Glyphosate is the most widely used herbicide on the planet, and its increasing use over time in the United States aligns well with the increasing rates of autism determined by the Centers for Disease Control. Based on the known mechanism of glyphosate toxicity, we hypothesize that a pregnant woman's exposure at midpregnancy to glyphosate-formulated herbicides (GFH) may produce, in her unborn child's brain, anatomic alterations of cortical neuron layering remarkably similar to those found in the brains of humans with autism. Glyphosate's known ability to chelate manganese ions combined with evidence of severely depleted serum manganese in cows exposed to glyphosate makes it likely that glyphosate would induce manganese deficiency in humans, interfering with the function of manganese-dependent enzymes. In particular, this would affect the maternal pituitary's manganese-dependent Protein Phosphatase 1 (PP1) enzyme, resulting in a significant reduction in maternal serum levels of Thyroid-Stimulating Hormone (TSH). A study of mid-pregnancy maternal TSH serum levels in human mothers has found a statistical correlation of reduced TSH to increased risk of autism in offspring. Since insufficient thyroid stimulation by TSH or by iodine deficiency would both induce hypothyroidism, effects of iodine deficiency can be expected to emulate effects of TSH deficiency. Cortical neuron disarrangements have been produced in the brains of offspring of rat dams fed an iodine-deficient diet, and such foci of disordered cortical neurons are characteristically found in human autistic brains. While the research literature on glyphosate's endocrine disrupting effects is limited, diverse evidence from animal studies reveals effects that suggest impaired thyroid function. If our hypothesis can be substantiated by a focused research effort, it would provide further justification for reducing or, ideally, eliminating glyphosate-formulated herbicide exposures in pregnant women.