Volume seven · original hypotheses · not peer reviewed
Each entry begins with evidence that already exists, names the thing current explanations cannot account for, and proposes a cause. Every one states its predictions as numbered commitments and says what result would refute it.
Skin barrier function collapses when the intercellular lipids undergo a phase transition rather than when the layer thins, so permeability should change sharply at a critical temperature and hydration, and emollients should work by shifting that transition.
Skin biophysicsWound healing is driven by an endogenous electric field rather than by chemical gradients alone, so healing rate should be predicted by the wound current and accelerated by applied fields, and drugs that block epithelial ion transport should delay closure.
Wound healingAcne is driven by sebum production rate rather than by bacterial colonisation, so sebum suppression should be the primary intervention and antibiotics should be understood as adjuncts that work partly through anti-inflammatory effects.
Sebaceous biologyDental caries occurs only below a critical plaque pH that depends on the saturation of calcium and phosphate, so caries risk should be predicted from the pH threshold and the mineral saturation rather than from sugar exposure or bacterial counts.
Oral microbiologyThe fracture toughness of enamel is set by its residual protein content rather than by its mineral density, so enamel that is equally mineralised can differ in crack resistance, and treatments that remove protein may weaken teeth while looking clean.
Biomineral mechanicsFluoride protects teeth by shifting the critical pH and the remineralisation kinetics rather than by killing bacteria, so its benefit should be independent of the oral flora and should appear at concentrations too low to inhibit bacterial growth.
Preventive dentistryEndurance performance is limited by heat dissipation rather than by oxygen delivery, so the limiting factor should change with ambient conditions, and cooling interventions should improve performance more than oxygen supplementation in the heat.
Exercise physiologyStrength gains from training are set by tendon stiffness rather than by muscle size, so force should increase before hypertrophy is measurable, and training that stiffens tendon should produce earlier gains than training that targets muscle alone.
Musculoskeletal adaptationFatigue is the output of a predictive model of remaining capacity rather than a central governor that protects the body, so it should be updated by unexpected evidence and should be manipulable by information at fixed physiology.
Fatigue theoryThe flavour of a fermented food is set by the sequence of microbial stages rather than by the final composition, so two fermentations ending with the same species and metabolites can taste different, and process control should target the trajectory.
Fermentation scienceMicrobial spoilage is governed by water activity rather than by microbial load, so two foods with the same contamination can differ in shelf life by months, and formulation should target water activity rather than preservative concentration.
Food safetyThe flavour of a spontaneous fermentation is set by which genus becomes dominant, and the winner is determined by the initial pH rather than by the diversity of the starting community, so flavour is predictable from a single early measurement.
Microbial ecologyThe evidence is published and cited. The tension is the anomaly the current explanation cannot absorb. The theory is the proposed cause. What this is not separates it from the nearest existing idea, which is the part most speculative writing skips. Predictions are numbered and falsifiable. What would refute it is the cheapest result that ends the argument.
These are not summaries of the literature and not reviews. They are claims, written to be argued with and tested. The evidence is real; the causal ordering is proposed. Several will turn out wrong, which is the intended condition of a hypothesis that can be checked.
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