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Part 4:
Both autism and mercury exposure are characterized by functional impairment to speech, language and behavior (Bernard 2001, Blaxill 2004b). Recent studies also suggest that the same key regions of the brain are affected in both cases (Limke 2004, Kates 2004). At the same time, episodes of severe mercury exposure reveal that there is no single manifestation of mercury poisoning. In fact, children exposed to high levels of mercury during gestation and infancy have suffered from strikingly different diseases.
Minamata disease resulted from in-utero exposure to mercury-contaminated fish. Children with Minamata disease had symptoms indistinguishable from mental retardation or cerebral palsy (Kondo 2000). Acrodynia resulted from mercury in infant teething powders in the early 1900s. Children with Acrodynia suffered peeling and reddened skin on their hands and feet, and heightened sensitivity to light (Warkany 1966).
Individual susceptibility played an important role in both disorders. Although thousands of children were treated with mercury-containing teething powders, only one in 500 to one in 1,000 children who were exposed developed Acrodynia (Warkany 1966). The role of individual sensitivity made it extremely difficult to link mercury exposure with what was, at the time, a new and bizarre disease. Similarly, when children have been exposed to high levels of mercury in foods, only a small group develop severe mercury poisoning while thousands are apparently unharmed (Jalili 1961, Kondo 2000).
Dr. James' findings clearly reveal a mechanism by which autistic children would be predisposed to mercury-related oxidative damage to their developing brain and nervous system. Several additional pieces of evidence strengthen the potential link between mercury exposure and autism in children with abnormal antioxidant capacity. These include:
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