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.
Keywords: encephalitis; autism; nitric oxide; cholesterol sulfate; ammonia; aluminum; mercury; lead; glyphosate; seizures; taurine
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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.
Seneff S, Lauritzen A, Davidson RM, Lentz-Marino L. Is Encephalopathy a Mechanism to Renew Sulfate in Autism? Entropy. 2013; 15(1):372-406.
Seneff, Stephanie; Lauritzen, Ann; Davidson, Robert M.; Lentz-Marino, Laurie. 2013. "Is Encephalopathy a Mechanism to Renew Sulfate in Autism?" Entropy 15, no. 1: 372-406.