Mercury and Autism: Accelerating Evidence?

The University of Northampton, Northampton, England, United Kingdom
Neuro endocrinology letters (Impact Factor: 0.8). 11/2005; 26(5):439-46.
Source: PubMed


The causes of autism and neurodevelopmental disorders are unknown. Genetic and environmental risk factors seem to be involved. Because of an observed increase in autism in the last decades, which parallels cumulative mercury exposure, it was proposed that autism may be in part caused by mercury. We review the evidence for this proposal. Several epidemiological studies failed to find a correlation between mercury exposure through thimerosal, a preservative used in vaccines, and the risk of autism. Recently, it was found that autistic children had a higher mercury exposure during pregnancy due to maternal dental amalgam and thimerosal-containing immunoglobulin shots. It was hypothesized that children with autism have a decreased detoxification capacity due to genetic polymorphism. In vitro, mercury and thimerosal in levels found several days after vaccination inhibit methionine synthetase (MS) by 50%. Normal function of MS is crucial in biochemical steps necessary for brain development, attention and production of glutathione, an important antioxidative and detoxifying agent. Repetitive doses of thimerosal leads to neurobehavioral deteriorations in autoimmune susceptible mice, increased oxidative stress and decreased intracellular levels of glutathione in vitro. Subsequently, autistic children have significantly decreased level of reduced glutathione. Promising treatments of autism involve detoxification of mercury, and supplementation of deficient metabolites.

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    • "VDAC NADH dehydrogenase is extremely sensitive to mercurial inhibition, which is consistent with the low-level effects of mercury in autism.40 A sensitivity to lead23 at VDAC SH groups could also point to lead-poisoning-related initiation of autism. "
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    ABSTRACT: Background The Voltage Dependent Anion Channel (VDAC) is involved in control of autism. Treatments, including coenzyme Q, have had some success on autism control. Data sources Correlation of porin redox activity and expression of autism is based on extensive literature, especially studies of antibodies, identification of cytosolic nicotinamide adenine dinucleotide reduced (NADH) dehydrogenase activity in the VDAC, and evidence for extreme sensitivity of the dehydrogenase to a mercurial. Evidence for a coenzyme Q requirement came from extraction and analog inhibition of NADH ferricyanide reductase in the erythrocyte plasma membrane, done in 1994, and reinterpreted when it was identified in VDAC in 2004. The effects of ubiquinol (the QH2 – reduced form of coenzyme Q) in children with autism were studied. Results A new role for coenzyme Q in the porin channels has implications on autism. Ubiquinol, the more active form of coenzyme Q, produces favorable response in children with autism. Agents which affected electron transport in porin show parallel effects in autism. Conclusion We propose a hypothesis that autism is controlled by a coenzyme Q-dependent redox system in the porin channels; this conclusion is based on the effects of agents that positively or negatively affect electron transport and the symptoms of autism. The full understanding of the mechanism of their control needs to be established.
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    • "Other possible reasons behind the initiation of autoimmunity and the production of autoantibodies in some autistic children may be attributed to the exposure to some environmental cross-reacting antigens, which initiate autoimmune reactions in genetically susceptible individuals [4]. These environmental antigens include food allergies to certain peptides as casein of milk and gluten of wheat [44,45], heavy metals exposure [46,47] and Hevea brasiliensis proteins in natural rubber latex [48]. In addition, infectious agents (for example, virus-induced autoimmunity) may play a causal in autism [1,49]. "
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    ABSTRACT: Increasing evidence of autoimmune phenomena in some individuals with autism could represent the presence of altered or inappropriate immune responses in this disorder. The role of the nucleosome in the induction of antibody response in some autoimmune-mediated tissue damage may provide novel targets for treatment. Due to the paucity of studies investigating the frequency of systemic auto-antibodies in autism, we are the first to investigate the frequency of antinucleosome-specific antibodies in a group of autistic children. Serum antinucleosome-specific antibodies were measured by ELISA in 60 autistic children, between the ages of 3 and 12 years, in comparison to 60 healthy children. Autistic severity was assessed using the Childhood Autism Rating Scale (CARS). Autistic children had significantly higher serum antinucleosome-specific antibodies than healthy children (P <0.001). The seropositivity of antinucleosome-specific antibodies was found in 46.7% of autistic children. Autistic children with a family history of autoimmunity (40%) had a significantly higher frequency of serum antinucleosome-specific antibodies (83.3%) than patients without such a history (22.2%, P <0.001). Serum levels of antinucleosome-specific antibodies were increased in some autistic children. However, these data should be treated with caution until further investigations are performed with a larger subject population to determine whether these antibodies have a role in the induction of autoimmunity in a subgroup of autistic children. The role of immunotherapy in children with autism should be also studied.
    Full-text · Article · Apr 2014 · Journal of Neuroinflammation
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    • "Geier et al. (2009) hypothesized that autism results from a combination of genetic and biochemical susceptibilities in the form of a reduced ability to excrete Hg and/or increased environmental exposure at key times during development. It was hypothesized that children with autism have a decreased detoxification capacity for Hg because of genetic polymorphism (Mutter et al., 2005). "
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    ABSTRACT: Many factors have been implicated in the onset of autism, including excess or deficiency in toxic or essential metals and impaired antioxidant systems. Exposure to metals is a putative risk factor for autism. Many metals can be implicated in autism as they typically disrupt enzyme functions and cell signaling processes and generate oxygen free radicals (ROS). Patients and methods Thirty-two autistic patients ranging in age from 2.6 to 12.7 years (mean age 5.6 years) were examined clinically. Twenty healthy children matched for age and sex were included as a control group. Serum mercury, lead, and nitric oxide were estimated in all patients. Results Eighteen patients presented with seizures and an epileptogenic focus in the electroencephalogram. The intelligent quotient assessment showed mental retardation in all patients: 18 had moderate retardation, two had severe retardation, and 12 had profound retardation. Assessment of the severity of autistic symptoms using the childhood autism rating scale indicated that six patients had mild, 12 had moderate, and 14 had severe autistic symptoms. The estimation of the level of mercury and lead in blood showed a significant increase compared with the control group (P= 0.0001). Furthermore, nitric oxide was significantly increased compared with the control group (P = 0.0001). These findings indicated a significant increase in both metal content and an imbalance in the oxidative status in the blood of autistic children. Conclusion Our findings suggest the hypothesis that exposure to metals and oxidative stress may be biomarkers of toxicity in autism. We recommend the consideration of supplementing autistic patients with antioxidants. We also recommend the study of introducing chelating agents for mercury and lead in patients with high toxic levels and their effect on clinical symptoms.
    Full-text · Dataset · Jun 2013
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