Abstract
In 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.
Highlights
An extensive review of the colloid and interface science literature has led us to conclude that the very earliest events in inflammation, disease, and sudden death are purely biophysical
We propose that the biophysical effects of pro-inflammatory cationic surfactants on cell membrane function, mediated by water, provide the provocation that induces sudden death syndrome (SDS)
Recent studies by Chen and Mehta and Kleinbongard demonstrated that human erythrocytes possess an active and functional erythrocytic nitric oxide synthase (eNOS) that is located within the plasma membrane
Summary
An extensive review of the colloid and interface science literature has led us to conclude that the very earliest events in inflammation, disease, and sudden death are purely biophysical. The literature amply supports the concept that our vascular system, including the molecular and humoral immune defense and lymphatic systems, acts as though it is a single organ [1] Both microvascular disease and endothelial dysfunction share a common initial pathophysiology. A better understanding of these earliest of biophysical events will enable a more rational approach to dealing with many of today’s idiopathic diseases. These diseases, are likely to be pluricausal [2] and highly stereotyped [3] in their clinical presentations, often with substantial overlap of symptoms
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