Mercury in the body produces a selenium deficiency state that increases toxicity.
Spiller HA. Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity. Clinical Toxicology. 2018;56(5):313-326.
This study makes the case that mercury’s multifaceted interactions with selenium are a central feature of mercury toxicity. The authors argue that “the previously suggested ‘protective effect’ of selenium against mercury toxicity may in fact be backwards”—because of mercury’s affinity for selenium, mercury can actually produce a selenium deficiency state that promotes oxidative stress and inhibits the body’s regenerative mechanisms. Depending on the form of mercury and other factors, selenium supplementation may have some benefits for restoring adequate selenium status and mitigating the toxicity of mercury, but it does not appear to promote increased elimination of mercury.
Increased susceptibility to ethylmercury-induced mitochondrial dysfunction in a subset of autism lymphoblastoid cell lines
Research confirms a link between environmental mercury exposure and an increased risk of autism and shows that some individuals are more susceptible than others.
Rose S, Wynne R, Frye RE, Melnyk S, James SJ. Journal of Toxicology. 2015, Article ID 573701.
The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, researchers compared mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. They also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. The findings suggest that the link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.
B-lymphocytes from a population of children with autism spectrum disorder and their unaffected siblings exhibit hypersensitivity to thimerosal.
Research has determined there is a subgroup of the population that has hypersensitivity to the toxicity of thimerosal yet thimerosal containing vaccines are administered to all without consideration to this important fact. We can ban peanuts from schools because a subpopulation is allergic to them, so why is thimerosal still contained in our vaccines?
Two medications (valproate and thalidomide) have been definitively shown to be causative with regards to autism spectrum disorder (ASD). Both of these medications share a common trait of inhibiting cell proliferation. Thus, these researchers set out to determine if thimerosal can inhibit cell proliferation using doses of thimerosal which reflect the concentrations that infants are exposed to via vaccinations. The design of this experiment was chosen to be able to distinguish between shared or different in utero environments among families with an ASD member. To accomplish this goal, B-cells were collected from, ASD individuals, their unaffected fraternal twins representing a shared in utero environment, and their unaffected nontwin siblings. In the same manner, B-cells were collected from control families with no history of ASD which were matched for age/sex/ethnicity and compared to ASD families. It was determined that there is a hypersensitivity to thimerosal among a subpopulation of ASD families. The target of thimerosal toxicity is the mitochondria and cell proliferation was inhibited at a dose that was lower than that required to cause cell death. Among the hypersensitive population, the dose of thimerosal that could inhibit cell proliferation was found to be only 40% of that needed to inhibit proliferation in the control group. Whether a twin or sibling was hypersensitive was dependent on having another family member with hypersensitivity. This finding implies there is a genetic component to thimerosal hypersensitivity. Among the ASD families with hypersensitivity oxidative stress was determined to be the contributing factor. Poor antioxidant status, high lactate levels, and elevated markers of oxidative stress are a common finding among individuals with ASD. In 2008 the case of Hannah Poling was awarded compensation under the United States National Vaccine Injury Compensation Program. It was claimed that her vaccines induced a mitochondrial encephalopathy that resulted in autism. Since the mitochondria is the most significant target of thimerosal toxicity, it is particularly poignant to know that a lowering of antioxidant status by any other additional conditions such as infections or co-exposure to other toxins would further sensitize mitochondria to the damaging effects of thimerosal. These researchers state that their work, “…supports a multi-insult model of ASD causation where many individuals have the genetic background that makes them vulnerable to a particular type of insult at a particular time in their brain development…”. Just like valproate and thalidomide which are the only 2 accepted causative agents for ASD, this research has demonstrated that thimerosal is also capable of inhibiting cell proliferation.