Regressive Autism: Putting Together the Pieces
Michael Wagnitz
March 12, 2007
Rates of autism spectrum disorders have been rising at an alarming rate according to the U.S. Department of Education, Office of Special Education, Data Analysis Services. Most of the new cases are regressive or late on-set autism. The diagnostic criteria for autism spectrum disorders are based on behavioral symptoms rather than a specific medical cause. In addition to psychological symptoms, many parents and physicians report conditions indicating a compromised immune system and gastrointestinal problems. This review looks at the most recent clinical studies indicating the causative agent may be mercury and tries to put this complicated puzzle together.
Autism is a term used to describe a condition which affects the immune, gastrointestinal and central nervous system. It has been shown that many of the physical and behavioral symptoms identified in children diagnosed with autism have been previously present in past cases of mercury poisoning (Bernard et al.2001).
Currently there is no known cause of autism identified in the medical literature, but by sifting through the most recently published clinical studies, one could make a compelling case that the causative agent is inorganic mercury (IHg). Analyses of first baby haircut samples have shown that autistic children retain seven times more mercury than neurologically typical controls (Holmes et al. 2003). Studies show that Macaca fascicularis primates that were dosed with chronic levels of methylmercury (MeHg) continued to accumulate IHg in the brain 6 months after the MeHg dosing had stopped. This clearance group showed a significant increase in microglial activity in the brain. Results from mercury speciation of the brain in these primates showed that MeHg concentration plateaued at about 12 months while the IHg fraction, derived from the demethylation of MeHg, continued to increase 6 months later. Autometallographic determination of the distribution of IHg by cell types showed microglial and astroglial cells contained significant more IHg deposits relative to other cells. This data suggests that IHg present in the brain is the toxic agent and responsible for the changes in the microglial and astroglial population (Charleston et al.1996).
Chronic microglial activation is recognized as an important component of neurodegenerative disease and neuroinflamation and contributes to neuronal dysfunction and injury. The recognition of microglial as the brains immune system and the understanding that chronic activation of this system leads to pathological consequences, has been the primary explanation for the current concept known as neuroinflamation (Streit et al. 2004). In a 2005 study brain tissue was obtained during autopsy from autistic patients. The author’s data show an active neroinflamatory process in the cerebral cortex, white matter and in the cerebellum of autistic patients. Immunocytochemical studies showed marked activation of the microglial and astroglial cells (Vargas et al.2005).
Another piece of the puzzle is provided in a recently published study comparing mercury brain levels in infant Macaca fascicularis primates exposed to injected ethylmercury and infant Macaca fascicularis primates exposed to equal amounts of ingested methylmercury (Burbacher et al. 2005). Primates exposed to the ethylmercuy retained twice as much IHg in their brains in comparison to the methylmercury exposed primates. These primates were exposed to mercury levels at a rate equal to what children in the United States received via standard childhood vaccines from 1991- 2003. This study did not take into account additional ethylmercury exposure from Rho D immunoglobulin injections that children of Rh negative mothers would have received during pregnancy nor does it look at mercury excretion issues.
While the Vargas study did not involve the testing for mercury, this future research, if undertaken, could provide a valuable piece to this puzzle.
References:
Bernard S, Enayati A, Redwood L, Roger H, Binstock T 2001 Autism: A novel form of mercury poisoning. Med. Hypotheses 56:462-471.
Holmes A, Blaxil M, Haley B. 2003. Reduced levels of mercury in first baby haircuts of autistic children. Int. Journal of Toxicology 22:277-285.
Charleston J, Body R, Bolender R, Mottet N, Vahter M, Burbacher T 1996. Changes in the number of astrocytes and microglia in the thalamus of the monkey Macaca fascicularis following long-term subclinical methylmercury exposure. Neurotoxicology 17:127-138
Streit W, Mrak R, Griffin W 2004. Microglia and neuroinflamation: a pathological perspective. Journal of Neuroinflamation 1:14
Vargus DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo Ca. 2005 Neuroglial activation and neuroinflamation in the brain of patients with autism. Annals of Neurology 57:67-81.
Burbacher T, Shen D, Liberato N, Grant K, Cernichiari E, Clarkson T. 2005. Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives. 113:1015-1021
About the Author:
Michael Wagnitz has over twenty years experience as a chemist working with trace metals analysis.
Autism is a term used to describe a condition which affects the immune, gastrointestinal and central nervous system. It has been shown that many of the physical and behavioral symptoms identified in children diagnosed with autism have been previously present in past cases of mercury poisoning (Bernard et al.2001).
Currently there is no known cause of autism identified in the medical literature, but by sifting through the most recently published clinical studies, one could make a compelling case that the causative agent is inorganic mercury (IHg). Analyses of first baby haircut samples have shown that autistic children retain seven times more mercury than neurologically typical controls (Holmes et al. 2003). Studies show that Macaca fascicularis primates that were dosed with chronic levels of methylmercury (MeHg) continued to accumulate IHg in the brain 6 months after the MeHg dosing had stopped. This clearance group showed a significant increase in microglial activity in the brain. Results from mercury speciation of the brain in these primates showed that MeHg concentration plateaued at about 12 months while the IHg fraction, derived from the demethylation of MeHg, continued to increase 6 months later. Autometallographic determination of the distribution of IHg by cell types showed microglial and astroglial cells contained significant more IHg deposits relative to other cells. This data suggests that IHg present in the brain is the toxic agent and responsible for the changes in the microglial and astroglial population (Charleston et al.1996).
Chronic microglial activation is recognized as an important component of neurodegenerative disease and neuroinflamation and contributes to neuronal dysfunction and injury. The recognition of microglial as the brains immune system and the understanding that chronic activation of this system leads to pathological consequences, has been the primary explanation for the current concept known as neuroinflamation (Streit et al. 2004). In a 2005 study brain tissue was obtained during autopsy from autistic patients. The author’s data show an active neroinflamatory process in the cerebral cortex, white matter and in the cerebellum of autistic patients. Immunocytochemical studies showed marked activation of the microglial and astroglial cells (Vargas et al.2005).
Another piece of the puzzle is provided in a recently published study comparing mercury brain levels in infant Macaca fascicularis primates exposed to injected ethylmercury and infant Macaca fascicularis primates exposed to equal amounts of ingested methylmercury (Burbacher et al. 2005). Primates exposed to the ethylmercuy retained twice as much IHg in their brains in comparison to the methylmercury exposed primates. These primates were exposed to mercury levels at a rate equal to what children in the United States received via standard childhood vaccines from 1991- 2003. This study did not take into account additional ethylmercury exposure from Rho D immunoglobulin injections that children of Rh negative mothers would have received during pregnancy nor does it look at mercury excretion issues.
While the Vargas study did not involve the testing for mercury, this future research, if undertaken, could provide a valuable piece to this puzzle.
References:
Bernard S, Enayati A, Redwood L, Roger H, Binstock T 2001 Autism: A novel form of mercury poisoning. Med. Hypotheses 56:462-471.
Holmes A, Blaxil M, Haley B. 2003. Reduced levels of mercury in first baby haircuts of autistic children. Int. Journal of Toxicology 22:277-285.
Charleston J, Body R, Bolender R, Mottet N, Vahter M, Burbacher T 1996. Changes in the number of astrocytes and microglia in the thalamus of the monkey Macaca fascicularis following long-term subclinical methylmercury exposure. Neurotoxicology 17:127-138
Streit W, Mrak R, Griffin W 2004. Microglia and neuroinflamation: a pathological perspective. Journal of Neuroinflamation 1:14
Vargus DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo Ca. 2005 Neuroglial activation and neuroinflamation in the brain of patients with autism. Annals of Neurology 57:67-81.
Burbacher T, Shen D, Liberato N, Grant K, Cernichiari E, Clarkson T. 2005. Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives. 113:1015-1021
About the Author:
Michael Wagnitz has over twenty years experience as a chemist working with trace metals analysis.
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