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A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States

DOI: 10.1186/1868-7083-4-6

Keywords: Autism, DNA methylation, Environmental epigenetics, Heavy metals, HFCS, PON1, SAM, Zn

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Abstract:

Autism is a developmental disorder defined by the American Psychiatric Association (APA) in the Diagnostic and Statistical Manual of Mental Disorders (DSM). The condition is considered a pervasive developmental disorder (PDD) that appears in the first three years of life and affects brain development impacting social and communication skills. Autism is defined by a common set of behaviors, including, but not limited to, observed deficits in nonverbal and verbal communication, lack of social reciprocity, and failure to develop and maintain appropriate peer relationships [1]. Recent estimates suggest that 31% of children with Autism Spectrum Disorder (ASD) also meet diagnostic criteria for Attention-Deficit/Hyperactivity Disorder (ADHD) and another 24% of children with ASD exhibit sub-threshold clinical symptoms for ADHD [2]. The number of children affected by this debilitating disorder remains unknown. As part of this review, we analyze the current United States (U. S.) Department of Education Special Education data to estimate the increase in autism prevalence from 2005 to 2010.The cause(s) of autism also remain(s) unknown. D'Amelio et al. found paraoxonase-1 (PON1) gene variants associated with autism in subgroups of the U. S. population but not in Italy [3]. They attributed the gene variation to greater household use of organophosphate (OP) pesticides in the U.S. compared to Italy. We think a more plausible explanation may lie in the U. S. food supply. As part of this investigation, we also reviewed and analyzed the U.S. Department of Agriculture (USDA) Food Availability Spreadsheets to identify which foods are most frequently consumed by Americans and of those which most frequently contain OP pesticide residue as reported by the U.S. Pesticide Data Program.During this investigation, we conducted a literature review of all studies published on autism since we published our first Mercury Toxicity Model [4], which explains how mercury exposure, nutritional deficienc

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