The cause of autism remains unknown but the increase in prevalence suggests environmental factors in its causation. There are well defined changes in the brain of patients with autism. These include prominent alterations of cortical neuronal migration and cerebellar Purkinje cells. Neuronal migration, via reelin regulation, requires the intervention of the thyroid hormone triiodothyronine (T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases. Experimental animal models have shown that transient intrauterine deficits of thyroid hormones (as brief as 3 days) result in permanent alterations of cerebral cortical architecture reminiscent of those observed in brains of patients with autism.
I have postulated that early maternal hypothyroxinemia (low T4) resulting in low T3 in the fetal brain during the period of neuronal cell migration (weeks 8–12 of pregnancy) may produce morphological brain changes leading to autism. Insufficient dietary iodine intake during pregnancy and a number of environmental antithyroid and goitrogenic agents can affect maternal thyroid function during pregnancy. A progressive decline in the levels of iodine in the US population, and in particular among women of reproductive age would increase the population at risk.
Environmental contaminants interfere with thyroid function including 60% of all herbicides, in particular 2,4-dichlorophenoxy acetic acid (2,4-D), acetochlor, aminotriazole, amitrole, bromoxynil, pendamethalin, mancozeb, and thioureas. Other anti-thyroid agents include polychlorinated biphenyls (PCBs), perchlorates, mercury, and coal derivatives such as resorcinol, phthalates, and anthracenes. A leading ecological study in Texas has correlated higher rates of autism in school districts affected by large environmental releases of mercury from industrial sources. Mercury is a well known antithyroid substance causing inhibition of deiodinases and thyroid peroxidase. The current surge of autism could be related to transient maternal hypothyroxinemia resulting from dietary and/or environmental exposure to antithyroid agents. Additional multidisciplinary epidemiological studies will be required to confirm this environmental hypothesis of autism.
Prof. Gustavo C. Román MD
Dr. Román was instrumental in the development of currently used criteria for Vascular Dementia (NINDS-AIREN Criteria) and created an international Neuroepidemiology research network that to this day continues to yield data. Dr. Román received the Commendation Medal of the US Department of Health and Human Services (DHHS), and the Distinguished Alumnus Medal from his Alma Mater the National University of Colombia. He is Honorary Member of the neurological societies of France, Spain, Cuba, Panama, Dominican Republic, Venezuela, Austrian Society of Tropical Medicine, Colombian Academy of Medicine and Society of Biological Psychiatry.
Dr. Román is Honorary Neuroepidemiology Professor, Universita degli Studi di Ferrara (Italy) and Honorary President of the Pan American Society of Neuroepidemiology. He served as advisor to the Food and Drug Administration (FDA), and is a reviewer for the Aging Systems and Geriatrics Study Section, and for the Fogarty Center of the NIH. He serves in the DHHS Subcommittee on Inclusion of Individuals with Impaired Decision-making in Research and he is Board Member, World Neurology Foundation. He was recently elected as Trustee to the board of directors of the World Federation of Neurology. Dr. Román is an internationally recognized expert in neuroepidemiology and his current areas of research include the study of environmental factors in stroke and autism.
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