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Entropy 2012, 14(10), 1953-1977; doi:10.3390/e14101953

Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?

Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge 02139, MA, USA
Note added by the Publisher: 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 issue an Expression of Concern 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 <a href=\\\\\\\\\\\\\\\'\\\\\\\\\\\\\\\'>possibly controversial articles</a>.
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Received: 28 September 2012 / Revised: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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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. View Full-Text
Keywords: autism; epigenetics; cholesterol sulfate; DNA methylation; sulfotransferases; heparan sulfate; folate; cobalamin; zinc autism; epigenetics; cholesterol sulfate; DNA methylation; sulfotransferases; heparan sulfate; folate; cobalamin; zinc

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Hartzell, S.; Seneff, S. Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism? Entropy 2012, 14, 1953-1977.

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