Published May 4, 2026 | Version v1

ROTATIONAL COHERENCE COLLAPSE AS THE UNIFIED MECHANISM OF SEVEN MAJOR DISEASES

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MS32 established the universal helix across ten empirical domains at 5.3σ. MS33 identified the bifurcation into creation and
maintenance modes governed by ACF at 6.4σ. MS34 established the two modes as phases of a continuous
thermodynamic cycle at 7.3σ. The present paper, MS35, applies the framework to biological disease.
The central proposition is that seven major diseases — cancer, Alzheimer's disease, Parkinson's disease, type 2 diabetes,
major depression, Huntington's disease, and ALS — are expressions of the same underlying event: the collapse of
rotational coherence at the mitochondrial and cellular scale below the ACF threshold of the creation mode. This
proposition is grounded in fifty years of independent peer-reviewed documentation of convergent mitochondrial dysfunction
across all seven diseases [Wallace 2005; Lin & Beal 2006; Bhatti et al. 2017].
The ATP synthase — a rotary molecular motor at 100–150 RPS confirmed by Nobel Prize work [Boyer & Walker 1997] — is
identified as the primary biological instantiation of the visitation frequency f v defined in MS33. The cell membrane potential
of −70 mV in healthy cells and −15 to −30 mV in diseased cells [Cone 1971; Hanahan & Weinberg 2011; Cross et al. 2007]
is identified as the biological measurement of ACF at and below the creation-mode threshold.
Primary statistical result (external evidence only): Fisher's method applied exclusively to the three independent
peer-reviewed biological domains (D17–D19) yields χ² = 42.83, df = 6, p = 1.26×10−7, σ = 5.16σ — crossing the 5σ
particle-physics discovery threshold using only auditable external data, with no dependence on the internal series chain.
Cumulative series result (df correction, v2.0): When the MS34 consolidated result (16 domains, df=32) is correctly
added, the total is χ² = 172.59, df = 38, p = 4.61×10−19, σ = 8.84. The v1.0 error (k=4, df=8) is corrected. Note: 75% of this
χ² mass originates from internal Zenodo preprints (MS32–MS34); this is declared explicitly in Section 4

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