The PMCHS framework wasn't born finished. This page traces, step by step, what was thought, published, then revised — so the current version of the model never gives the impression of having always existed in this form.
The research begins from a specific question: could mast cells play a role in sudden infant death syndrome (SIDS)? This initial intuition — a maternal mast cell terrain as a transversal risk factor — becomes the throughline for everything that follows.
Published on Zenodo/OSF (DOI 10.5281/zenodo.19816705), after rejections from medRxiv (no institutional affiliation) and PsyArXiv. This first preprint lays out the initial framework: PMCHS as a predominantly maternal epigenetic terrain, centered on the NR3C1/KITLG axis, four mast cell degranulation phenotypes, and the first data from the international survey (N≈423).
Published on Zenodo/OSF (DOI 10.5281/zenodo.20480196). This second preprint formalizes the link between the maternal mast cell terrain, disrupted synaptic pruning via microglial activation, locus coeruleus hyperactivation, and non-integrated primitive reflexes as an early neurodevelopmental marker.
Revisiting the model, the thesis shifts on a central point: non-integrated primitive reflexes are no longer seen as the origin of locus coeruleus hyperreactivity, but as a downstream consequence, with its own cascade. The origin of the terrain is repositioned toward an early rupture in safety and attachment — for example, unresponded infant distress that "teaches" the infant that adults are unreliable.
Direct consequence: mast cell/immune dysregulation itself stops being seen as a parallel or upstream driver, and becomes a consequence of chronic locus coeruleus hyperreactivity.
The causal model is restructured around a simpler principle: the locus coeruleus (chronic hyperactivation) becomes the central upstream node, from which several branches of consequences emerge — behavioral regulation mechanisms, immune dysregulation (mast cells), general interoceptive hypoesthesia (HIG), and dissociation/fawning responses. Primitive reflexes remain in the model, but as one downstream branch among others, no longer as the starting point.
Preprint 2 is currently under revision (version 5): adding a section on the thoracic postural mechanism (somatic amplification loop), four new references, and correcting orphan citations pointing to a now-retracted Melillo paper.
The current model places the locus coeruleus as the central causal node, with mast cells, HIG, behavioral regulation mechanisms and primitive reflexes as observable consequence branches — rather than independent drivers of the terrain.
The model keeps evolving. Among the threads currently being explored and not yet formally integrated: the link between May-Thurner syndrome/pelvic venous congestion and lipedema as a regional mast-cell-mediated trigger; the folate/FRAA mechanism in autism; and the exact place of collagen degradation in the model (a consequence of chronic mast cell activity rather than a primary structural defect). These threads will be added to this timeline as they are formalized.