Three visual representations of the PMCHS model: the estrogenic amplification loop, the transgenerational cumulative burden, and the causal architecture centered on the locus coeruleus.
A self-sustaining cycle triggered by estrogen signaling, specifically concerning the role of estrogen in tissue inflammation — notably in the pathogenesis of lipedema and obesity — which amplifies the local mast cell terrain over time independently of a new triggering factor. Distinct from the transgenerational cumulative burden below, which is a different kind of mechanism.
Source: "Estrogenic amplification loop" pillar, see Current biological model.
A mechanism distinct from the estrogenic loop above: four factors that accumulate from generation to generation — mitochondrial transmission, epigenetic amplification, combined parental load, and fetal microchimerism — progressively aggravating the PMCHS terrain passed on to the next child.
⚗️ Source: synthesis of personal research notes on fetal microchimerism and mitochondrial transmission — not yet integrated into published preprints or the (V4) revision of Preprint 2. See the detail in Proposed mechanisms.
The current state of the model (September 2026): an early rupture of safety/attachment upstream, the locus coeruleus as the hyperactivated central relay, and four branches of observable consequences downstream.
Source: "Current state of the model" section, see Model evolution and Proposed mechanisms.