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.
Highlights
Autism spectrum disorders (ASD), with early childhood autism at their core, are loosely defined by social, cognitive, and memory deficits leading to atypical neurodevelopment [1]
We argue that this transformation is facilitated by endothelial nitric oxide synthase, operating in red blood cells and platelets, as well as the endothelial cells lining the capillary walls, and by neuronal nitric oxide synthase
Encephalitis can be viewed as a response of the body to the need to augment the supply of sulfate to the brain and to the blood stream, under conditions of extreme deficits
Summary
Autism spectrum disorders (ASD), with early childhood autism at their core, are loosely defined by social, cognitive, and memory deficits leading to atypical neurodevelopment [1]. The signaling cascade under consideration here suggests that metabolic and biophysical changes associated with encephalitis can activate an innate ability to produce sulfate that would ordinarily require sunlight exposure This is where high fever and seizures play an important role, in providing the necessary energy to catalyze the production of sulfate from sulfur-containing precursor molecules such as homocysteine, 3-mercaptopyruvate, and, especially, taurine. The reasonable expectation is that the child would experience the sulfur deficiency in utero, potentially leading to reprogramming of neural development strategies Another phenomenon seen in connection with ASD is an increase in plasma levels of nitric oxide (NO) [45], which can be induced by the epigenetic reprogramming to compensate for insufficient sulfate supplies [14]. A likely consequence of excess NO synthesis is the production of excess ammonia, with consequences in the brain, as shown in Section 4, explaining why ASD is associated with overproduction of GSSG
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