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Oxygen radicals damage the brain and nervous systemAutistic children's inability to combat oxidative stress can lead to many health problems. GLUTATHIONE and antioxidant precursors havebeen examined as treatments for metabolicconditions like PKU that create long-termoxidative stress (Baielli 2003). GLUTATHIONE works as an antioxidant, keeping in check the potentially destructive process of oxidative stress caused both by normal metabolism and environmental contaminants.
Oxidative stress is caused by oxygen radicals — highly unstable chemicals that react with and destroy healthy cells. Autistic children showed a significant impairment in every one of five measurements of the body's ability to maintain a healthy GLUTATHIONE defense.These findings raise serious concerns about children's overall exposure to environmental contaminants. These free oxygen radicals are produced by the body in manageable amounts as byproducts of normal body metabolism, but their prevalence can be exacerbated by exposure to environmental chemicals. When this one, submitted by mom Lisa Wilson, landed in our inbox, we were especially moved. Mercury is of particular concern, however, because of its proven toxicity to the developing brain and nervous system, and documented high exposures from a variety of sources.One of every six pregnancies is exposed to methyl mercury above EPA's safe level from maternal consumption of contaminated seafood (CDC 2002, Mahaffey 2004).
Oxygen radicals damage cells by reacting with proteins, DNA, carbohydrates, and fats, setting off chain reactions that can only be stopped by a cell's antioxidant defense system. Wilson says her 11-year-old son, Jonathan, wrote the "script" for a video about autism and then recorded it with the help of a friend. Thimerosal, a preservative in vaccines that is 49 percent ethyl mercury, was a major source of mercury exposure from 1988 through 2002 when it was removed from childhood immunizations at the urging of the Public Health Service and the American Academy of Pediatrics. In the process they disrupt cell functions and interfere with signals sent between cells in the body, which can lead to auto-immunity (Klein 2003).Oxidative damage is counteracted by the body's antioxidant systems, which convert oxygen radicals into harmless byproducts. Elemental mercury from dental amalgams is another potentially important source, but its contribution to overall mercury exposure is less well studied.The incidence of autism increased 10-fold from 6 in 10,000 in the 1980s (Blaxill 2004), to about 60 in 10,000 today (Autism Alarm, PDF file). Oxidative stress occurs when oxygen radicals overwhelm the capacity of the body's antioxidant systems.
Finding treatment that addresses your child’s needs, rather than focusing on what to call the problem, is the most helpful thing you can do.
These new findings significantly strengthen the possibility that mercury could cause or contribute to autism and other neurodevelopmental disorders by identifying a metabolic imbalance common to nearly all autistic children that would make these children poorly equipped to mount a defense against a number of neurotoxic compounds, including mercury.Finally, these findings raise serious concerns about the studies that have allegedly proven the safety of mercury in vaccines. The epidemiologic studies used to dismiss a causal relationship between autism and thimerosal have assumed that all children have the same resistance to chemical exposure. It damages cell membrane structure (lipids), the cell machinery that performs the essential work of the cells (proteins), and the body's ability to regulate cell growth and protein synthesis (DNA and RNA). Oxidative stress is associated with premature aging of cells, and can lead to tissue inflammation, damaged cell membranes, autoimmunity and cell death (Klein 2003). Drug companies responded with vaccinations supplied in multiple dose containers preserved with the mercury-based antibacterial thimerosal. GLUTATHIONE is the most important antioxidant for metals detoxification and excretion.The brain and nervous system are particularly vulnerable to oxidative stress due to limited antioxidant capacity. Neither the CDC, nor the Food and Drug Administration (FDA), which monitors the safety of vaccinations, expressed concerns at that time about the relatively high doses of mercury that newborn babies and infants would be exposed to through these shots.A dramatic nationwide increase in autism followed directly on the heels of the abrupt rise in thimerosal exposure (Blaxill 2001).
The brain makes up about two percent of a person's mass but consumes 20 percent of their metabolic oxygen. Rates rose from 6 in 10,000 children in the 1980s to 60 in 10,000 today (Blaxill 2004a, American Academy of Pediatrics 2004). Some brain cells, like neurons, cannot make GLUTATHIONE, but instead rely on surrounding astrocyte cells to provide useable GLUTATHIONE precursors.
On May 17, 2004, the IOM published its final report on the possible link between thimerosal and autism.
Because the brain has limited access to the bulk of antioxidants produced by the body, neurons are the first cells to be affected by a shortage of antioxidants, and are most susceptible to oxidative stress. Researchers studying antioxidant protection of neurons are finding short windows during development of high vulnerability to oxidative stress (Perry 2004).Children are more vulnerable than adults to oxidative stress due to their naturally low GLUTATHIONE levels from conception through infancy (Erden-Inal 2003, Ono 2001). Risks created by this natural deficit in detoxification capacity in infants are compounded by the fact that mercury and other environmental chemicals that invoke oxidative stress are found at higher concentrations in the developing infant than in their mothers and appear to accumulate in the placenta.In addition to this natural variability in antioxidant status with age, a person's genes play a strong role in their ability to make antioxidants in response to oxidative stress. A host of genes determine the speed and responsiveness of antioxidant production and recycling.
Experimental chelation therapy in chromium, lead, and boron intoxication with N-acetylcysteine and other compounds. People with gene deletions for two types of GLUTATHIONE genes (GST M1 and T1) are more likely to have allergic reactions to the mercury-based preservative thimerosal (Westphal 2000).Environmental chemicals that provoke oxidative stress could contribute to autism or other health problemsDuring a typical day children and pregnant women are exposed to many different types of environmental chemicals that cause oxidative stress.
These exposures add up, creating special concerns for infants and small children due to age-related sensitivity that derives from naturally low GLUTATHIONE levels. Mercury Linked to Autism-Like Damage in Mice: Institute of Medicine Says Study Does Not Support Link Between Mercury, Autism in Humans. These findings represent a potential milestone in our understanding of individual vulnerability to toxic substances, including, but not limited to, mercury.
This natural age-related vulnerability is exacerbated in individuals with impaired GLUTATHIONE ratios. If these children were exposed to a high dose of any compound that produced significant oxidative stress, they would be less able to detoxify and excrete the compound.Pervasive environmental contaminants like air pollutants from power plants and auto exhaust, pesticides, heavy metals and food additives all produce some degree of oxidative stress. Jill James, now of the University of Arkansas for Medical Sciences, has uncovered a unique and consistent metabolic imbalance in autistic children when compared to normal healthy children (James 2004a, 2004b).
Fine particulate matter and diesel exhaust both provoke tremendous oxidative stress and deplete GLUTATHIONE (Li 2002).
This impairment manifests as a severe deficit in the body's most important antioxidant and metals detoxifier, GLUTATHIONE.
When compared to normal health children, autistic children showed a significant impairment in every one of five measurements of the body's ability to maintain a healthy GLUTATHIONE defense.These findings are strong evidence that if these children were exposed to a potentially toxic dose of mercury or other compound they would be much less able to mount an effective defense. When they dosed pregnant mice with these pesticides the male offspring showed permanent alterations to neurological systems and enhanced susceptibility as an adult to paraquat (Barlow 2004).PCBs induce a concentration-dependent increase in oxygen radicals. Reduced antioxidant defense may characterize a group of individuals who are demonstrably more sensitive to the effects of a range of toxic chemical exposures, and shed light on increasing rates of related learning and behavioral disorders. Modulation of antioxidant defense systems by the environmental pesticide maneb in dopaminergic cells. Arsenic and chromium in pressure-treated wood, mercury in fish and vaccines, lead in paint, and metals in soil or drinking water are chronic if not daily sources of oxidative stress in the child's environment.GLUTATHIONE is one of the bodies most important mechanism of heavy metal detoxification and excretion.
James' results do not prove that mercury causes autism, they significantly strengthen this possibility.
GLUTATHIONE binds with these compounds as well as other metals—cadmium, lead, mercury, and nickel (Stohs 1995).
The epidemiologic studies used to dismiss a causal relationship between mercury and autism assumed that all children have the same resistance to chemical exposure.
Thimerosal induces DNA breaks, caspase-3 activation, membrane damage, and cell death in cultured human neurons and fibroblasts. Given James' finding that autistic children would be much more sensitive to certain chemical contaminants, studies that do not acknowledge these vulnerabilities cannot be used to dismiss the relationship between environmental chemicals, including mercury, and the disease.


For example, cells treated with chemicals to inhibit GLUTATHIONE recycling are much more sensitive to manganese toxicity (Desole 1997). People chronically exposed to arsenic in drinking water have increased oxidative damage and decreased antioxidant potential (Wu 2001).Numerous studies link thimerosal with oxidative stress to the brain and neurological system at concentrations similar to those that were experienced by children vaccinated in the 1990s.
According to the EPA's top mercury scientist, one out of every six children born in the United States is exposed to levels of methyl mercury during pregnancy that exceed what the Agency considers safe (Mahaffey 2004). Researchers measured mercury concentrations between 10 and 30 nanomoles per liter (nM) in premature infants given a single Hepatitis B shot at birth (Stajich 2000). The principal source of high fetal methyl mercury exposure is maternal consumption of contaminated seafood, primarily canned tuna.
Mercury concentrations ranging from 4 to 21 nM are reported in young children when measurements were collected 3 to 20 days after vaccination (Pichichero 2002). Pregnant women who eat significant quantities of large ocean-going fish could expose their babies to amounts of mercury that are well above the government's recommended safe levels.In March, 2004, the Food and Drug Administration revised their mercury seafood advisory to include a specific warning about consumption of canned albacore tuna. Four recent studies of thimerosal toxicity to human brain cells report oxidative damage, interruption of methylation, and decreased cell energy resulting from thimerosal exposure in the range of exposure overlapping with those for vaccinated children in the 1990s (Waly 2004, Baskin 2003, Ueha-Ishibashi 2004, Makani 2002).
Pregnant women and children are advised to eat no more than one six ounce can of albacore tuna per week. Several studies documented the protective benefits of antioxidants, especially GLUTATHIONE, which attenuate the damages caused by thimerosal (Makani 2004, James 2005, Shanker 2003).Impaired antioxidant production provides a common rationale for many disparate features of autistic disordersThe identification of reduced antioxidant capacity as a common impairment in autistic children is an important breakthrough that should guide research into the autism epidemic. The advisory, however, provides no consumption advice for a number of fish where high mercury levels are a concern, including tuna steaks, sea bass, halibut, and many others. It strongly suggests that GLUTATHIONE is a factor that mediates the relationship between environmental chemicals and autism, and for the first time provides a plausible biological link between several trademark features of the disorder that have baffled researchers searching for a single gene or chemical exposure that is triggering autism.For example, scientists have failed to explain why autism rates are much higher in males, why autism manifests in some children after a period of healthy development, and why autistic children develop intestinal and autoimmune disorders at high rates. The Environmental Working Group has filed a legal challenge to the FDA mercury seafood advisory, charging that it is not based on the best available science on seafood contamination and mercury risk levels to the developing fetus.But contaminated seafood is not the only source of mercury exposure for the developing fetus or infant. Antioxidant imbalance, particularly GLUTATHIONE deficit, may be the unifying factor that links these apparently disparate symptoms and provides a clue to interventions that could treat autism.
Mercury amalgam dental fillings are a potentially significant source of fetal mercury exposure, although precise amounts are not well characterized. Each of these seemingly disconnected features of autism are strongly associated with GLUTATHIONE capacity.Autism rates higher, GLUTATHIONE levels lower in malesMales make up 70 percent of all autism cases, as well as the majority of children diagnosed with learning disabilities and attention deficit disorder. And from 1988 through about 2002, children were exposed to significant doses of mercury from birth through six months of age in the form of a mercury-based preservative, thimerosal, used in routine childhood immunizations. New research attributes weaker antioxidant capacity in young males with greater vulnerability in their brain and nervous systems, potentially effecting vulnerability to mercury and autism.
Children born to Rh negative mothers were also exposed to mercury in-utero when their mothers received a mercury-containing RhoGAM shot. Women and girls, in contrast, have lower levels of inactive antioxidant chemicals (Rush 2003). Estrogen is a powerful antioxidant that confers substantial benefits against free-radical mediated damage in aging.
The health impact of mercury exposure through vaccinations has been the source of intense debate because of significant changes in the vaccination regimen from 1988 through 1991 that increased neonatal and infant exposure to mercury.Drug companies were similarly silent on the matter, although internal company documents show that they were aware of the potent neurotoxic effects of mercury as early as the 1940s. Notably, the FDA banned the sale of topically applied thimerosal antibiotics in the 1980s due to severe, even crippling, adverse skin reactions in sensitive individuals.The amount of mercury in the standard battery of childhood immunizations more than doubled between 1988 and 1991 when these additional shots were added to the early childhood vaccination regimen. Studies using tissue samples from newborn infants reveal significantly higher GLUTATHIONE levels, GLUTATHIONE production, and cell survival in response to oxidative stress in cells from girls compared to boys (Lavoie 1997).
Throughout the 1990s, children received nine mercury-containing vaccinations within their first six months of life, including the unprecedented injection of a mercury-containing vaccine at birth, and up to three shots given in a single day at 2-, 4-, and 6-months.
Studies of brain injury in newborns have found that inherently stronger GLUTATHIONE capacity in females protects their brain cells from damage after a traumatic injury. The average two-month old baby vaccinated with thimerosal-containing shots in the 1990s received a single day dose of mercury that was between 100 and 125 times the government's long-term safe exposure level.Drug companies used thimerosal as a vaccine preservative to allow multiple injections to be shipped and stored in single containers. GLUTATHIONE concentrations remain constant in females but they drop by as much as 80 percent in males after a brain injury (Du 2004).
Similar studies found increased brain damage to children younger than four years old when their antioxidant systems are immature and GLUTATHIONE levels are lower (Fan 2003).GLUTATHIONE deficit may be responsible for intestinal disorders in autistic childrenThe reduced concentrations of GLUTATHIONE Dr.
After more than a decade of nationwide, high childhood exposures, it was removed from childhood vaccinations between 1999 and 2002, at the urging of the Public Health Service and the American Academy of Pediatrics, but is still present in most flu vaccines.
James measured in study children may explain common intestinal ailments noted in autistic children. In these 'leaky gut' disorders undigested proteins pass through the gut and cause oxidative damage to the brain and nervous system (White 2003).
Rates of autism in the United States increased from fewer than 6 cases per 10,000 children in the 1980s to more than 60 per 10,000 children today (Blaxill 2004a). This is similar to PKU, a metabolic disorder in which the toxic accumulation of undigested phenylalanine causes oxidative damage leading to autistic-like symptoms. Mitochondria from females exhibit higher antioxidant gene expression and lower oxidative damage than males.
The American Academy of Pediatrics and the Centers for Disease Control (CDC) currently estimate that autism affects one in every 166 children (AAP 2004). Autoimmunity can be triggered when genetically susceptible people are exposed to an environmental chemical or virus.
Oxidative stress also plays an important role in autoimmunity by disrupting cell signaling. T lymphocytes are made less active or hypo-responsive when they are exposed to oxygen radicals. T lymphocytes regain normal responsiveness when the antioxidants N-acetyl cysteine (Cemerski 2002) and other GLUTATHIONE precursors are added to the system (Hehner 2000).A recent investigation reported chronic inflammation in the brains of autistic patients, resulting from an over-active immune system, a sign of autoimmunity (Vargas 2004). The inflammation indicates that the brain is responding to a process that is stressing or damaging brain cells, a process which might include oxygen radicals.The weight of the evidence supports a fresh look at the mercury-autism hypothesisBoth autism and mercury exposure are characterized byfunctional impairment to speech, language and behavior(Bernard 2001, Blaxill 2004b). Jill James of the University of Arkansas School of Medicine has documented a unique metabolic profile in 95 autistic children with regressive autism. Recent studies also suggestthat the same key regions of the brain are affected in bothcases (Limke 2004, Kates 2004). At the same time, episodesof severe mercury exposure reveal that there is no singlemanifestation of mercury poisoning. GLUTATHIONE, a potent antioxidant, is the body's most important tool for detoxifying and excreting metals.Autistic children have significant differences in every measure of antioxidant capacity and oxidative stressThe James study shows that children with regressive autism have consistently elevated levels of oxidative stress as compared to normal healthy children. In fact, childrenexposed to high levels of mercury during gestation andinfancy have suffered from strikingly different diseases.Minamata disease resulted from in-utero exposure tomercury-contaminated fish. Individuals with reduced GLUTATHIONE antioxidant capacity will be under chronic oxidative stress and will be more vulnerable to toxic compounds that act primarily through oxidative damage, including mercury (James 2004). Children with Minamata diseasehad symptoms indistinguishable from mental retardation orcerebral palsy (Kondo 2000).
Oxidative stress plays a key role in several important degenerative diseases of the brain and nervous system, including Alzheimer's, Parkinson's, Huntington's disease, and schizophrenia (Shulz 2000, Granot 2004). The role of individual sensitivity made it extremely difficult to link mercury exposure with what was, at the time, a new and bizarre disease.


Similarly, when children have been exposed to high levels of mercury in foods, only a small group develop severe mercury poisoning while thousands are apparently unharmed (Jalili 1961, Kondo 2000).Dr. James' findings clearly reveal a mechanism by which autistic children would be predisposed to mercury-related oxidative damage to their developing brain and nervous system. Several additional pieces of evidence strengthen the potential link between mercury exposure and autism in children with abnormal antioxidant capacity.
Organic mercury actively transported through the blood—brain barrier accumulates in the highest concentrations in the cerebellum, especially the neuronal cells (Limke 2004). The cerebellum is the brain region associated with movement and cognition, and a key region targeted by toxic chemicals (Fonnum 2000), and a region of impairment in autistic patients (McAlonan 2004).Dr.
Glutathione deficiency potentiates manganese toxicity in rat striatum and brainstem and in PC12 cells.
She found that astrocytes have higher levels of GLUTATHIONE compared to neurons and were more resistant to the cytotoxic effects of thimerosal (James 2005). Mercury was less toxic to human brain cells pretreated with GLUTATHIONE or a GLUTATHIONE precursor N-acetyl cysteine, which is used as a treatment for mercury intoxication and it is thought to speed mercury excretion from the body (Ballatori 1998). Similar studies have documented oxidative damages of mercury and GLUTATHIONE protection to T cells, astrocytes, neurons and fibroblasts (Makani 2002, Shanker 2003).Immune symptomsIn the summer of 2004, researchers at Columbia's Mailman School of Public Health reported symptoms similar to autism in thimerosal-exposed mice. Innate gender-based proclivity in response to cytotoxicity and programmed cell death pathway.
Thimerosal was administered to three strains of laboratory mice at exposures that replicated infant exposure in the 1990s. Only the mouse strain with a predisposition to autoimmunity was affected by thimerosal exposure.
These mice had significant growth delay, reduced locomotion, exaggerated response to novelty, and changes in the brain and nervous system that were suggestive of autism (Hornig 2004).Metal metabolism and regressionUnlike most substances that are toxic to the brain, there is a significant lag time between exposure to either mercury or thimerosal, and the emergence of the symptoms of mercury poisoning.
Pooled analysis and meta-analysis of Glutathione S-Transferase M1 and Bladder Cancer: a HuGE review. The delay between first exposure and on-set of symptoms of mercury poisoning has been attributed to the gradual depletion of the brain's compensatory responses, chiefly GLUTATHIONE and other antioxidants (Weiss 2002).Autism often is diagnosed after a period of seemingly healthy development. Regressive children lose previously acquired skills such as speech and mobility, or fail to progress in their development. The role that oxidative stress and environmental chemicals play in regressive autism is unknown, but studies finding reduced metal excretion in autistic children point to different dynamics in regressive autism.A recent publication by physician Amy Holmes reported that autistic children had significantly lower levels of mercury in their hair relative to non-autistic children, suggesting greater accumulation of mercury in the body due to reduced excretion capabilities (Holmes 2003). Hair samples were analyzed from 94 autistic children and 45 non-autistic children between one and two years of age and the autistic children had significantly lower levels of mercury in their hair samples (0.47 vs.
In autistic children there was no correlation, hair levels were always low, even in cases where elevated maternal mercury exposure was reported.Regressive cases had higher concentrations of mercury in hair indicating less impaired mercury metabolism. This indicates that children least able to excrete mercury might experience autistic symptoms immediately while regressive cases of those with some capacity to detoxify and get rid of mercury would at first appear normal, but would then build up mercury to a critical point before their excretion capacity was overwhelmed and autistic symptoms surfaced. Arsenic-induced oxidative stress and its reversibility following combined administration of N-acetylcysteine and meso 2,3-dimercaptosuccinic acid in rats. Prenatal exposure to methylmercury changes dopamine-modulated motor activity during early ontogeny: age and gender-dependent effects. Metabolism of dichloromethane (methylene chloride) to formaldehyde in human erythrocytes: influence of polymorphism of glutathione transferase theta (GST T1-1). Enhancement of T cell receptor signaling by a mild oxidative shift in the intracellular thiol pool. Press Release: MMR Vaccine and Thimerosal-Containing Vaccines Are Not Associated With Autism, IOM Report Says. Metabolic biomarkers of increased oxidative stress and methylation capacity in children with autism.
Personal communication with EWG.James SJ, Slikker W 3rd, Melnyk S, New E, Pogribna M, Jernigan S. Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors.
Neuroanatomic variation in monozygotic twin pairs discordant for the narrow phenotype for autism.
Polychlorinated biphenyl mixture aroclor 1254-induced oxidative stress plays a role in dopaminergic cell injury. Use of a stratified oxidative stress model to study the biological effects of ambient concentrated and diesel exhaust particulate matter. Disruption of intraneuronal divalent cation regulation by methylmercury: are specific targets involved in altered neuronoal development and cytotoxicity in methylmercury poisoning? Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway.
Oxidative stress induced by phenylketonuria in the rat: Prevention by melatonin, vitamin E, and vitamin C. Opening Statement, Institute of Medicine News Conference on the Institute of Medicine Report on Thimerosal and Neurodevelopmental Outcomes, October 2001. Antioxidants are required during the early critical period, but not later, for neuronal survival. Plasma glutathione peroxidase in healthy young adults: influence of gender and physical activity. Declining Minamata male birth ratio associated with increased male fetal death due to heavy methylmercury pollution. Methylmercury-induced reactive oxygen species formation in neonatal cerebral astrocytic cultures is attenuated by antioxidants. The cerebral lesions in a patient with generalized glutathione deficiency and pyroglutamic aciduria (5-oxoprolinuria). 18(2)321-336.Tandon SK, Singh S, Prasad S, Khandekar K, Dwivedi VK, Chatterjee M, Mathur N.
Reversal of cadmium induced oxidative stress by chelating agent, antioxidant or their combination in rat.
Effect of thimerosal, a preservative in vaccines, on intracellular Ca(2+) concentration of rat cerebellar neurons. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal.
Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization. Association of blood arsenic levels with increased reactive oxidants and decreased antioxidant capacity in a human population of northeastern Taiwan.



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