Abstract
Autism spectrum disorder (ASD) is a developmental disability that can create significant challenges in behavior and communication. The prevalence of ASD is over 2% among 8-year-old children and the prevalence is similar across the globe. We suggest there are multiple critical periods during the fetal period and early post-natal years that set conditions for neurotypical development or for autism, via mechanisms that impact immunity. One critical period requires folate, a key methyl donor, with insufficient folate conditioning for ASD. Another critical period is altered by oxidative stress or inflammation, possibly linked to insufficient taurine to support microglial immunity, causing inflammatory-triggered alterations of neurotypical development, or by excessive oxidation related to low cysteine availability. We propose that supplementing reduced folate and taurine early in development, including both fetal and post-natal periods, may be most effective in reducing the severity of ASD symptoms by facilitating neurotypical passage through critical neurodevelopmental periods.
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