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December 13, 2004

Overloaded?: Conclusion

Conclusion: The Promise of Prevention and Treatment

The findings by James and her colleagues significantly strengthen the evidence of a connection between mercury and autism, but they have much broader significance for public health and pollution control policies in general. The research strongly suggests it may be possible to identify individuals susceptible to toxic chemical exposure. If confirmed, these findings would argue strongly that environmental policies designed to protect the average person from chemical exposures are grossly insufficient to protect the public health.

Public health protections from chemical pollutants commonly include a ten-fold margin of safety to account for individual differences in susceptibility. An additional ten-fold safety factor may be included to account for the increased vulnerability of children. However even this 100-fold safety factor may not account for the reduced capacity of a vulnerable child to combat oxidative stress during crucial developmental periods.

Children with the metabolic profile James has identified are very likely to be more susceptible to a vast number of common pollutants, from arsenic in drinking water and wooden play-sets, to air pollution from cars and power plants. Environmental and health officials must evaluate the adequacy of current laws and policies to protect individuals with a heightened sensitivity to chemicals exposure.

At the same time, James' work may point to a potential treatment for autistic and other children whose diseases stem from bad glutathione ratios. After identifying a common vulnerability in autistic children, Dr. James and her research partners administered micronutrients to a subset of study participants in an attempt to remedy imbalanced metabolic profiles. Children received daily supplements of glutathione precursors folinic acid (5-formyl THF) and betaine for three months, followed by methyl B12 (methyl cobalamin) for an additional month. At the end of the intervention, glutathione measurements had improved in all children (James 2004a). The physician administering the dietary intervention noted improved speech and cognition but the study was not designed to quantify the benefits. Follow-up studies are underway to include more children and document improvements in their health outcomes.


Glutathione and antioxidant precursors have been examined as treatments for metabolic conditions like PKU that create long-term oxidative stress (Baielli 2003). A small pilot study found that glutathione supplements caused a 42 percent decline in disability for patients with Parkinson's disease (Sechi 1996). Antioxidants are also proposed to treat metal toxicity, particularly arsenic (Flora 1999), borate (Banner 1986), cadmium (Tandon 2003), chromate (Banner 1986), copper (Henderson 1985), lead (Tandon 2003), and mercury (Ballatori 1998).

Oxidative damage to brain cells during pregnancy and early life can lead to permanent changes to brain structure and functioning, resulting in autism. In order to fully protect brain cells, glutathione and antioxidant precursors must be administered in advance of environmental exposures that stress or kill brain cells. Nonetheless, bolstering glutathione recycling in children already diagnosed with autism could ameliorate many downstream effects of glutathione depletion including intestinal function, auto-immunity, and cellular inflammation. Dr. James is hopeful that the success of the intervention "implies that certain aspects of autism may be treatable" (James 2004a).