targets did not cover — a follicular channel whose net occlusion drive (androgen-driven sebum, infundibular hyperkeratinisation and Cutibacterium acnes, minus clearance) can rise until the duct snaps shut into a comedo. This page emerges that duct as the same R19 jamming switch the barrier and wound pages use, running on a newly measured sebaceous master-gene γ — PRDM1/Blimp1, the sebaceous-lineage master — with no constant fitted to a lesion.
| Quantity | Value | Meaning |
|---|---|---|
| Master gene (measured) | PRDM1 γ = 1.3432 | fetched from NCBI, cached, vendored — the same promoter-ΔG pipeline that reproduces MITF/EDAR byte-for-byte |
| γ reproduces offline | yes | recomputed from the cached promoter (1.343156) — not refitted |
| Spinodal | 0.599 | substrate-derived from γ (sets the occlusion regime scale) |
| Healthy net occlusion | -0.30 | the healthy duct sits patent in the OFF basin (yes) |
Committing the master gene on the biology before reading γ is the discipline that makes the next result a prediction rather than a fit: PRDM1 turns out to carry the lowest γ in the whole organ atlas, so its functional spinodal opens earliest. The substrate therefore predicts the sebaceous programme is among the first to become switchable — an emergence-order statement graded by sign [V] Simulation-verified, not chosen to land anywhere.
The duct is a hysteretic two-state jam, not a reversible threshold
Run as the R19 switch, the duct does not drift smoothly from open to closed. As the net occlusion rises it stays patent, then snaps shut discontinuously at the upper spinodal (a jump of about 2.01 at net occlusion ≈ 1.00); coming back down it does not reopen at the same level but only at a lower spinodal (net occlusion ≈ -1.00), tracing a hysteresis loop of width about 2.01. Discontinuous closure (yes) and a finite hysteresis loop (yes) are the signature of a first-order jam — the simulation-verified core [V] Simulation-verified of this page, taken straight from the substrate with nothing tuned. The clinical reading is immediate: a comedo, once formed, does not clear the moment the drive eases slightly — it has to be pushed back below a distinctly lower threshold, which is why effective therapy attacks several occlusion inputs at once.
The package is explicit about what it does not claim. The hysteresis shape — discontinuity, the loop, the patent set-point — is verified [V] Simulation-verified; the occlusion set-points themselves are dimensionless regime scales [F] Forced (substrate). The absolute comedo and lesion counts, the Hurley-stage extent and the sebum excretion rate remain open [O] Open (obstacle stated), inheriting the new sebaceous target's standing obstacle — a per-gland calibration. The duct is graded on direction, discontinuity, hysteresis and reversibility, never on a fitted magnitude.
Two occlusion diseases are this one jam at two depths
With the jam established, acne vulgaris and hidradenitis suppurativa follow as the same switch driven to two different depths, and each established therapy is the same occlusion drive reversed — no new physics between them.
| Disease | Occlusion handle | Covered as |
|---|---|---|
| Acne vulgaris | standing high net occlusion (sebum + hyperkeratinisation + C. acnes) | drive past the upper spinodal → comedo; the C. acnes amplifier makes it inflammatory; comedolytic + sebostatic + antimicrobial reopens it |
| Hidradenitis suppurativa | the same jam in deeper apocrine-bearing follicles | a heavier plug ruptures into the dermis → a scarring sinus-tract sub-state acne lacks; biologics de-inflame, deroofing/excision resets the scar |
Acne vulgaris: a standing occlusion drives the duct over the spinodal
Acne is a standing elevated occlusion drive: androgen-driven sebum plus infundibular hyperkeratinisation plus the C. acnes amplifier carry the net occlusion to about 1.10, past the upper spinodal, so the duct jams into a comedo (yes) and the C. acnes amplifier makes the lesion inflammatory (yes). The therapeutic structure falls straight out of the hysteresis: a single agent that only nudges the drive is often insufficient (retinoid monotherapy clears: no), because the duct must be driven below the lower spinodal — but a combined comedolytic + sebostatic + antimicrobial regimen (or isotretinoin) does exactly that and the duct reopens (yes). Treating only the inflammation leaves the duct mechanically jammed but non-inflammatory (still jammed: yes) — the comedonal residue the clinic knows well.
Hidradenitis suppurativa: the same jam deeper, with an irreversible rupture branch
Hidradenitis suppurativa is the same occlusion jam in deeper apocrine-gland-bearing follicles, driven heavier (net occlusion about 1.50) so the plug reaches a load at which it ruptures into the dermis instead of extruding (yes) — a chronic scarring sinus-tract sub-state the superficial comedo never reaches. This produces the page's sharpest clinical contrast: dropping the occlusion drive all the way down to the same sub-acne level that clears acne (yes — the jam itself would open) still leaves the ruptured tract in place (yes). So an anti-inflammatory biologic calms the active disease but cannot reopen a structural scar; only physical reset — deroofing or excision — resolves the tract (yes). The same drive-down, opposite outcome, is the substrate's clean account of why isotretinoin clears acne but not established hidradenitis tracts.
The discriminant: opposite occlusion modes from one jam
As with the static diseases and the hair cycle, the decisive evidence is that clinically opposite behaviours fall out of the same jam driven differently, with no constant changed between them.
| Axis | One pole | Opposite pole | Reproduced |
|---|---|---|---|
| Reversibility | superficial acne (drive-down reopens it) | deep HS rupture (same drive-down leaves the scar) | yes |
| Inflammatory sign | with C. acnes (inflammatory) | without C. acnes (comedonal, still jammed) | yes |
| Plug depth | hidradenitis suppurativa (heavier load) | acne (lighter load) | yes |
All three opposite pairs reproduce (yes). That one occlusion switch yields a reversible superficial comedo and an irreversible deep sinus tract, an inflammatory and a comedonal lesion, and a lighter and a heavier plug — from occlusion depth and the C. acnes amplifier alone, on a single measured PRDM1 γ with no new parameter — is the strongest internal evidence that these occlusion diseases are jamming dynamics, not bespoke fits.
Grades and reproducibility
Every mechanism here is a simulation-verified shape or sign [V] Simulation-verified — discontinuous closure, the hysteresis loop, the patent set-point, the comedo direction, the reopening on reversed knobs, the deep rupture branch and its drive-down irreversibility. Every clinical mapping rests on a cited anchor [L] Cited anchor. The occlusion set-points are forced regime scales [F] Forced (substrate). Every absolute magnitude is open [O] Open (obstacle stated) — comedo and lesion counts, Hurley-stage extent, sebum excretion rate — inheriting the sebaceous target's obstacle (a per-gland calibration). No disease introduces a new constant; each is a named perturbation of the one jam.
The sebaceous pipeline is deterministic on its own terms: two independent runs hash to an identical SHA-256, separate from the core battery, the pathology layer and the hair-cycle layer. Crucially, adding this organ does not touch the core T1–T5+oncology battery, whose result hash is unchanged at 1fb59f556e01….