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Entropy 2013, 15(1), 372-406; doi:10.3390/e15010372

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

1,* , 2
1 Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, MA 02139, USA 2 Independent Researcher, Houston, TX 77084, USA 3 Internal Medicine Group Practice, PhyNet, Inc., Longview, TX 75604, USA 4 Biochemistry Laboratory Director, Mount Holyoke College, South Hadley, MA 01075, 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: 8 October 2012 / Revised: 14 January 2013 / Accepted: 15 January 2013 / Published: 22 January 2013
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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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.
Keywords: encephalitis; autism; nitric oxide; cholesterol sulfate; ammonia; aluminum; mercury; lead; glyphosate; seizures; taurine encephalitis; autism; nitric oxide; cholesterol sulfate; ammonia; aluminum; mercury; lead; glyphosate; seizures; taurine
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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Seneff, S.; Lauritzen, A.; Davidson, R.M.; Lentz-Marino, L. Is Encephalopathy a Mechanism to Renew Sulfate in Autism? Entropy 2013, 15, 372-406.

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