The first half of Janet Kern, Boyd Haley, David Geier, Paul King, Lisa Sykes and Mark Geier’s paper on Thimerosal toxicity laid the groundwork for a the relationship between Thimerosal and abnormal sulfation, decreased GSH, and lower cellular thiol levels in ASD individuals. With a nuanced analysis of existing research, Kern et al. pointed out that Thimerosal has the potential to affect each of the three biomarkers in a negative manner. In the second half of their paper, the researchers discuss this relationship and its connection to autism in further detail.
GSH Availability in the ASD Brain
Though Kern et al. underscored the inverse relationship between GSH levels in the blood and the severity of ASD symptoms, recent research reveals that GSH isn’t just insufficient in the plasma of ASD individuals; it’s insufficient in the brain, too. These low levels are particularly evident in the brain’s cerebellum, which is responsible for the majority of fine motor cognitive performance; this area showed signs of oxidative stress and neurodegeneration. GSH is an important thiol; among its many duties, GSH is responsible for regulating and maintaining a healthy immune system, as well as suppressing inflammation. When our bodies don’t have enough GSH, many processes are disrupted. In short, lower GSH levels make individuals more vulnerable to brain insults. While this relationship is rather clear-cut and reinforced by a number of studies, its connection to Thimerosal was still largely indirect. That is until a recent study proved that GSH concentrations in lymphoblastoid cells (LCLs) from children with ASD were more significantly reduced when introduced to Thimerosal than GSH concentrations of LCLs from a control group of children; the LCLs of ASD subjects also demonstrated increased levels of GSH oxidation than when exposed to Thimerosal, while the control group did not. Researchers of the study concluded that these lower levels of GSH thiols and increased levels of oxidation could hinder the brain’s antioxidant defense and detoxification capacity.
Studies have also shown that some ASD individuals and immediate family members have a hypersensitivity to Thimerosal that control groups with no family presence of ASD do; in fact, those with hypersensitivity to Thimerosal only needed to be exposed to 40% of the Thimerosal quantity the control group was exposed to to demonstrate sensitivity.
Consider too, that through Thimerosal exposure via vaccines and mercury in breast milk, infants can receive more than 4.5 times the amount of Hg in their first six months of life than what’s sanctioned as safe by the EPA, the Centers for Disease Control, the World Health Organization, and the Food and Drug Administration. Research has shown that even when mercury exposure is at a level the EPA deems safe, cognitive function declines. As Kern et al. point out, the reason for this disparity is likely the fact that the EPA bases its recommendation based on Hg ingestion, rather than injection; Hg injection is shown to result in more adverse effects.
Exposure to Thimerosal in the first year of life is particularly dangerous because infants lack an adequate reserve of GSH; studies have revealed that fetal and infant tissue is more vulnerable to Hg toxicity than tissue from older children and adults. Thus, the time of Thimerosal exposure becomes an important factor in its level of toxicity.
As David and Mark Geier have already shown in research, nothing explains the symptoms of ASD more accurately than Hg toxicity. Ultimately, Kern et al. conclude that the combination of low GSH levels, abnormal sulfation chemistry, limited thiol availability, and redox increase an individual’s vulnerability to Thimerosal, and in turn, their vulnerability to regressive autism. Such would better explain why some ASD individuals experience the adverse effects of Thimerosal exposure more acutely and maintain more severe brain insults. Such also makes for a strong case against the continued presence of Thimerosal in vaccines in the United States and around the world.