What the PMCHS model predicts, and what could in principle be tested or observed to confirm or refute it.
A formal cohort study, independent of the initial survey (and therefore less exposed to self-selection bias), should find a maternal-to-paternal transmission ratio significantly higher than expected under sex-independent transmission.
Not formally testedCirculating HMGB1 levels should be measurably higher in people presenting the histaminergic degranulation phenotype, and correlated with reported symptom severity.
Not testedNR3C1 methylation scores should differ measurably (hypermethylation) in people with a suspected PMCHS terrain compared to controls, particularly where childhood trauma is reported.
Not testedUnder prolonged mast cell stabilization (quercetin, luteolin, cromoglycate), a measurable improvement in thirst and satiety perception (via a standardized scale yet to be defined) should be observable.
Preliminary clinical signal reportedIndirect markers of locus coeruleus activity (e.g. heart rate variability or pupillary reactivity) should be abnormal in people with a suspected PMCHS terrain — including those whose archaic reflexes are well integrated, since these are now considered a consequence rather than the origin.
Not testedIf the observed collagen degradation is indeed a consequence of chronic mast cell activity rather than a primary structural defect, prolonged mast cell stabilization should be accompanied by stabilization or improvement of connective-tissue fragility markers (indicators to be defined).
Not testedA retrospective case-control study should find a higher prevalence of maternal mast cell terrain (or suggestive family history) in families that have experienced sudden infant death syndrome than in the general population. 9.7% of PMCHS survey respondents report such a history — a signal worth formal investigation, not yet proof.
Preliminary signal (survey, N=423)