Beecham JE and Stephanie Seneff
The causes of autism spectrum disorder (ASD) are not well understood. Only a minority of cases are explainable by specific abnormalities in DNA sequence, whereas the majority are widely assumed to be linked to epigenetic effects, and/or likely impacted by environmental factors. Here, we postulate autism causation via environmental and/or dietary sourced toxin acting intermittently in utero on human fetuses to disrupt neurodevelopment in a nondose dependent manner. Our theory is informed by a mini-review and correlation of selected studies from the research literature related to autism, including radiologic, anatomic, metabolic, neurodevelopmental, pharmacologic and MRI studies. In reviewing and analyzing evidence, we focus on data supporting interaction of the theorized harmful glycine mimetic at one or more of the following calcium inflow regulatory factors for neurons: the N-methyl D-aspartate (NMDA) receptor, the glycine receptor (GlyR) and/or the glycine transporter protein 1 (GlyT1). We postulate this harmful glycine mimetic to act by exerting a direct molecular disruption to calcium regulatory factors for neurons. This disruption appears to occur in a time sensitive, rather than a strictly dose-dependent manner, leading to haphazard disorganizations of the normally carefully choreographed steps of early neuronal migration. Within this analysis, we find support for the contention that a strong candidate for the putative harmful glycine mimetic is glyphosate, the active ingredient in the pervasive herbicide Roundup®. In addition to glyphosate’s molecular similarity to glycine, glyphosate is known to have a propensity to avidly bind minerals such as manganese and magnesium, which minerals are implicated in the normal functioning of several neuronal calcium inflow regulatory factors. Our theory highlights areas deserving of further study.
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