Fwd: Major New Study Implicating the Biological Plausibility of Mercury Causi...

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From: mgeier@...Sent: 6/17/2011 1:45:41 P.M. Eastern Daylight TimeSubj: Major New Study Implicating the Biological Plausibility of Mercury Causing Autism

Dear Everyone,

Please, find attached to this email a new study, "The Plausibility of a Role for Mercury in the Etiology of Autism: A Cellular Perspective" published in the peer-reviewed journal of Toxicological & Environmental Chemistry by researchers from Swinburne University (including the Swinburne Autism Bio-Research Initiative) saved as The Plausibility of a Role of Mercury in the Etiology of Autism - In Press1a.pdf in Adobe Acrobat Format. As per previous emails, this new study is one of literally dozens of peer-reviewed academic studies published in the last several months directly implicating a causal role for mercury in autism spectrum disorders, and this new study has more than 10 pages of peer-reviewed academic journal citations in support of its conclusions.

This article describes that autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development.

Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis.

This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism.

This investigators concluded their study by stating [emphasis added], "From a cellular perspective, it would appear that the existing scientific literature supports the biological plausibility of a Hg-based autism pathogenesis. Hg has well-known effects relating to the disruption of sulfur chemistry leading to elevated oxidative stress which, in turn, results into broader physiological/organ affects, particularly to the CNS. Oxidative stress was consistently elevated in autism. Although this is not unique to autism (as many disease states are associated with this biochemical characteristic), it does suggest that autism is more than just a neurological disease but also a disease which reflects dysfunction at various metabolic levels. Nevertheless, research studies identifying Hg’s effects on glial cells and mitochondria that are consistent with findings in autistic patients, lend further support to the Hg-autism hypothesis...This population level approach to reducing Hg exposure has not, as of yet, been comprehensively introduced..."