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Open AccessCorrection Correction on Davidson, R.M.; Lauritzen, A.; Seneff, S. Biological Water Dynamics and Entropy: A Biophysical Origin of Cancer and Other Diseases. Entropy 2013, 15, 3822-3876
Entropy 2015, 17(9), 6238; doi:10.3390/e17096238
Received: 14 August 2015 / Accepted: 28 August 2015 / Published: 8 September 2015
Viewed by 833 | PDF Full-text (604 KB) | HTML Full-text | XML Full-text
Abstract The authors wish to make the following correction to their paper [1]. The correct reference 190 in the reference list should be: [...] Full article
Open AccessReview Biological Water Dynamics and Entropy: A Biophysical Origin of Cancer and Other Diseases
Entropy 2013, 15(9), 3822-3876; doi:10.3390/e15093822
Received: 3 June 2013 / Revised: 26 August 2013 / Accepted: 30 August 2013 / Published: 13 September 2013
Cited by 19 | Viewed by 3981 | PDF Full-text (708 KB) | HTML Full-text | XML Full-text
Abstract
This paper postulates that water structure is altered by biomolecules as well as by disease-enabling entities such as certain solvated ions, and in turn water dynamics and structure affect the function of biomolecular interactions. Although the structural and dynamical alterations are subtle, they
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This paper postulates that water structure is altered by biomolecules as well as by disease-enabling entities such as certain solvated ions, and in turn water dynamics and structure affect the function of biomolecular interactions. Although the structural and dynamical alterations are subtle, they perturb a well-balanced system sufficiently to facilitate disease. We propose that the disruption of water dynamics between and within cells underlies many disease conditions. We survey recent advances in magnetobiology, nanobiology, and colloid and interface science that point compellingly to the crucial role played by the unique physical properties of quantum coherent nanomolecular clusters of magnetized water in enabling life at the cellular level by solving the “problems” of thermal diffusion, intracellular crowding, and molecular self-assembly. Interphase water and cellular surface tension, normally maintained by biological sulfates at membrane surfaces, are compromised by exogenous interfacial water stressors such as cationic aluminum, with consequences that include greater local water hydrophobicity, increased water tension, and interphase stretching. The ultimate result is greater “stiffness” in the extracellular matrix and either the “soft” cancerous state or the “soft” neurodegenerative state within cells. Our hypothesis provides a basis for understanding why so many idiopathic diseases of today are highly stereotyped and pluricausal. Full article
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Open AccessReview Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases
Entropy 2013, 15(4), 1416-1463; doi:10.3390/e15041416
Received: 15 January 2013 / Revised: 10 April 2013 / Accepted: 10 April 2013 / Published: 18 April 2013
Cited by 47 | Viewed by 214643 | PDF Full-text (518 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of
[...] Read more.
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate's inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy: the disruption of homeostasis by environmental toxins. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Is Encephalopathy a Mechanism to Renew Sulfate in Autism?
Entropy 2013, 15(1), 372-406; doi:10.3390/e15010372
Received: 8 October 2012 / Revised: 14 January 2013 / Accepted: 15 January 2013 / Published: 22 January 2013
Cited by 6 | Viewed by 5406 | PDF Full-text (777 KB) | HTML Full-text | XML Full-text
Abstract
This paper makes two claims: (1) autism can be characterized as a chronic low-grade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is
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This paper makes two claims: (1) autism can be characterized as a chronic low-grade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessReview Is Endothelial Nitric Oxide Synthase a Moonlighting Protein Whose Day Job is Cholesterol Sulfate Synthesis? Implications for Cholesterol Transport, Diabetes and Cardiovascular Disease
Entropy 2012, 14(12), 2492-2530; doi:10.3390/e14122492
Received: 8 October 2012 / Revised: 28 November 2012 / Accepted: 4 December 2012 / Published: 7 December 2012
Cited by 8 | Viewed by 4809 | PDF Full-text (618 KB) | HTML Full-text | XML Full-text
Abstract
Theoretical inferences, based on biophysical, biochemical, and biosemiotic considerations, are related here to the pathogenesis of cardiovascular disease, diabetes, and other degenerative conditions. We suggest that the “daytime” job of endothelial nitric oxide synthase (eNOS), when sunlight is available, is to catalyze sulfate
[...] Read more.
Theoretical inferences, based on biophysical, biochemical, and biosemiotic considerations, are related here to the pathogenesis of cardiovascular disease, diabetes, and other degenerative conditions. We suggest that the “daytime” job of endothelial nitric oxide synthase (eNOS), when sunlight is available, is to catalyze sulfate production. There is a striking alignment between cell types that produce either cholesterol sulfate or sulfated polysaccharides and those that contain eNOS. The signaling gas, nitric oxide, a well-known product of eNOS, produces pathological effects not shared by hydrogen sulfide, a sulfur-based signaling gas. We propose that sulfate plays an essential role in HDL-A1 cholesterol trafficking and in sulfation of heparan sulfate proteoglycans (HSPGs), both critical to lysosomal recycling (or disposal) of cellular debris. HSPGs are also crucial in glucose metabolism, protecting against diabetes, and in maintaining blood colloidal suspension and capillary flow, through systems dependent on water-structuring properties of sulfate, an anionic kosmotrope. When sunlight exposure is insufficient, lipids accumulate in the atheroma in order to supply cholesterol and sulfate to the heart, using a process that depends upon inflammation. The inevitable conclusion is that dietary sulfur and adequate sunlight can help prevent heart disease, diabetes, and other disease conditions. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessReview Is Cholesterol Sulfate Deficiency a Common Factor in Preeclampsia, Autism, and Pernicious Anemia?
Entropy 2012, 14(11), 2265-2290; doi:10.3390/e14112265
Received: 12 September 2012 / Revised: 21 October 2012 / Accepted: 6 November 2012 / Published: 8 November 2012
Cited by 5 | Viewed by 4323 | PDF Full-text (447 KB) | HTML Full-text | XML Full-text
Abstract
In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed
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In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed to a severe depletion of cholesterol sulfate. Through studies on the Vaccine Adverse Event Reporting System (VAERS) database, we demonstrate a strong statistical relationship among the signs and symptoms associated with autism and those associated with preeclampsia, pernicious anemia, and serious adverse reactions to vaccines. We show that VAERS reports associated with symptoms typical of pernicious anemia produce both a set of symptoms that are highly correlated with preeclampsia and another set highly correlated with autism. We explain this observation via an argument that, in a severe reaction, the cascade of events subsequent to vaccination reflects a profuse production of nitric oxide (NO) and consequential destruction of both red blood cells (RBCs) and cobalamin. This may explain the diverse signs and symptoms associated with both preeclampsia and severe vaccine adverse reactions. We argue that excess NO synthesis, induced by the aluminum and antigen in vaccines, results in hemolysis of RBCs, which allows hemoglobin to scavenge the excess NO, converting it to nitrate. The NO is also scavenged by cobalamin, leading to its inactivation and contributing to subsequent pernicious anemia. Finally, we demonstrate that severe adverse reactions to vaccines can be associated with life-threatening conditions related to the heart and brain, as well as stillbirth, when the vaccine is administered to a woman in the third-trimester of pregnancy, as demonstrated by statistical analysis of the Gardasil records. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessArticle Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure
Entropy 2012, 14(11), 2227-2253; doi:10.3390/e14112227
Received: 24 September 2012 / Revised: 16 October 2012 / Accepted: 5 November 2012 / Published: 7 November 2012
Cited by 16 | Viewed by 53660 | PDF Full-text (441 KB) | HTML Full-text | XML Full-text
Abstract
Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC
[...] Read more.
Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC Vaccine Adverse Events Reporting System (VAERS) database. Our results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessReview Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
Entropy 2012, 14(10), 1953-1977; doi:10.3390/e14101953
Received: 28 September 2012 / Revised: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
Cited by 9 | Viewed by 4050 | PDF Full-text (415 KB) | HTML Full-text | XML Full-text
Abstract
Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the
[...] Read more.
Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessReview The Initial Common Pathway of Inflammation, Disease, and Sudden Death
Entropy 2012, 14(8), 1399-1442; doi:10.3390/e14081399
Received: 29 June 2012 / Revised: 19 July 2012 / Accepted: 20 July 2012 / Published: 2 August 2012
Cited by 11 | Viewed by 5497 | PDF Full-text (1223 KB) | HTML Full-text | XML Full-text
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
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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. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)

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