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Entropy 2012, 14(8), 1399-1442; doi:10.3390/e14081399

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

1,*  and 2
1 Internal Medicine Group Practice, PhyNet, Inc., Longview, TX 75604, USA 2 Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, MA 02140, USA
Expression of Concern Note added on 17 September 2015 by the Editors: The editors of the journal have been alerted to concerns over potential bias in opinions and bias in the choice of citation sources used in this article. We note that the authors stand by the content as published. Since the nature of the claims against the paper concern speculation and opinion, and not fraud or academic misconduct, the editors would like to make readers aware that the approach to collating literature citations for this article was likely not systematic and may not reflect the spectrum of opinions on the issues covered by the article. Please refer to our policy regarding possibly controversial articles.
* Author to whom correspondence should be addressed.
Received: 29 June 2012 / Revised: 19 July 2012 / Accepted: 20 July 2012 / Published: 2 August 2012
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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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.
Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Davidson, R.M.; Seneff, S. The Initial Common Pathway of Inflammation, Disease, and Sudden Death. Entropy 2012, 14, 1399-1442.

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