Because Dr. Haley’s chelator is a mirror of glutathione, which is also a chelator, it is interesting to read Dr. Jill James, of the University of Arkansas School of Medicine, her research has documented a unique metabolic profile in 95 autistic children with regressive autism. Regressive autism is a form of the disease in which children develop normally for a certain period before losing previously acquired language or behaviors and being diagnosed with autism. The metabolic profile in the James study children manifests as a severe imbalance in the ratio of active to inactive glutathione in autistic children, compared to a group of healthy control children. Glutathione, a potent antioxidant, is the body’s most important tool for detoxifying and excreting metals and its production in the body is dependent on good nutrition.
The James study shows that children with regressive autism have consistently elevated levels of oxidative stress as compared to normal healthy children. Individuals with reduced glutathione antioxidant capacity will be under chronic oxidative stress and will be more vulnerable to toxic compounds that act primarily through oxidative damage, including mercury. Thus when we treat for mercury toxicity it is a good idea to include glutathione (probably the best way is with suppositories or IV) selenium, bicarbonates and magnesium.
 Magnesium deficiency (MgD) has been associated with production of reactive oxygen species, cytokines, and eicosanoids, as well as vascular compromise in vivo. Although MgD-induced inflammatory change occurs during “chronic” MgD in vivo, acute MgD may also affect the vasculature and consequently, predispose endothelial cells (EC) to perturbations associated with chronic MgD. As oxyradical production is a significant component of chronic MgD, we examined the effect of acute MgD on EC oxidant production in vitro. In addition we determined EC; pH, mitochondrial function, lysosomal integrity and general cellular antioxidant capacity. Decreasing Mg2+ (< or = 250microM) significantly increased EC oxidant production relative to control Mg2+ (1000microM). MgD-induced oxidant production, occurring within 30min, was attenuated by EC treatment with oxyradical scavengers and inhibitors of eicosanoid biosynthesis. Coincident with increased oxidant production were reductions in intracellular glutathione (GSH) and corresponding EC alkalinization. These data suggest that acute MgD is sufficient for induction of EC oxidant production, the extent of which may determine, at least in part, the extent of EC dysfunction/injury associated with chronic MgD. Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production.Wiles ME, Wagner TL, Weglicki WB. The George Washington University Medical Center, Division of Experimental Medicine, Washington, D.C., USA. email@example.com Life Sci. 1997;60(3):221-36.