The Possible Link between Autism and Glyphosate Acting as Glycine Mimetic – A Review of Evidence from the Literature with Analysis
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 non- dose 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.
The available evidence appears to link research findings in autism to defects in early (including in utero) neurodevelopment . Scientific studies are still ongoing to determine which governing factors for human neurodevelopment act at which steps to influence neuron migration and/or gene expression. However, in view of the rising incidence of autism diagnosis, we hold that it is time to consider the theory herein advanced that human fetal neurodevelopment might be altered by exposure to intermittent doses of a relatively small number of molecules of a putative harmful glycine-mimetic.
The theory that such a toxin is originating from environmental and/or dietary sources is supported by the finding that the brains of at least some of the control subjects in the studies by Suzuki et al.  and Stoner et al.  had findings similar to the findings in the brains of autistics. Similarly, the plasma amino acid changes documented by Aldred et al.  in autistics were present also in their family members. Similarly, the fact that studies of gut microbiota of autistics compared to gut microbiota of their non-autistic siblings  have not shown significant differences could be explained by the presence in food for both groups of a harmful glycine mimetic acting as a biocide.
Importantly, the theory herein advanced holds that an environmental or dietary sourced exposure to a human fetus of such a putative harmful glycine mimetic would likely not follow a standard dose response curve. We believe evidence  supports the view that the effects on neurodevelopment in the fetus of such theorized harmful glycine mimetic exposure are dependent on factors such as timing of exposure, and on location of molecular interactions. This theory, if proven, might have far reaching implications, such as precluding, at least for pregnant women, the supposed utility of safe allowable limits in food or on crops of the putative harmful glycine mimetic.
In essence, neurodevelopment is unlike other natural processes, in that a small number of molecules disrupting neurodevelopment at just the wrong time could have devastating autism-causing and long lasting outsized effects.