Special Issue "Biosemiotic Entropy: Disorder, Disease, and Mortality"
Quicklinks
A special issue of Entropy (ISSN 1099-4300).
Deadline for manuscript submissions: closed (31 October 2012)
Special Issue Editor
Guest Editor
Prof. Dr. John W. Oller, Jr.
Department of Communicative Disorders, University of Louisiana at Lafayette, P. O. Box 43170, Lafayette, LA 70504-3170, USA
Website: http://www.ucs.louisiana.edu/%7Ejxo1721/index.html
E-Mail: joller@louisiana.edu
Interests: biosemiotics; etiology of communication disorders; measurement of human abilities and severity of disabilities; intelligence theory; pragmatic information; pragmatic mapping theory; systems grammar
Special Issue Information
Dear Colleagues,
The simplest and most informative linguistic messages are the kind found in ordinary true narratives. Such valid messages ― laden with pragmatic information ― provide the limiting antithesis of biosemiotic entropy. Generalizing from linguistic to biological systems, and taking account of some of the countless ways any complex arrangement of symbols can be rendered senseless, the thesis to be explored in this special issue is that the corruption of biological messages from genetics upward to epigenetics, proteins, cells, tissues, and the organs of viable organisms ― which can be described as biosemiotic entropy ― is, unsurprisingly, the proximate cause of disorders, diseases, and mortality. We invite contributions ― pro, con, or offering any plausible alternative ― to the idea that corrupted biological messages account for (but, of course, are not limited to) anaphylaxis, preeclampsia, sudden death syndrome, immune disorders, autism, and so forth. Empirical and theoretical articles are invited exploring pathways by which toxins, disease agents, and their interactions, and/or injuries from microwave, electromagnetic, radiological, or other energy sources can be shown to increase biosemiotic entropy. Empirically grounded arguments showing how cascading series of effects lead to certain injuries, diseases, and/or known disorders are preferred.
Prof. Dr. John W. Oller, Jr.
Guest Editor
Submission
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Entropy is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs).
Keywords
- abstraction theory
- autism
- biosemiotic entropy
- immune disorders
- mortality theory
- pragmatic mapping
- pragmatic information
- preeclampsia
- theoretical linguistics
- theory of true narratives
Published Papers (9 papers)
|
Received: 29 June 2012; in revised form: 19 July 2012 / Accepted: 20 July 2012 / Published: 2 August 2012
Show/Hide Abstract
| Download PDF Full-text (1223 KB)
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.
|
|
Received: 28 September 2012; in revised form: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
Show/Hide Abstract
| Download PDF Full-text (415 KB)
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 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.
|
|
Received: 13 September 2012; in revised form: 18 October 2012 / Accepted: 19 October 2012 / Published: 25 October 2012
Show/Hide Abstract
| Download PDF Full-text (467 KB)
Abstract: In this review, we discuss an immunological-driven sign termed the Completed Self, which is related to a holistic determination of health vs. disease. This sign (human plus commensal microbiota) forms the human superorganism. The worldwide emergence of an epidemic of chronic diseases has caused increased healthcare costs, increased premature mortality and reduced quality of life for a majority of the world’s population. In addition, it has raised questions concerning the interactions between humans and their environment and potential imbalances. Misregulated inflammation, a host defense-homeostasis disorder, appears to be a key biomarker connecting a majority of chronic diseases. We consider the apparent contributors to this disorder that promote a web of interlinked comorbid conditions. Three key events are suggested to play a role: (1) altered epigenetic programming (AEP) that may span multiple generations, (2) developmental immunotoxicity (DIT), and (3) failure to adequately incorporate commensal microbes as a newborn (i.e., the incomplete self). We discuss how these three events can combine to determine whether the human superorganism is able to adequately and completely form during early childhood. We also discuss how corruption of this event can affect the risk of later-life diseases.
|
|
Received: 24 September 2012; in revised form: 16 October 2012 / Accepted: 5 November 2012 / Published: 7 November 2012
Show/Hide Abstract
| Download PDF Full-text (441 KB)
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 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.
|
|
Received: 12 September 2012; in revised form: 21 October 2012 / Accepted: 6 November 2012 / Published: 8 November 2012
Show/Hide Abstract
| Download PDF Full-text (447 KB)
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 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.
|
|
Received: 8 October 2012; in revised form: 28 November 2012 / Accepted: 4 December 2012 / Published: 7 December 2012
Show/Hide Abstract
| Download PDF Full-text (618 KB)
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 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.
|
|
Received: 1 November 2012; in revised form: 30 December 2012 / Accepted: 11 January 2013 / Published: 16 January 2013
Show/Hide Abstract
| Download PDF Full-text (6400 KB)
Abstract: Biosemiotic entropy involves the deterioration of biological sign systems. The genome is a coded sign system that is connected to phenotypic outputs through the interpretive functions of the tRNA/ribosome machinery. This symbolic sign system (semiosis) at the core of all biology has been termed “biosemiosis”. Layers of biosemiosis and cellular information management are analogous in varying degrees to the semiotics of computer programming, spoken, and written human languages. Biosemiotic entropy — an error or deviation from a healthy state — results from errors in copying functional information (mutations) and errors in the appropriate context or quantity of gene expression (epigenetic imbalance). The concept of biosemiotic entropy is a deeply imbedded assumption in the study of cancer biology. Cells have a homeostatic, preprogrammed, ideal or healthy state that is rooted in genomics, strictly orchestrated by epigenetic regulation, and maintained by DNA repair mechanisms. Cancer is an eminent illustration of biosemiotic entropy, in which the corrosion of genetic information via substitutions, deletions, insertions, fusions, and aberrant regulation results in malignant phenotypes. However, little attention has been given to explicitly outlining the paradigm of biosemiotic entropy in the context of cancer. Herein we distill semiotic theory (from the familiar and well understood spheres of human language and computer code) to draw analogies useful for understanding the operation of biological semiosis at the genetic level. We propose that the myriad checkpoints, error correcting mechanisms, and immunities are all systems whose primary role is to defend against the constant pressure of biosemiotic entropy, which malignancy must shut down in order to achieve advanced stages. In lieu of the narrower tumor suppressor/oncogene model, characterization of oncogenesis into the biosemiotic framework of sign, index, or object entropy may allow for more effective explanatory hypotheses for cancer diagnosis, with consequence in improving profiling and bettering therapeutic outcomes.
 |
|
Received: 8 October 2012; in revised form: 14 January 2013 / Accepted: 15 January 2013 / Published: 22 January 2013
Show/Hide Abstract
| Download PDF Full-text (777 KB)
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 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.
 |
|
Received: 15 January 2013; in revised form: 10 April 2013 / Accepted: 10 April 2013 / Published: 18 April 2013
Show/Hide Abstract
| Download PDF Full-text (518 KB) | 
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 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.
|
Planned Papers
The below list represents only planned manuscripts. Some of these
manuscripts have not been received by the Editorial Office yet. Papers
submitted to MDPI journals are subject to peer-review.
Type of Paper: Article
Title: Is Cholesterol Sulfate Deficiency a Major Factor in Preeclampsia and in Autism-related Increased Risk to Adverse Reactions to Vaccines?
Authors: Stephanie Seneff 1, Robert Davidson 2 and Jingjing Liu 1
Affiliations: 1 Computer Science and Artificial Intelligence Laboratory, MIT, 32 Vassar Street, Cambridge, MA 01890, USA; E-Mails: Seneff@csail.mit.edu (S.S.); jingl@csail.mit.edu (J.L.)
2 Internal Medicine Group Practice, PhyNet, Inc. Longview, TX 75605, USA; E-Mail: patrons99@yahoo.com (R.D.)
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 to a severe depletion of cholesterol sulfate. Through studies on the VAERS (Vaccine Adverse Event Reporting System) database, we demonstrate a strong statistical relationship among the symptoms associated with autism and the symptoms 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 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 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.
Keywords: autism; preeclampsia; nitric oxide; cobalamin; cholesterol sulfate; red blood cells; vaccines
Type of Paper: Review
Title: Multiple Layers of Patterns Affect the Risk of Chronic Diseases
Author: Rodney R. Dietert
Affiliation: Department of Microbiology and Immunology, Cornell University, Ithaca, NY USA; E-Mail: rrd1@cornell.edu
Abstract: Chronic diseases are the greatest killer worldwide. They cause not only a majority of mortality but also disability, reduced quality of life and the overburdening of our healthcare systems. When viewed across a lifetime, these diseases and conditions exist as an interconnected web of comorbid health risks. These disease patterns frequently emerge during childhood beginning with a root entryway condition (e.g., childhood asthma or type 1 diabetes) then progress to include additional chronic diseases with aging. Misregulated inflammation is a pivotal cellular-molecular signal for these interlinked patterns of disease. Beyond the biosemiotic patterns that link these diseases to each other, there are additional layers of patterns that feed into the chronic disease web. These include: patterns of direct environmental insult (e.g., toxic chemicals, drugs, radiation, diet,), physical-psychological trauma patterns, cognitive-perception patterns, and transgenerational epigenetic patterns. This review will discuss how these additional patterns over-lay the interconnected web of chronic diseases and affect the likelihood of disorder (inflammatory-immune dysfunction), disability and/or premature death. Consideration of these multiple- layered patterns may provide a useful strategy for both individual- and population-based risk reduction of chronic diseases.
Last update: 5 October 2012
