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The Initial Common Pathway of Inflammation, Disease, and Sudden Death†
AbstractIn reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.
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Davidson, R.M.; Seneff, S. The Initial Common Pathway of Inflammation, Disease, and Sudden Death. Entropy 2012, 14, 1399-1442.View more citation formats
Davidson RM, Seneff S. The Initial Common Pathway of Inflammation, Disease, and Sudden Death. Entropy. 2012; 14(8):1399-1442.Chicago/Turabian Style
Davidson, Robert M.; Seneff, Stephanie. 2012. "The Initial Common Pathway of Inflammation, Disease, and Sudden Death." Entropy 14, no. 8: 1399-1442.
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