The thirteen major skin diseases are not new physics: each is one verified mechanism (T1–T5 or the oncology kernel) driven off its set-point, and each treatment is the same knob reversed. They pass a clinical-sign plus intervention-reversal battery and a five-way opposite-sign discriminant — psoriasis/ichthyosis, melasma/vitiligo, hyperhidrosis/ectodermal-dysplasia — with no constant added.
Thirteen common skin diseases are reproduced as signed perturbations of the six verified mechanisms. Opposite entities — psoriasis/ichthyosis, melasma/vitiligo, hyperhidrosis/ectodermal-dysplasia — emerge from opposite drive signs on a single R19 switch, every intervention is the same knob reversed, and the layer adds no constant while the core-battery hash stays fixed.
Disease is mechanism off its set-point; treatment is the same knob reversed
The previous pages established six verified mechanisms — the water barrier (T1), wound closure (T2), the melanin screen (T3), turnover (T4), thermoregulation (T5), and the carcinogenesis kernel. This page covers the major skin diseases without adding any new physics: each disease is one of those mechanisms driven away from its set-point, and each established treatment is the same control pushed back. Thirteen diseases pass a clinical-sign plus intervention-reversal battery and a five-way opposite-sign discriminant, with no constant introduced.
| Disease | Target | Covered as |
|---|---|---|
| Atopic dermatitis | T1 | chronic barrier-reserve collapse |
| Contact dermatitis | T1 | acute insult past the discontinuous collapse |
| Ichthyosis (dynamics) | T1+T4 | desquamation retention near the spinodal |
| Psoriasis | T4 | differentiation-spinodal threshold + autonomous acceleration |
| Chronic / diabetic / pressure wound | T2 | non-closure below the critical unjamming drive |
| Vitiligo | T3 | discontinuous melanocyte-viability loss |
| Melasma / hyperpigmentation | T3 | regulated melanin overshoot |
| Albinism / OCA (dynamics) | T3→onco | screen removed → hazard relative risk |
| Hypohidrotic ectodermal dysplasia (dynamics) | T5 | capped sweat → danger band at lower load |
| Primary hyperhidrosis | T5 | lowered recruitment threshold |
| Heat stroke | T5 | capacity exceeded → runaway |
| Skin cancer (melanoma / SCC / BCC) | onco | intermittent-vs-cumulative + pigment-loss burst |
| Actinic keratosis | onco | SCC precursor (fewer multistage hits) |
Barrier failures (T1): atopic, contact, ichthyosis
Atopic dermatitis is a chronic erosion of barrier reserve: the depth of the intact-barrier basin falls to about 0.55 of healthy, and barrier repair (emollient) restores it to about 0.90 — the knob moved back, not a new mechanism. Contact dermatitis is the acute mode of the same T1 switch: an external irritant clears the spinodal and the barrier collapses discontinuously rather than drifting. Ichthyosis sits on the retention side: a weak desquamation drive holds the corneum near its spinodal, raising stratum-corneum residence about 6.6× (critical slowing), reversed by a keratolytic that restores a strong shedding drive.
Turnover off both poles (T4): psoriasis versus ichthyosis
Psoriasis is the turnover mechanism past its differentiation spinodal: below threshold transit is homeostatic (about 28 days), but above it the exit drive becomes autonomous and self-accelerating, compressing transit about 20.8× toward the cited 3–5-day psoriatic window (against the 28–40-day healthy window). Anti-proliferative therapy lowers the exit drive back below the spinodal. Psoriasis (acceleration) and ichthyosis (retention) are the two opposite signs of one turnover switch.
Wound non-closure (T2): chronic, diabetic, pressure wounds
A chronic wound is re-epithelialisation held below its own unjamming drive. With the vertex-model threshold q* = 3.81 fixed (cited), a free-edge drive of 0.1 stays below the package's critical unjamming drive of 0.15, so the edge never crosses q*, the sheet stays jammed, and the gap does not close. Raising the drive to 0.25 (debridement, growth factor, or a re-epithelialisation cue) carries it over the threshold and the wound closes — the same T2 unjam→migrate→rejam cycle, restored.
Pigment off both poles (T3): vitiligo, melasma, albinism
Vitiligo drives the melanocyte viability switch below its spinodal: melanin collapses discontinuously to 0.0 and the delivered-ultraviolet attenuation returns to 1.0 (no screen at all), so the patch is photoprotection-deficient — repigmentation needs active phototherapy (hysteresis). Melasma is the opposite sign of the same MITF switch: a standing pro-melanogenic drive raises regulated melanin about 3.12×, reversed by removing the driver. Albinism removes the functional screen upstream, so the ultraviolet reaching DNA stays full and the shared multistage hazard rises to a relative risk of about 2.58× versus pigmented skin — an exogenous sunscreen brings it back to about 1.13×.
Thermoregulation off both poles (T5): ectodermal dysplasia, hyperhidrosis, heat stroke
Hypohidrotic ectodermal dysplasia caps the sweat appendage's maximum capacity, so the evaporative interface flux is limited and the danger band is reached at a lower load: onset moves from 3.1 (healthy) to 1.8 (disease), and at a test load of 2.5 the core measure runs to 4.60 against 2.05 healthy — external cooling caps the load below that onset. Primary hyperhidrosis is the opposite sign of the same EDAR switch: the recruitment threshold is lowered (onset 0.2 against 0.3), so the gland fires sub-threshold, and threshold-raising therapy reverses it. Heat stroke is the capacity limit of the healthy controller: above saturation the regulated temperature–load slope (0.77) jumps to the runaway slope (2.00) and core temperature climbs without bound.
Oncology: skin cancer and its precursor
The carcinogenesis page's single convex multistage rate carries straight into disease. Squamous-cell carcinoma is near-linear in cumulative dose (linear to r = 0.999); melanoma is intermittent-sensitive, the same dose in bursts raising relative risk up to about 5.67×; and a chronic-exposure tan protects against melanoma by about 2.63× (the paradox). The pigment-loss diseases above couple in here: removing the screen raises the burst relative risk to about 10.59×. Actinic keratosis is the same kernel with fewer hits crossed — early field damage of high prevalence (0.96) sitting above invasive squamous-cell carcinoma (0.18) at the same dose, with only a small per-lesion fraction completing the remaining hits.
The discriminant: opposite diseases from opposite drive signs
The decisive test is that opposite clinical entities fall out of the same switch driven in opposite directions, with no constant changed between them. Each pole below is the literal sign-flip of its partner on one R19 control.
| Switch | Positive-drive pole | Negative-drive pole | Reproduced |
|---|---|---|---|
| Turnover | psoriasis (accelerated) | ichthyosis (retention) | yes |
| Barrier reserve | intact (full reserve) | atopic (collapsed reserve) | yes |
| Melanin | melasma (overshoot) | vitiligo (loss) | yes |
| Sweat recruitment | hyperhidrosis (excess) | ectodermal dysplasia (deficit) | yes |
| Photoprotection | healthy tan (screened) | pigment loss (unscreened) | yes |
All five opposite pairs reproduce (yes). That a single switch generates psoriasis and ichthyosis, melasma and vitiligo, hyperhidrosis and the ectodermal-dysplasia deficit from opposite signs alone is the strongest internal evidence that the lesions are dynamics, not bespoke parameters.
Grades and reproducibility
Every disease mechanism here is a simulation-verified shape, control, or sign [V] Simulation-verified; every clinical mapping rests on a cited anchor [L] Cited anchor; and every absolute magnitude is open [O] Open (obstacle stated), each inheriting the obstacle of its parent target — absolute TEWL (T1 lipid permeability), absolute closure rate (T2 cell speed), absolute melanin optical density (T3 extinction coefficient), absolute transit days (T4 per-cell calibration), absolute set-point and sweat rate (T5 per-gland output and heat capacity), and absolute incidence and relative-risk magnitude (oncology population baseline and dose calibration). No disease introduces a new constant; each is a named perturbation of an existing knob.
The pathology pipeline is deterministic on its own terms: two independent runs hash to an identical SHA-256, separate from the core battery. Crucially, adding this disease layer does not touch the core T1–T5+oncology battery, whose result hash is unchanged at 1fb59f556e01….