Neurological and Immune Reactive Conditions Affecting Kids

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The incidence of neurotoxic, allergic, and immune reactive conditions, such as autism, schizophrenia, ADD, dyslexia, allergies, asthma, eczema, psoriasis, and childhood diabetes, has been increasing rapidly in recent years. A report by the National Research Council in 2000 found that 50% of all pregnancies in the U.S. result in prenatal or postnatal mortality, significant birth defects, developmental disabilities or otherwise chronically unhealthy babies, and recent studies published in JAMA found similar trends continuing with huge increases in children’s chronic conditions. Incidence of chronic developmental conditions in infants more than doubled between 1988 and 2006, especially asthma, learning and behavioral problems, and obesity. There has been a similar sharp increase in developmental disabilities in Canadian children over the last two decades, including learning disabilities and behavioral problems, asthma and allergies, and childhood cancer. Studies have documented that the primary cause of the increased developmental conditions are increased toxic exposures, including increased use of vaccines with toxic and inflammatory ingredients.

The U.S. Dept. of Education indicates that over 5 million children attending school have neurological-related disabilities reported by state agencies, other than ADD. A random sample of Oregon high school students found that over 16% had been diagnosed with depression. According to the American Academy of Pediatrics between 6 to 12% of all school age children are affected by ADHD and a similar number have some degree of dyslexia. The Centers for Disease Control shows 5.4 million schoolchildren have been diagnosed with ADHD. That’s 10%. In fact from the years 2003 to 2007, the number of kids between four and 17 with AD/HD jumped by one million. That’s a 22% increase. However, large surveys of elementary level student records find much higher levels—with over 20% of elementary school boys in some areas being treated for ADD. Studies have found that long-term use of stimulant drugs commonly causes significant adverse neurological and health effects, and options are available to deal with such conditions without such adverse effects including dealing with the underlying causes. Estimates of the percentage of children with mood or anxiety orders are as much as 20%.

Most of the increases in children’s neurological or developmental conditions have been found to be related to major increases in brain and immune system inflammation related to increased exposure to toxic chemicals or dietary excitoxins of the 4 million U.S. children born each year. At least 1 in 6 had one of the neurological conditions previously listed. One of the main causes of increased exposures to toxic metals, such as mercury and aluminum, and other toxins is the greatly increased vaccination schedule for infants in recent years compared to 1983 and prior. Another major source of mercury exposure is dental amalgam fillings. U.S. EPA has estimated that over 3 million of these are related to lead or mercury toxicity, with at least 25% of U.S. children getting mercury exposure at dangerous levels.

Researchers have found that the most striking differences between autistic and normal brains were loss of the purkinje cell layer in the cerebellum and activation of the microglia, which are cells that are central to the inflammatory response. The inflammatory response is your body’s defense against invasion, but in autism, it seems there is an inflammatory war going on in the brains of autistic children and adults. According to Psychology Today, other studies have shown that autism is possibly an autoimmune disease of some kind—the immune system is not only fighting external invaders or “bad guys” in the body, such as viruses, bacteria, or newly-formed cancer cells, but the body has also started to attack presumably healthy tissues of the body. In the evolutionary medicine paradigm, autoimmune disorders are diseases of civilization, caused by our highly inflammatory diets and stressful lifestyles.

Studies indicate that over 60,000 children are born each year with neurodevelopmental impairments due to prenatal exposure to methylmercury. Two other sources of mercury exposure appear to have been more common and at higher levels than this: 1) ethyl mercury from vaccines and 2) mercury vapor from amalgam dental fillings with mothers’ mercury fillings being the largest source of mercury in the fetus and a significant source of mercury in infants. Vaccines have unacceptable levels of many toxins, such as mercury thimerosal, aluminum, formaldehyde, endotoxins, and altered strains of viruses that cause brain inflammation and immune effects on infants, with some more susceptible to such effects than others based on genetics and other synergistic toxic exposures. Another study has found results that suggest that EMR radiation—radiation generated by such as cell phones and cell phone towers—may be another significant factor in autism. The study found a significant correlation between measured heavy metal concentrations, exposure to EMR, and autism.

A survey of thousands of parents of autistic children or children with Asperger’s by the Autism Association found that chelation/detoxification was by far the most effective treatment for autism, noting that chelation/detoxification was also much safer than most drug treatments for autism spectrum conditions. This is consistent with the findings of most autism treatment clinic tests that found that most autistic children tested are highly mercury and metal toxic. Another significant factor in some autism cases has been found to be Lyme disease. A study at the U.S. CDC found “statistically significant association” between neurological developmental disorders such as autism, attention deficit disorder (ADD), and speech disorders with exposure to mercury from thimerosal-containing vaccines before the age of 6 months. An analysis of the U.S. CDC VAERS database for adverse reactions from vaccines regarding effects of the diptheria-tetanus-pertusis vaccine found that those receiving DTaP and DTucP vaccines with thimerosal had significantly higher rates of autism, speech disorders, and heart arrest than those receiving DtaP vaccine without thimerosal, and that the rate of these increases exponentially with dose. The head of the CDC admitted that mercury can cause autism in susceptible children. An analysis of the U.S. Dept. of Education’s report on the prevalence of various childhood conditions among school children found that the rate of autism and speech disorders increased with increasing levels of thimerosal exposure from vaccines. Mercury has been well documented to cause birth defects, spontaneous abortions, and neurological problems, so autism-related effects are not surprising.

A follow-up study using DMSA as a chelator found that, overall, urinary mercury concentrations were significantly higher in children with autistic spectrum disorders than in a matched control population, and that vaccinated cases showed significantly higher urinary mercury concentrations than vaccinated controls. This is consistent with other studies that found that those who are poor are more likely to accumulate mercury and have adverse health effects. Changes in hospitals’ birth procedures, such as immediate cord clamping, have also been found to be a factor in the increase in neurological developmental problems.

Children with autism had significantly (2.1-fold) higher levels of mercury in baby teeth and blood but have similar levels of lead and similar levels of zinc. Baby teeth are a good measure of cumulative exposure to toxic metals during fetal development and early infancy. A study of environmental mercury levels in Texas school districts found a 61% increase in autism and a 43% increase in special education cases for every 1,000 pounds of mercury released into the environment. Autism prevalence diminished by 2% for every ten miles of distance from a mercury source.

Another study found similar results and estimated economic costs due to disability or lower IQ. Fossil fuel-burning power plants were the largest source of the widespread mercury pollution, but dental amalgam was the largest source in sewers and a significant source of environmental mercury in water bodies, fish, and air emissions. Children with autism also had significantly higher usage of oral antibiotics during their first twelve months of life. Children exposed to high levels or mercury and/or toxic metals have been found to have weakened immune system and increased susceptibility to pathogens. Tylenol, antibiotics, and milk are documented to increase the effects of mercury.

A survey released recently indicates a strong correlation between rates of neurological disorders, such as ADHD and autism, and childhood vaccinations. The survey found vaccinated boys were 155% more likely to have neurological disorders compared to their unvaccinated peers. Vaccinated boys were 224% more likely to have ADHD, and 61% were more likely to have autism. For older vaccinated boys in the 11-17 age bracket, the results were even more pronounced. Vaccinated boys were 158% more likely to have a neurological disorder, 317% more likely to have ADHD, and 112% more likely to have autism. Other studies have found similar results regarding a connection to vaccines and toxic metals. Studies have also found a significant link between food additives (food colorings and food preservatives) and ADHD.


Asthma is a chronic inflammatory disorder of the airways, characterized by wheezing, shortness of breath, chest tightness, mucus production, etc. At least 7.2% of the adult population has asthma, and asthma in children has become much more prevalent. Asthma is closely tied to immune system reactions of the humoral system, as controlled by cell signaling cytokines. Allergic antigens bind to immune mast cells and basophils, and when these come into contact with IgE antibody, a hypersensitivity response of the immune system leads to inflammation and bronchoconstriction.

It has been suggested that infant and childhood vaccinations may be contributing to the increasing prevalence of asthma. The strongest evidence in support of a possible association between vaccination and asthma comes from a prospective study of a cohort of children born in 1977 in Christchurch, New Zealand. In that study, there was no evidence of asthma after five to ten years of follow-up among 23 children who received neither pertussis nor oral polio vaccine, whereas asthma developed in 20% of 1184 children who had been vaccinated. A study of 1934 patients followed from birth to age twelve in a general medical practice in the UK found a 1.4-fold increased risk of asthma associated with whole cell pertussis vaccination. An association between pertussis vaccination and asthma was also reported in two cross-sectional surveys.

There are theoretical reasons to suspect a possible association of asthma with vaccination. One possible mechanism is that vaccines or their adjuvants may have direct IgE-potentiating effects. Another possibility is that vaccination may shift the immunologic balance toward a more allergenic response. It has also been suggested that vaccination may indirectly affect the tendency to develop allergies and perhaps asthma by preventing diseases in childhood, such as measles, which may protect against developing allergic conditions later in life. In the case of pertussis, the disease has been suggested to increase the occurrence of atopy and asthma, and it may be that the vaccine could have similar effects.

Also according to the U.S. FDA, at least 26 million have allergies, at least 17 million have asthma, and 15 million have systemic eczema. Childhood diabetes is increasing rapidly. Although Russian and U.S. studies from the 1980s found that thimerosal was highly toxic and recommended that its use as a medical preservative should be discontinued, its use was not discontinued. One study found five times higher rate of allergy among a group vaccinated with pertussis vaccine (DPT) as opposed to an unvaccinated group, and three other studies found increased asthma, allergies, and eczema among the vaccinated group.

Vaccines given to infants in the first six months of their lives commonly cause asthma. Over the last twenty years, the percent of diabetes cases below twenty years old has increased from 2% to over 30%, and there was a 70% in cases under forty years of age between 1990 and 1998. Studies in the U.S. and Sweden have confirmed vaccinations to be a major factor in the increased diabetes cases. Currently over 16 million have diabetes. DPT vaccinations have also been linked to sudden infant death syndrome (SIDS). DPT vaccines are mostly given at two, four, and six months of age, and 85% of SIDS cases occur during this age span.

One study found babies die at a rate 8 times the normal rate within three days of DPT shots, while another found that among SIDS victims 61% had DPT within the 2 previous weeks and 13% within 24 hours of DPT vaccination. According to Dr. Harris Coulter, SIDS was so infrequent in the pre-vaccination era that it was not even mentioned in the statistics, but it started to climb in the 1950s with the spread of mass vaccination against childhood diseases. A monitoring study of infant breathing patterns after DPT vaccinations showed large increases in breathing difficulties. including episodes of ceased breathing, which continued for months after DPT in some cases. Some cases of seizures after DPT were also observed. Another study found significantly higher rates of heart arrest in those getting DpaT vaccines with mercury thimerosal compared to those without. Prenatal exposure to mercury has also been found to predispose animals and infants to seizures and epilepsy. Many adverse reactions and adverse health effects related to the Gardasil HPV vaccine, including death, have been recorded.

The computer records from the National Vaccine Injury Compensation Program, obtained by Gannett News Service using the Freedom of Information Act, as part of a four month study of federal immunization policy, reveal:

Of 253 infant death cases awarded more than $61 million by the U.S. Court of Federal Claims in the 1990s under the compensation program, 224, or 86 percent, were attributed to vaccination with DTP, the diphtheria, tetanus and pertussis (whooping cough) shot. In these cases, mortality was originally attributed to SIDS in 90, or 40%, of them. The Vaccine Court has awarded at least nine judgments in favor of children who have become autistic or have had serious damage from MMR vaccine. The effect of metals in vaccines on peptides from milk and gluten has been suggested as another mechanism causing apnea in infants and some SIDS cases.

Andrew Wakefield has published about 130-140 peer-reviewed papers looking at the mechanism and cause of inflammatory bowel disease and has extensively investigated the brain-bowel connection in the context of children with developmental disorders, such as autism. One of his studies has been highly criticized, but the criticisms have been documented to be for political reasons rather than science; therefore Wakefield’s study has been vindicated. A large number of replication studies have been performed around the world by other researchers, confirming the curious link between brain disorders, such as autism, and gastrointestinal dysfunction.

A team from the Wake Forest University School of Medicine in North Carolina is examining 275 children with regressive autism and bowel disease—and of the 82 tested so far, 70 prove positive for the measles virus. Dr Stephen Walker said: “Of the handful of results we have in so far, all are vaccine strain, and none are measles.” This research proves that in the gastrointestinal tract of a number of children who have been diagnosed with regressive autism, there is evidence of measles virus. What it means is that the study done earlier by Dr. Wakefield and published in 1998 is correct. Out of 771 total claims filed by parents between 1990 through mid-1998, 660 (or 86%) claims contained assertions that DTP was the cause of death. 43% were classified by medical authorities at time of death as SIDS cases. A second federal database tends to draw a similar connection. This one, analyzing the 1990s through the Food and Drug Administration’s reports, contains 460 reports of children who died within three days of receiving shots containing DTP. Of those 460 reports, 266 (or 58%) of the claims listed SIDS as a reaction.

That database is called VAERS (Vaccine Adverse Event Reporting System). It was ordered by Congress to track dangerous reactions to the shots all babies must receive as admission to our society. In typical federalese, the FDA refers to death as an adverse event “or a reaction.” By law, reports of reactions to DTP and other vaccines are supposed to be made religiously by doctors, pharmaceutical companies, and public health clinics, but former FDA commissioner David A. Kessler has estimated the reports “represent only a fraction of the serious adverse events”—perhaps as few as 10%. Dr. Marcel Salive, chief of the FDA’s epidemiology staff, says, “Any number you get, take with a grain of salt.” Some spokespersons at various government and medical institutions have continued to deny the strong evidence that vaccines are a major factor in autism and other conditions; however, they can identify no credible evidence to support their opinion.

Most criticisms have been found to have significant connections to special interests and no credible paper or clinical evidence has been provided to support their position that has not been credibly debunked in Congressional Hearings and other documentation. Vaccines contain immune adjuvants such as aluminum and mercury thimerosal that cause stimulation and activation of the immune system. This has been found to cause high levels of brain inflammation with increased free radicals and inflammatory cytokines over prolonged periods of time, as long as a year from one vaccination. Brain inflammation has been found to be a major factor in irritability, anxiety, depression, insomnia, and neurological conditions, including ADHD, schizophrenia, and autism. Aluminum has also been found to significantly increase the effects of other toxins, such as mercury, through synergistic effects. Autistic children have been found to have on average three times as much aluminum in erythrocytes as non-autistic children. Evidence supports a link between the aluminum hydroxide used in vaccines, and symptoms associated with Parkinson’s, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and Alzheimer’s.

With large numbers of vaccines being given in recent years in rapid succession, the brain of infants becomes increasingly overexcited and inflamed, resulting in brain damage and disruption of brain development. Vaccine adjuvants, mercury from mother’s amalgam fillings, and dietary excitotoxins such as MSG and soy products have all been found to be major factors in the brain inflammation causing large numbers of developmental neurological conditions in children. Mercury has been found to cause an increase in inflammatory Th2 cytokines. In the pancreas, the cells responsible for insulin production can be damaged or destroyed by the chronic high levels of cytokines, with the potential of inducing type II diabetes—even in otherwise healthy individuals with no other risk factors for diabetes. Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam fillings and normalizing of blood sugar. In addition to this mechanism, other links between vaccines and diabetes have been found, and there is evidence that vaccines are the number one cause of Type I diabetes in young children.

The largest increase in neurological and immune conditions has been in infants, with an increase in autism cases to over 500,000, an over 900% increase to a level of approx. 1 per 500 infants in the last decade, making it the 3rd most common chronic childhood condition. For 1999 through 2002, the number of professionally diagnosed in California with full syndrome autism has doubled. There have been similar increases in ADD and dyslexia to over 10 million, similar large numbers (over 10%) with childhood depression or anxiety, and over 10 % of infants— approximately 15 million in the U.S. with systemic eczema. Studies researching the reason for these rapid increases in infant reactive conditions seem to implicate earlier and higher usage of vaccines containing mercury (thimerosal) as a likely connection. A recent study comparing pre- and post-vaccination mercury levels, found a significant increase in both preterm and term infants after vaccination, with post-vaccination mercury levels approximately 3 times higher in the preterm infants as compared with term infants.

The study found mercury blood levels up to 23.6 ug/L and received an average dose of 16.7 ug/kg. Just this one vaccination gave an exposure to mercury that is many times the U.S. ATSDR adult minimum risk level (MRL) for mercury of .3/ug/kg body weight per day. Recent research provides evidence that the use of hepatitis B vaccines with thimerosal in newborns appears to be very harmful. The first phase of this monkey study, published in 2009 in the journal Neurotoxicology, focused on the first two weeks of life. Baby monkeys received a single vaccine for Hepatitis B, mimicking the U.S. vaccine schedule, and were compared with matched, unvaccinated monkeys. The vaccinated monkeys, unlike their unvaccinated peers, suffered the loss of many reflexes that are critical for survival.

It has been estimated that, if all of the vaccines recommended by the American Association of Pediatrics are given and all contained thimerosal, by age 6 months an infant would have received 187 micrograms of ethyl mercury, which is more than the EPA/ATSDR health standard for organic mercury and by age three, the typical child would have received over 235 micrograms of mercury thimerosal from vaccinations, which is considerably more than federal mercury safety guidelines (in addition to significant levels from other sources for many). Infants during this period have undeveloped blood brain barriers and much of the mercury goes to the brain, resulting in significant adverse neurological effects in those that are most susceptible. Neonatal administration of the vaccine preservative thimerosal has been found to produce lasting impairment of nociception (pain sense) and apparent activation of opioid system (controls pain, reward and addictive behaviors) in rats, which is similar to brain problems in some children with autism. The mercury load was calculated and injected into the rats that corresponded to what infants receive with vaccines in many countries including the U.S. The bioaccumulation in the brain and toxic effects of ethyl mercury are comparable to that of methyl, with mercury accumulation in the brain and physical effects actually being more extensive.

Researchers on autism have found and are in agreement that autism is primarily caused by various disruptions in the body’s homeostasis that result in a cascade of systemic problems characterized by the term autism. Vaccines and mercury have been found to be something that is capable of causing such a disruption in the body’s homeostasis in susceptible individuals.

Brain inflammation has been found to be a major factor in autism, and in the sometimes related metabolic syndrome. Causes of oxidative stress and lipid peroxidative-related brain inflammation that have been documented include vaccines, mercury, aluminum, excitotoxins, such as MSG, aspartame, food additives, and overconsumption of high-fructose corn sweetener. These cause high glutamate levels in the brain and oxidative damage, resulting in inflammation of the brain and immune system, as well as damage to brain microglia cells and the mitochondrial DNA, high triglycerides, metabolic syndrome, etc. These have been found to be factors in most chronic neurological diseases including autism and diabetes.

The brain has elaborate protective mechanisms for regulating neurotransmitters such as glutamate, which is the most abundant of all neurotransmitters. When these protective regulatory mechanisms are damaged or affected, chronic neurological conditions, such as autism, can result. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS, causing increased glutamate and calcium related neurotoxicity. Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage.

Nitric oxide related toxicity caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD), has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity. Mitochondrial DNA mutations or dysfunction is fairly common and is found in at least 1 in every 200 people, and toxicity affect this population more than those with less susceptibility to mitochondrial dysfunction. These inflammatory processes damage cell structures, including DNA, mitochondria, and cell membranes. They also activate microglia cells in the brain, which control brain inflammation and immunity. Once activated, the microglia secretes large amounts of neurotoxic substances such as glutamate, an excitotoxin, which adds to inflammation and stimulates the area of the brain associated with anxiety. Inflammation also disrupts brain neurotransmitters, resulting in reduced levels of serotonin, dopamine, and norepinephrine. Some of the main causes of such disturbances that have been documented include vaccines, mercury, aluminum, other toxic metals, MSG, aspartame, etc.

Inflammation induced by vaccine adjuvants, like aluminum and mercury, or by excitotoxins, like MSG, has been found to play a significant role in insulin resistance (type II diabetes) and in high levels of LDL cholesterol. Type II diabetes is an epidemic among young Americans and greatly increases the incidence of heart attack, blindness, stoke, infertility, and early death. There is also evidence that the diet drink sweetener aspartame can cause or increase the effects of diabetes and hypoglycemia. Iron overload has also been found to be a cause of insulin resistance/type II diabetes. Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions. Mercury and cadmium inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes.

Impairment of Methionine Synthase Function and Impairment of Folate-dependent Methylation

The authors of two studies about thimerosal developmental effects write:

“Our studies… provide evidence that mercury, aluminum, other heavy metals and the vaccine preservative thimerosal potently interfere with [methionine synthase] activation and impair folate-dependent methylation. 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. Mercury exposure has been found to cause oxidative damage, reactive oxygen species, and depletion of glutathione in the brain. Oxidative damage and depletion of glutathione have been found to be factors in neurological conditions such as bipolar disorder, schizophrenia, depression, etc. Repetitive doses of thimerosal leads to neurobehavioral deteriorations in autoimmune susceptible mice, increased oxidative stress and decreased intracellular levels of glutathione in vitro. Subsequent to vaccination, autistic children have significantly decreased level of reduced glutathione. Since each of these agents has been linked to developmental disorders, our findings suggest that impaired methylation, particularly impaired DNA methylation in response to growth factors, may be an important molecular mechanism leading to developmental disorders.”

Stajich, Pichichero, Waly, et al. write:

“A single thimerosal-containing vaccination produces acute ethylmercury blood levels of 10-30nM…, and blood samples in 2-month-old infants, obtained 3-20 days after vaccination, contain 3.8-20.6n methylmercury. Our studies therefore indicate the potential for thimerosal to cause adverse effects on [methionine synthase] activity at concentrations well below the levels produced by individual thimerosal-containing vaccines. A second study notes that it has been found that those with autism generally had higher levels of exposure to mercury from their mother’s amalgam fillings or other sources prenatally. Another study on mice supported the autism/thimerosal connection. Many other studies have documented the vaccine/thimerosal connection to autism.”

Because of the evidence, the FDA has completed a study and written a letter to vaccine manufacturers asking that mercury be removed from vaccines. The updated letter stated:
“The Center for Biologics Evaluation and Research (CBER) has completed its evaluation of the use of thimerosal in vaccines. Our review concluded that reducing or eliminating thimerosal from vaccines is merited. The letter pointed to a joint statement by the American Academy of Pediatrics and the United States Public Health Service in 1999, which ‘called for the removal of thimerosal from vaccines as soon as possible.’”

A Congressional Committee after holding a hearing has also called for elimination of mercury in vaccines as soon as possible. However, it has been documented that most children still receive high levels of mercury in vaccines and that aluminum in vaccines have similar significant adverse neurological effects.

Many thousands of parents have reported that their child got such conditions after vaccination, and tests have confirmed high levels of mercury and aluminum in most of those tested, along with other toxic exposures. An additional source of thimerosal to the fetus of women who are RH negative is the 30 micrograms in the RhoGAM shot the mother receives, which has been found to be a significant factor in autism incidence. Mothers of children with neurodevelopmental disorders, autism, or ADHD treated by two clinics were compared to a set of mothers from a control group of children for Rh-Negativity. Prior to 2002 when thimerosal use in vaccines was reduced, the group of mothers of children with neurodevelopmental disorders or conditions were more than 25% more likely to have Rh-Negativity than mothers of the control group. After 2002, there was no significant difference in Rh-negativity incidence between mothers of children with ND disorders versus controls.

Underweight infants that get the same dose of thimerosal as other infants have also been found to be at special risk. Many of those diagnosed with high mercury levels have been found to have significant improvement after mercury detoxification. Thimerosal had been previously removed from similar preservative uses in eye drops and eye medications after evidence of a connection to chronic degenerative eye conditions.

After over 15,000 lawsuits were filed in France over adverse effects of the hepatitis B vaccine, the French Minister of Health ended the mandatory hepatitis B vaccination program for all school children. Adverse effects included neurological disorders and autoimmune disorders, such as multiple sclerosis and lupus. Some hospitals in the U.S. also quit recommending certain vaccinations. Dr. Loren Koller recognized that more is involved in the vaccine effects than just ethylmercury. He mentions aluminum and even the viral agents beings used as other possibilities. This is especially important in the face of Dr. R. K. Gherardi’s identification of macrophagic myofascitis, a condition causing profound weakness and multiple neurological syndromes, one of which closely resembled multiple sclerosis. Both human studies and animal studies have shown a strong causal relationship to the aluminum hydroxide or aluminum phosphate used as vaccine adjuvants. More than 200 cases have been identified in European countries and the United States and have been described as an emerging condition. In two children aged 3 and 5, doctors at the All Children’s Hospital in St. Petersburg, Florida described chronic intestinal pseudo-obstruction, urinary retention, and other findings indicative of a generalized loss of autonomic nervous system function (diffuse dysautonomia). The three-year-old had developmental delay and hypotonia (loss of muscle tone). A biopsy of the children’s vaccine injection sites disclosed elevated aluminum levels. In a study of some 92 patients suffering from this emerging syndrome, eight developed a full-blown demyelinating CNS disorder (multiple sclerosis). This included sensory and motor symptoms, visual loss, bladder dysfunction, cerebellar signs (loss of balance and coordination) and cognitive and behavioral disorders.

Dr. Gherardi, the French physician who first described the condition in 1998, collected over 200 proven cases. One third of these developed an autoimmune disease, such as multiple sclerosis. Of critical importance is his finding that, even in the absence of obvious autoimmune disease, there is evidence of chronic immune stimulation caused by the injected aluminum, known to be a very powerful immune adjuvant. The reason this is so important is that there is overwhelming evidence that chronic immune activation in the brain (activation of microglial cells in the brain) is a major cause of damage in numerous degenerative brain disorders, from multiple sclerosis to the classic neurodegenerative diseases (Alzheimer’s disease, Parkinson’s, and ALS). In fact, I have presented evidence that chronic immune activation of CNS microglia is a major cause of autism, ADD, and Gulf War Syndrome. Dr. Gherardi emphasizes that once the aluminum is injected into the muscle, the immune activation persists for years. In addition, we must consider the effect of the aluminum that travels to the brain itself. Numerous studies have shown harmful effects when aluminum accumulates in the brain. A growing amount of evidence points to high brain aluminum levels as a major contributor to Alzheimer’s disease and possibly Parkinson’s disease and ALS (Lou Geherig’s disease). This may also explain the ten times increase in Alzheimer’s disease in those receiving the flu vaccine five years in a row.

Mucocutaneous lymph node syndrome (Kawasaki syndrome) is an autoimmune disease that manifests as a multi-systemic necrotizing medium vessel vasculitis that is largely seen in children under 5-years-of-age, which affects many organs, including the skin, mucous membranes, lymph nodes, and blood vessel walls, but the most serious effect is on the heart where it can cause severe aneurysmal dilations in untreated children. Medical literature, epidemiological findings, and some case reports have suggested that mercury plays a pathogenic role. Several patients with Kawasaki’s disease have presented elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria, which are seen in children with acrodynia—known to be caused by mercury, are similar to those seen in Kawasaki’s disease. Genetic depletion of glutathione S-transferase, a susceptibility marker for Kawasaki’s disease, is known to be also a risk factor for acrodynia and also increases susceptibility to mercury. Coinciding with the largest increase (1985-1990) from 75microg to 187.5microg of thimerosal (49.6% ethyl mercury) in vaccines, which are routinely given to infants in the U.S. by six months, the rates of Kawasaki’s Disease increased ten times, and later between 1985-1997 the rates increased by twenty times. Since 1990, 88 cases of patients developing Kawasaki’s Disease some days after vaccination have been reported to the Centers of Disease Control (CDC), including 19% manifesting symptoms the same day.

Although vaccinations appear to be the largest source of mercury in many infants, mercury has been found to be transmitted from the mother to the fetus through the placenta, and mercury accumulates in the fetus at higher levels than in the mother’s blood. Infants of mothers who had dental work involving amalgam during pregnancy had significantly higher levels of mercury in hair tests. Breast milk of women who have amalgam fillings is the second largest source of mercury in infants and young children, but eating a lot of fish has also been found to be a significant source. Milk increases the bioavailability and retention of mercury by as much as double, and mercury is often stored in breast milk and the fetus at much higher levels than that in the mother’s tissues. Inorganic mercury has been shown to be excreted to milk from plasma to a higher extent than methylmercury.

Mercury is transferred mainly by binding to cassein. The level of mercury in breast milk was found to be significantly correlated with the number of amalgam fillings, with milk from mothers with 7 or more fillings having levels in milk approximately ten times that of amalgam-free mothers. The mercury in milk sampled ranged from 0.2 to 6.9 ug/L. Prenatal mercury exposure can also developmentally damage the metals detox system of the liver, which can lead to accumulation and toxicity of later metals exposure.

A group of Chinese children with autism were diagnosed as having mercury toxicity from eating fish. Overall, it was estimated that the children examined received an estimated median mercury dose of 0.40 micrograms mercury/kilogram bodyweight/week (0.06 micrograms mercury/kilogram bodyweight/day). This is a remarkably low dose of mercury, considering that children receiving thimerosal-containing childhood vaccines on average received ten to twenty micrograms mercury/kilogram bodyweight/day and the US Environmental Protection Agency (EPA) methylmercury safety limit is 0.1 micrograms mercury/kilogram bodyweight/day), and yet these children had very serious adverse outcomes.

A recent study found that prenatal mercury exposures and susceptibility factors, such as ability to excrete mercury, appear to be major factors in those with chronic neurological conditions like autism. Infants whose mothers received prenatal Rho D immunoglbulin injections containing mercury thimerosal or whose mothers had high levels of amalgam fillings had a much higher incidence of autism. While the hair test levels of mercury of infants without chronic health conditions like autism were positively correlated with the number of the mothers amalgam fillings, vaccination thimerosal exposure, and mercury from fish, the hair test levels of those with chronic neurological conditions, such as autism, were much lower than the levels of controls and those with the most severe effects had the lowest hair test levels, even though they had high body mercury levels. This is consistent with past experience of those treating children with autism and other chronic neurological conditions.

Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals. Those with the genetic allele ApoE4 protein in the blood have been found to detox metals poorly and to be much more to chronic neurological conditions than those with types ApoE2 or E3.

Mercury and toxic metals enzymes required to digest milk casein and wheat gluten, resulting in dumping morphine-like substances in the blood that are neurotoxic and psychotic as a major factor in schizophrenia, autism, and ADHD. A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids appears to be a major part of the connection to these allergic/immune reactive conditions. For example, mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV), which are required in the digestion of the milk protein casein or wheat protein gluten, and the same protein that is cluster differentiation antigen 26 (CD26), which helps T lymphocyte activation. CD26 or DPPIV is a cell surface glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors. Studies involving large samples of patients with autism, schizophrenia, or mania found that over 90% of those tested had high levels of the milk protein beta-casomorphine-7 in their blood and urine, defective enzymatic processes for digesting milk protein, and similarly for the corresponding enzyme needed to digest wheat gluten. Like casein, gluten breaks down into molecules with opioid traits, called gluteomorphine or gliadin. As with caseomorphin, it too can retain biological activity if the enzymes needed to digest it are not functioning properly.

Proteins in bovine milk are a common source of bioactive peptides. The peptides are released by the digestion of caseins and whey proteins. In vitro, the bioactive peptide beta-casomorphin 7 (BCM-7) is yielded by the successive gastrointestinal proteolytic digestion of bovine beta-casein variants A1 and B, but this was not seen in variant A2 or in goats milk. In hydrolysed milk with variant A1 of beta-casein, BCM-7 level is 4-fold higher than in A2 milk. Variants A1 and A2 of beta-casein are common among many dairy cattle breeds. A1 is the most frequent in Holstein-Friesian (0.310-0.660), Ayrshire (0.432-0.720) and Red (0.710) cattle. In contrast, a high frequency of A2 is observed in Guernsey (0.880-0.970) and Jersey (0.490-0.721) cattle. In children with autism, most of whom have been found to have been exposed to high levels of toxic metals through vaccines, mothers’ dental amalgams, or other sources; higher levels of BCM-7 is found in the blood.

BCM-7 appears to play a significant role in the aetiology of human diseases. Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from ischaemic heart disease. It appears that the populations that consume milk containing high levels of beta-casein A2 have a lower incidence of cardiovascular disease and type 1 diabetes. Beta-casomorphin-7 has opioid properties including immunosuppression, which account for the specificity of the relation between the consumption of some but not all beta-casein variants and diabetes incidence. BCM-7 has also been suggested as a possible cause of sudden infant death syndrome (SIDS). In addition, neurological disorders, such as autism and schizophrenia, appear to be associated with milk consumption and a higher level of BCM-7.

The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin, and IgG and IgM for casein. Beta-casomorphine-7 is a morphine-like compound that results in neural dysfunction, as well as being a direct histamine releaser in humans and inducing skin reactions. Similarly, many also had a corresponding form of gluten protein with similar effects. Elimination of milk, wheat products, and sulfur foods from the patient’s diet has been found to improve the condition. A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects. The behavioral improvements were accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio. Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors. As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detoxification. As mercury levels are reduced, the protein binding is reduced and improvement in the enzymatic process occurs. The neurotoxic effects of such opioid mechanisms has also been found to be a factor in multiple sclerosis, and low dose naltrexone (LDN) has been found to often be effective in reducing MS symptoms and exerbations.

Lactose (milk sugar), which is a major component of milk, is a disaccharide sugar made up of the simple sugars glucose and galactose. Lactase is an enzyme that facilitates digestion of lactose. Over 50% of non-Caucasians are lactose intolerant, and about 20% of Caucasians are also lactose intolerant. Infants are most lactose tolerant, but lactase activity declines dramatically over time so adults have about 5 to 10% of the level of activity in infants. Only a relatively small percentage of people retain enough lactase activity to absorb significant amounts of lactose throughout their adult life. Lactose intolerance results in undigested lactose in the intestines, which often causes gas, bloating, abdominal discomfort, and proliferation of bacteria in the intestines. In addition to inhibiting the enzymes required to digest milk casein and whey, chronic mercury exposure in animals has also been found to inhibit lactase and glucose-6-phosphatase needed to digest lactose and other polysaccharides. Thus chronic exposure to mercury and toxic metals also increases lactose intolerance and digestion problems of carbohydrates in general. Digestive problems have been found to commonly be improved by reducing chronic mercury and toxic metal exposures. Lactose intolerance can also be alleviated to some degree by supplemental enzymes, using fermented milk products such as yogurt or kefir, or using only small amounts of milk products spread throughout the day.

Studies have also found heavy metals deplete glutathione and bind to protein-bound sulfhydryl SH groups, resulting in inhibiting SH-containing enzymes and production of reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl radical. In addition to forming strong bonds with SH and other groups like OH, NH2, and Cl in amino acids which interfere with basic enzymatic processes, toxic metals exert part of their toxic effects by replacing essential metals such as zinc at their sites in enzymes. An example of this is mercury’s disabling of the metallothionein protein, which is necessary for the transport and detoxification of metals. Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally binds with cuprous ions, thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function.

Another large study found a high percentage of autistic and PDD children are especially susceptible to metals due to the improper functioning of their metallothionein detoxification process, and with proper treatment, most recover or significantly improve. Mercury has also been found to play a part in neuronal problems through blockage of the P-450 enzymatic process. Another study found accelerated lipofuscin deposition—consistent with oxidative injury to autistic brain in cortical areas serving language and communication. Compared with controls, children with autism had significantly higher urinary levels of lipid peroxidation. Double-blind, placebo-controlled trials of potent antioxidants—vitamin C or carnosine—significantly improved autistic behavior.

Mercury-induced reactive oxygen species and lipid peroxidation has been found to be a major factor in mercury’s neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide dismutase (SOD). This has been found to be a major factor in neurological and immune damage caused by the heavy metals, including damage to mitochondria and DNA, as well as chronic autoimmune conditions and diseases.

Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes such as cysteine dioxygenase, gamma-glutamyltranspeptidase (GGT), and sulfite oxydase, along with neurotransmitter amino acids which have been found to be significant factors in many autistics, plus enzymatic processes involving vitamins B6 and B12, with effects on the cytochrome-C energy processes as well. For example, the vitamin B6 activating enzyme, B6-kenase, is totally inhibited in the intestine at extremely low (nanamolar) concentrations. Epson salts (magnesium sulfate) baths, supplementation with the p5p form of vitamin B6, N-acetyl cysteine, and vitamin B12 shots are methods of dealing with these enzymatic blockages that have been found effective by those treating such conditions. Mercury has also been found to have adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium. Supplementing with these minerals has also been found to be effective in the majority of cases, and lithium oratate has even been found to cause regeneration of neurons in damaged areas of the brain, such as the hippocampus. Another of the results of these toxic exposures and enzymatic blockages is the effect on the liver and dysfunction of the liver detoxification processes, which autistic children have been found to have. All of the autistic cases tested were found to have high toxic exposures/effects and liver detoxification profiles outside of normal.

Other aspects of gastrointestinal dysfunction that is found in the majority of autism cases are intestinal inflammation, enterocolalitis, lymphondular hyperplsia, abnormal intestinal permeability, or malabsorption. The intestinal damage also causes improper functioning of the buffering mechanism that maintains blood PH and enzyme functions. Such damage to the intestines and gastrointestinal processes are known from animal studies to be caused by mercury and other toxic metals. Inorganic mercury is the predominant excretionary form in the intestines, whatever the source’s form. All forms are absorbed by the intestines, and inorganic mercury accumulates in intestinal tissues, especially in young animals or infants, which are known to have poor biliary excretion of mercury. Children in the U.S. are exposed to high levels of mercury thimerosal, a highly toxic organic form of mercury. Organic mercury in primate studies is found to cause paneth cells in the intestines to be enlarged and packed with secretionary granules. This is also common in autistic children.

Along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions. Mercury as well as thimerosal, aluminum, and other toxic metals have direct neurotoxic effects on brain nucleoid binding proteins through their effect on Ca2+ATPase and Na+/K+ATPase activity. The effects on the neurological and immune systems of exposure to various toxic substances, such as toxic metals and environmental pollutants, have been found to have additive or synergistic effects and to be factors in increasing eczema, allergies, asthma, delayed food allergies, and sensitivity to other lesser allergens. Most of the children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds. Other than the organochlorines or toxic metals, three common pollutants that have been documented to have effects on such conditions are traffic and industrial pollutants nitrogen oxide, power plant residual oil fly ash, and organochlorine pollutants.

Mercury has also been found to cause reduced acetylycholine levels and to be a factor in autism. When the author succeeded in removing excessive metal deposits using cilantro and up-regulation techniques, he found Acetylcholine suddenly increased towards a normal level, short-term memory, and the ability to concentrate and think clearly improved significantly; often those who had abnormal or anti-social and irritable behavior returned to more acceptable behavior.

Another effect of mercury and toxic metals is a reduction in B-lymphocyte. Many studies dealing with autistic patients and further work with such patients have found toxic metal exposure causes a tendency to be more seriously affected by viruses and to develop intestinal disorders, including leaky gut, lymphoid modular hyperplasia, and a high incidence of parasites. Gut disease with inflammation has become increasingly evident in autism. Enterocolitis and lymphonodular hyperplasia are found in nearly 90% of regressed autistic children. Widespread inflammatory changes with poor intestinal digestive enzyme activity, abnormal intestinal permeability, and malabsorption have been reported in various autistic subgroups. Studies have found that mercury has similar effects on animals.

A mechanism by which vaccines such as MMR trigger autism by causing a loss of homeostasis between the amino acids glycine and glutamate has been demonstrated. Also, mercury exposure has been shown to disrupt immune system homeostasis, making the systems more susceptible to infectious agents such as measles virus and other viruses. The stabilizer in MMR and a few other vaccines is hydrolyzed gelatin, a substance that is approximately 21% glycine. It appears that, based on studies, the use of that form of glycine triggers an imbalance between the amino acid neurotransmitters responsible for the absorption rate of certain classes of cells throughout the body. It is that wide-spread disruption that apparently results in the systemic problems that encompass the mind and the body characterized in today’s ‘classic’ autism. Metals by binding to SH radicals in proteins and other such groups can cause autoimmunity by modifying proteins which via T-cells activate B-cells that target the altered proteins inducing autoimmunity as well as causing aberrant MHC II expression on altered target cells. Studies have found that various protein-related disorders, such as misfolded proteins, are found in some autism cases.

Studies have also found mercury, aluminum, and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein. While zinc binding with MBP stabilizes the association with brain myelin, mercury and cadmium have been found to interfere with zinc binding to MBP and thus cause dysfunction and auto-immunities. Dr. Stejskal recently began testing children with autism. Her preliminary results on eighteen autistic children and eleven controls found that five of eighteen autistic children had a positive proliferative (“allergic”) response on MELISA to thimerosal vs. 1/11 controls. Similar results were recently found for methylmercury (6/10 autistics vs. 0/11 controls) and inorganic mercury (6/18 autistics vs. 0/11 controls). Most importantly, 13/16 autistics tested positive for reactivity to the mercury-MBP vs. only 3/10 controls. The mercury-MBP reactivity is presumed to be caused by the mercury reconfiguring the three-dimensional MBP, to which the body generates the allergic (autoimmune) response. In another study, a significant percentage of children with autism developed anti-SK, anti-gliadin and anti-casein peptides, and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. These antibodies are synthesized as a result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69, indicating that they are specific. The study found that bacterial antigens (SK), dietary peptides (gliadin, casein) and thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules bind to CD26 or CD69 and induce antibodies against these molecules. Immune mechanisms are thus seen to be a major factor in neurotoxicity of metals seen in conditions such as autism and ADD.

Parathyroid Hypertensive Factor (PHF) is produced by the parathyroid gland and is measurable by the University of Alberta. Preliminary PHF determinations on over 100 patients through the Pfieffer Treatment Center have revealed very high levels for autistic patients. Heavy metals are known to block calcium L-channels at the cell membrane, whereas PHF is known to open calcium L-channels and stimulate phosphodiesterase. Calcium L-channels perform numerous functions, including initiation of transcriptional events which support learning, memory, and endocrine secretion. Mercury inhibits L-channels at micromolar concentration in an irreversible manner in hippocampal neurons. Hypothetically, elevated PHF may serve to at least partially compensate Hg-inhibition of L-channels. Mercury is also a potent inhibitor of cAMP, cellular levels of which presumably further decrease with PHF-stimulation of phosphodiesterase. Thus, in the context of mercury toxicity, PHF may play both adaptive and maladaptive roles. The very mechanism of mercury-induced auto-immune disease in mercury-sensitive rats is related to L-channel signaling. This process involves induction of interleukin-4 gene expression, which is mediated by protein kinase C-dependent calcium influx through L-channels. PHF hypothetically may affect the autoimmune response.

An IRB approved study assessing urinary levels of porphyrins found an apparent dose-response effect between autism severity and increased urinary coproporphyrins. Each group of ASDs had significantly increased median coproporphyrin levels versus controls. A significant increase (1.7-fold) in median coproporphyrin levels was observed among non-chelated ASD patients versus chelated ASD patients. Mercury toxicity was found to be associated with elevations in urinary coproporphyrin (cP), pentacarboxyporphyrin (5cxP), and precoproporphyrin (prcP) (also known as keto-isocoproporphyrin) levels. Two cohorts of autistic patients in the U.S. and France had urine porphyrin levels associated with mercury toxicity. Another study using chelation therapy on a group of autistic patients found significant improvement during the study period.

Following other studies showing higher than normal androgen levels in most autistic patients, a study found increased androgen levels in virtually all of a group of autistics. Morning blood samples collected following an overnight fast, compared to the pertinent reference means, showed significantly increased relative mean levels for: serum testosterone (158%), serum free testosterone (214%), percent free testosterone (121%), DHEA (192%), and androstenedione (173%). A medical hypothesis has suggested that some autism spectrum disorders (ASDs) may result from interactions between the methionine cycle-transsulfuration and androgen pathways following exposure to mercury. A study following treatment including chelation using DMSA and Lupron brought significant improvement in the majority of patients.

A significant overall improvement from the 70-79th percentile of severity at baseline to the 40-49th percentile of severity at the end of the study was observed for patients treated for a median of approximately 4 months. Significant improvements in sociability, cognitive awareness, behavior, and clinical symptoms/behaviors of hyperandrogenemia were also observed. Significant decreases in blood androgens and increases in urinary heavy metal concentrations were observed. Minimal drug adverse effects were found. Another disorder caused by metals/vaccine exposure is pyrroluria, which about 50% of autistic and schizophrenic children have been found to have. Hypothyroidism during pregnancy may be a cause of developmental delays, reduced IQs, and autism.

Studies have documented that mercury causes hypothyroidism, damage of thyroid RNA, autoimmune thyroiditis, and impairment of conversion of thyroid T4 hormone to the active T3 form. These studies and clinical experience indicate that mercury and toxic metal exposures appear to be the most common cause of hypothyroidism, and the majority treated by metals detoxification recover or significantly improve.

The estimated prevalence of hypothyroidism from a large federal health survey, NHANES III, was 4.6%, but the incidence was twice as high for women as for men. Many with sub-clinical hypothyroidism are not aware of their condition. Another large study found that 11.7% tested had abnormal thyroid TSH levels with 9.5% being hypothyroid and 2.1% hyperthyroid. According to survey tests, 8 to 10% of untreated women were found to have thyroid imbalances so the actual level of hypothyroidism is higher than commonly recognized. Even larger percentages of women had elevated levels of antithyroglobulin (anti-TG) or antithyroid peroxidase antibody (anti-TP). Tests have found approximately 30% of pregnant women have low free T4 in the first trimester.

Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain. Hypothyroidism of the adults causes most frequently dementia and depression. Nearly all the hyperthyroid patients show minor psychiatric signs and sometimes psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur. These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission and play an important role in regulating central noradrenergic and GABA function.

Studies indicate that slight thyroid deficiency/imbalance (sub-clinical) during the perinatal period can result in delayed neuropsychological development in neonate and child or permanent neuropsychiatric damage in the developing fetus or autism or mental retardation. Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result in significantly reduced IQs and causes psychomotor deficits. Women with the highest levels of thyroid-stimulating-hormone (TSH) and lowest free levels of thyroxin 17 weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age eight. Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children.

Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. Without treatment, many of the women with thyroiditis go on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About 7.5% of pregnant women develop thyroiditis after birth. Studies have also established a connection between maternal thyroid disease and babies born with heart defects.

Infants of women with hypothyroxinemia at twelve weeks’ gestation had significantly lower scores on the Neonatal Behavioral Assessment Scale orientation index compared with subjects. Regression analysis showed that first-trimester maternal free thyroid hormone T4 was a significant predictor of orientation scores. This study confirmed that maternal hypothyroxinemia constitutes a serious risk factor for neurodevelopmental difficulties that can be identified in neonates as young as three weeks.

Mercury (especially mercury vapor from dental amalgam or organic mercury) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, thyroid gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces, and likewise rapidly crosses the placenta and accumulates in the fetus, including the fetal brain and hormone glands at levels commonly higher than the level in the mother. Milk from mothers with seven or more mercury amalgam dental fillings was found to have levels of mercury approximately ten times that of amalgam free mothers. The milk sampled ranged from 0.2 to 57 ug/L. In a population of German women, the concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L. A Japanese study found that the average mercury level in samples tested increased 60% between 1980 and 1990. The study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening but more so in the linguistic pathway. The level of mercury in umbilical cord blood, meconium, and placenta is usually higher than that in mothers’ blood.

Alterations of cortical neuronal migration and cerebellar Purkinje cells have been observed in autism. Neuronal migration, via reelin regulation, requires triiodothyronine (T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases. Experimental animal models have shown that transient intrauterine deficits of thyroid hormones (as brief as three days) result in permanent alterations of cerebral cortical architecture reminiscent of those observed in brains of patients with autism. Early maternal hypothyroxinemia resulting in low T3 in the fetal brain during the period of neuronal cell migration (weeks eight to twelve of pregnancy) may produce morphological brain changes leading to autism. Insufficient dietary iodine intake and a number of environmental antithyroid and goitrogenic agents can affect maternal thyroid function during pregnancy.

Mercury can have significant effects on thyroid function even though the main hormone levels remain in the normal range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely affects the activity of selenoenzymes, including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases (5-Di and 5′-DI) in the fetal brain, even though thyroxine (T4) levels are normal. Gpx activity is severely inhibited, while 5-DI levels are decreased and 5′-DI increased in the fetal brain, similar to hypothyroidism. Thus normal thyroid tests will not pick up this condition.

Mercury reduces the blood’s ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc and vitamin B12; depresses enzyme isocitric dehydrogenase (ICD) in fetus; and causes reduced iodine uptake, autoimmune thyroiditis, and hypothyroidism. Because of the evidence of widespread effects on infants, the American Association of Clinical Endocrinologists advises that all women considering becoming pregnant should get a serum thyrotropin test so that hypothyroidism can be diagnosed and treated early. Since mercury and toxic metals are common causes of hypothyroidism, another test that should be considered is a hair element test for mercury or toxic metal exposures and essential mineral imbalances. An ecological study in Texas has correlated higher rates of autism in school districts affected by large environmental releases of mercury from industrial sources.

In addition to large numbers of cases affecting infants, allergic contact eczema is the most frequent occupational disease; the most common cause of contact eczema is exposure to toxic metals. The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium. The highest level of sensitization is to infants, who are most reactive to thimerosal, a form of mercury that has been used as a preservative in vaccines and eye drops. Many with immune reactive conditions like eczema and psoriasis recover after tests and treatment for the cause of the immune reactivity

There has been strong suggestive and clinical evidence for a connection between toxic metals and autism spectrum conditions, and recent studies using government databases have confirmed the connection. There also appear to be subgroups of exposure and symptom patterns among the many different types of persuasive developmental disorders (PDD) including autism, Asperger’s syndrome, obsessive compulsive disorder (OCD), dyslexia, ADD/ADHD, learning disabilities, childhood depression, etc. Some of the apparent subgroups of autism include:

  • the group with blocked enzymatic processes needed to properly digest casein and gluten,
  • a group related to blockage by toxic metals of methionine synthase function,
  • a group related to mother’s hypothyroid condition during the first trimester of pregnancy(due to metals effects),
  • a group of general brain-related encephalies and/or immune effects of toxic exposures,
  • the Singh subgroup of autoimmune reactions to brain myelin sheath or other autoimmunity,
  • the reduced B lymphocyte/MMR subgroup with intestinal leaky gut and/or involvement of measles virus, and
  • the Megson/DPT visual abnormality related group.

Since most children have been found to have high levels of toxic exposure, most of those affected appear to have symptoms related to both the first subgroup plus often one or more of the other exposures/subgroups. The Megson group is often helped significantly by treatment with vitamin A from cod liver oil and urocholine. Thousands of autistic children are being treated for metals toxicity using chelation protocols after tests have documented high exposures to mercury and other toxic metals, and the majority has shown significant improvement. In a large survey of parents of autistic children by the Autism Research Institute, treating autism, chelation/detoxification with nutritional support was found to be by far the most effective and least harmful treatment of all treatments surveyed, with over 73% of those using chelation protocol improving significantly after treatment. Autism treatment clinics testing and treating autism usually find high toxic metal body burdens and successful cognitive and behavioral treatment results as toxic metal body burden declines and metabolic imbalances are improved. Most of those using the chelation/nutrition protocol recovered or significantly improved and are doing well in school.

Most children with autism have been found to have gastrointestinal damage and leaky gut, as well as damaged enzymatic process and damaged systems that control blood PH. This results in digestive dysfunction, inability to absorb minerals and nutrients, nutritional deficiencies, damage to autonomic nervous system, and neurological and behavioral problems. Supplements to deal with these nutritional deficiencies and imbalances are needed to alleviate these problems. These problems also cause proliferation of unfriendly bacteria, yeast, and parasites, for which supplementation with probiotics and Saccharomyces boulardii yeast is helpful. Treatment is complicated and individual, usually requiring detoxification as well as protocols to deal with the dysfunctional gastrointestinal, immune, and hormone systems.

Some deficiencies usually found include sulfates, magnesium, zinc, essential fatty acids, vitamins A and E, selenium, etc. Supplementation for these and other essential minerals and nutrients are needed due to the dysfunctional digestive systems. A large double blind study of autistic patients found a nutritional approach using 400 mg carnosine, 50 IU vit E, and 5 mg of zinc two times per day to be highly beneficial. Large numbers of autistic children have shown significant improvement after detoxification and biomedical nutritional treatment. A program found to significantly improve most children with autism spectrum conditions is Brain Balance. Properly formulated nutritional treatments have also been found to be effective in treating ADHD and depression.

Physical activity has been found to help kids who may be restless or hyperactive or who have been diagnosed with ADHD. Even emotional disturbances can be improved with exercise, as the activity provides an outlet for energy and reduces the natural inclination of children to act out. Use of exercise therapy, along with Emotional Freedom Technique (EFT), was found to have significant benefits. Exercise at school was also found to significantly increase reading and math ability of students, in addition to helping control obesity.


1. Weiss B, Landrigan PJ. The developing brain and the environment. Environ Health Perspect. 2000; 107(3).

2. Frith CD, et al. More dyslexia in English speaking countries. Science. 2001.

3. Stanley F. Before the bough breaks: 21st century kids in crisis. Zonta International Conference, Gothenburg Sweden. 2002.

4. Perrin J. The increase of childhood chronic conditions in the U.S. JAMA. 2007; 297(24): 2755-9.

5. Van Cleave J, et al. National longitudinal survey of youth-child (NLSY) cohort (1988 – 2006). JAMA. 2010; 303: 623-630, 665-666.

6. Silhan P, Arenberger P. Standard epicutaneous tests in ambulatory care of patients. Cas Lek Cesk. 1999;138(15): 469-73.

7. Rook GAW, Stanford JL. Give us this day our daily germs. Immunol Today. 1998; 19: 113-6.

8. Kemp T, Pearce N, Fitzharris P, et al. Is infant immunization a risk factor for childhood asthma or allergy? Epidemiology. 1997; 8: 678-80.

9. Odent MR, Culpin EE, Kimmel T. Pertussis vaccination and asthma: Is there a link? JAMA. 1994: 592-3.

10. Blomfield R. Childhood vaccination should have been included in asthma study. BMJ. 1998; 317: 205

11. Farooqi IS, Hopkin JM. Early childhood infection and atopic disorder. Thorax. 1998; 53: 927-32.

12. Hurwitz EL, Morgenstern H. Effects of diphtheria-tetanus-pertussis or tetanus vaccination on allergies and allergy-related respiratory symptoms among children and adolescents in the United States. J Manipulative Physiol Ther. 2000; 23: 81-90.

13. Hedenskog S, Bjorksten B, Biennow M, Granstrom G, Granstrom M. Immunoglobulin E response to pertussis toxin in whooping cough and after immunization with a whole cell and an acellular pertussis vaccine. Int Arch Allergy Appl Immunol. 1989; 89: 156-61.

14. Mark A, Bjorksten B, Granstrom M. Immunoglobulin E responses to diphtheria and tetanus toxoids after booster with aluminium-adsorbed and fluid DT vaccines. Vaccine. 1995; 13: 669-73

15. Mu HH, Sewell WA. Regulation of DTH and IgE responses by IL-4 and IFN-gamma in immunized mice given pertussis toxin. Immunology. 1994; 83: 639-45.

16. Pauwels R, Van Der Straeten M, Platteau B, Bazin B. In vivo effects of Bordetella pertussis vaccine on IgE synthesis. Allergy. 1983; 38: 239-46.

17. Ryan M, Murphy G, Ryan E, et al. Distinct T-cell subtypes induced with whole cell and acellular pertussis vaccines in children. Immunology. 1998; 93: 1-10.

18. Shaheen SO, Aaby P, Hall AJ, et al. Measles and atopy in Guinea-Bissau. Lancet. 1996; 347: 1792-6.

19. von Hertzen LC, Haahtela T. Could the risk of asthma and atopy be reduced by a vaccine that induces a strong T-helper type 1 response? Am J Respir Cell Mol Biol. 2000; 22: 139-42.

20. Nilsson L, Kjellman NIM, Bjorksten B. A randomized controlled trial of the effect of pertussis vaccines on atopic disease. Arch Pediatr Adolesc Med. 1998; 152: 734-8.

21. Johnston IDA, Bland JM, Ingram D, Anderson HR, Warner JO, Lambert HP. Effect of whooping cough in infancy on subsequent lung function and bronchial reactivity. Am Rev Respir Dis. 1986; 143: 270-5.

22. Wjst M, Dold S, Retmeir P, Fritzsch C, von Mutius E, Hiemann HH. Pertussis infection and allergic sensitization. Ann Allergy. 1994; 73: 450-4.

23. Brasch J, Geier J, Schnuch A. Differentiated contact allergy lists serve in quality improvement. Hautarzt. 1998; 49(3): 184-0.

24. Manzini BM, Ferdani G, Simonetti V, Donini M, Sedernari S. Contact sensitization in children. Pediatr Dermatol. 1998; 15(1): 12-1.

25. Romaguera C, Vilaplana J. Contact dermatitis in children: 6 years’ experience. Contact Dermatitis. 1998; 39(6): 277-80.

26. Sun CC. Allergic contact dermatitis of the face from contact with nickel and ammoniated mercury. Contact Dermatitis. 1987; 17(5): 306-9.

27. Xue C, He Z, Zhang H, Li S. Study on the contact allergen in patients with dermatitis and eczema. Wei Sheng, Yen Chiu. 1997; 26(5): 296-8.

28. Aberer W, Holub H, Strohal R, Slavicek R. Palladium in dental alloys- the dermatologists responsibility to warn? Contact Dermatitis. 1993; 28(3): 163-5.

29. Sterzl I, Prochazkova J, Stejaskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.

30. Stejskal V. MELISA: A new technology for diagnosing and monitoring of metal sensitivity. Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine. Baltimore, MY. 1998.

31. Redhe O, Pleva J. Recovery from asthma, allergies, ALS after removal of dental amalgam fillings. Int J of Risk & Safety in Medicine. 1994; 4: 229-236.

32. Kurek M, Przybilla B, Hermann K, Ring J. An opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy Immunol. 1992; 97(2): 115-20.

33. Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology. 1990; 29(5): 445-52.

34. Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J Inorg Biochem. 1996; 62(4): 271-9.

35. Ariza ME, Bijur GN, Williams MV. Lead and mercury mutagenesis: Role of H 2, superoxide dismutase, and xanthine oxidase. Environ. Mol. Mutagen. 1998; 31: 352-361.

36. Naidu BV, Fraga C, Salzman AL, Szabo C, Verrier ED, Mulligan MS. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant. 2003; 22: 784-93.

37. Liaudet L, Szabo G, Szabo C. Oxidative stress and regional ischemia-reperfusion injury: The peroxynitrite—PARP connection. Coronary Artery Dis. 2003; 14: 115-122.

38. Naidu BV, Fraga C, Salzman AL, Szabo C, Verrier ED, Mulligan MS. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant. 2003; 22: 784-93.

39. Virag L, Szabo E, Gergely P, Szao C. Peroxynitrite- induced cytotoxicity: Mechanisms and opportunities for intervention. Toxicology Letters. 2003; 140: 113-124.

40. Grisham MB, Hernandez LA, Granger DN. Xanthine oxidase and neutrophil infiltration in intestinal ischemia. Am J Physiol. 1986; 251(4.1): G567-74.

41. Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents: Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol. 1978; 20(6): 729-35.

42. Boadi WY, et al. In vitro effect of mercury on enzyme activities. Environ Res. 1992; 57(1): 96-106.

43. Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT. Gastrointestinal abnormalities in children with autistic disorder. J Pediatr. 1999; 135: 559-63.

44. McFadden SA. Phenotypic variation in xenobiotic metabolism and adverse environmental response: Focus on sulfur-dependent detoxification pathways. Toxicology. 1996; 111(1-3): 43-65.

45. Markovich, et al. Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol Appl Pharmacol. 1999; 154(2): 181-7.

46. Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem. 1991; 266(19): 12695-702.

47. Perry TL, et al. Hallevorden-Spatz disease: Cysteine accumulation and cysteine dioxygenase deficiency. Ann Neural. 1985; 18(4): 482-489.

48. Ceaurriz, et al. Role of gamma-glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.

49. Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996; 10(6): 435-40.

50. Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptidyl peptidase IV from human placenta. Eur J Biochem. 1982; 126(2): 359-65.

51. Kar NC, Pearson CM. Dipeptyl peptidases in human muscle disease. Clin Chim Acta. 1978; 82(1-2): 185-92.

52. Sastry KV, Gupta PK. Changes in the activities of some digestive enzymes, exposed chronically to mercuric chloride. J Environ Sci Health B. 1980; 15(1): 109-19.

53. Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993; 44(1): 13-8.

54. Stefanovic V, et al. Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem. 1998; 8(5): 278-84.

55. Crinnion WJ. Environmental toxins and their common health effects. Altern Med Rev. 2000; 5(1): 52-63.

56. Cohly HH, Panja A. Immunological findings in autism. Int Rev Neurobiol. 2005; 71: 317-41.

57. , Ilback NG, Wesslen L, Fohlman J, Friman G. Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis). Toxicol Lett. 1996; 89(1): 19-28.

58. Ilback NG, Lindh U, Wesslen L, Fohlman J, Friman G. Trace element distribution in heart tissue sections studied by nuclear microscopy is changed in Coxsackie virus B3 myocarditis in methyl mercury-exposed mice. Biol Trace Elem Res. 2000; 78(1-3): 131-47.

59. Crompton P, Ventura AM, de Souza JM, Santos E, Strickland GT, Silbergeld E. Assessment of mercury exposure and malaria in a Brazilian Amazon riverine community. Environ Res. 2002; 90(2): 69-75.

60. Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: A novel form of mercury poisoning. Med Hypotheses. 2001; 56(4): 462-71.

61. Holmes A. Autism: Treatments.

62. Redwood L. Mercury and autism. Vitamin Research News. 2001; 15(5): 1-12.

63. Cutler AH. Amalgam Illness: Diagnosis and Treatment.

64. IHMA.

65. Cade JR, et al. Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism. 1999.

66. University of Florida. UF researchers cite possible link between autism, schizophrenia, and diet. 1999.

67. Cade R, et al. Autism and schizophrenia: Intestinal disorders. Nutritional Neuroscience. 2000.

68. Autistic spectrum and dietary intervention: Links & books.

69. Sun ZJ, Cade JR, et al. Beta-casomorphin induces Fos-like immunoreactivity in discrete brain regions relevant to schizophrenia and autism. Autism. 1999; 3(1): 67-83.

70. Cade JR, Sun ZJ. Peptide found in schizophrenia and autism causes behavioral changes in rats. Autism. 1999; 3(1): 85-95.

71. Leboyer M, et al. Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone. Encephale. 1993;19(2): 95-102.

72. Lucarelli S, et al. Food allergy and infantile autism. Panminerva Med. 1995; 37(3): 137-41.

73. Hoggan R. Application of the exorphin hypothesis to attention deficit hyperactivity disorder: A theoretical framework. Thesis. University of Calgary.1998.

74. Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen. 1994; 114(12): 1432-4.

75. Reichelt KL, et al. Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychopharmocol. 1981; 28: 627-43.

76. Lucarelli S, Cardi E, et al. Food allergy and infantile autism. Panminerva Med. 1995; 37(3): 137-41.

77. Shel L. Autistic disorder and the endogenous opioid system. Med Hypotheses. 1997; 48(5): 413-4.

78. Kost NV, Sokolov CO, et al. Beta-Casomorphins-7 in infants on different type of feeding and different levels of psychomotor. Peptides. 2009.

79. Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides. 1984; 5(6): 1139-47.

80. Singh MM, Kay SR. Wheat gluten as a pathogenic factor in schizophrenia. Science. 1976; 191(4225): 401-2.

81. Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides. 1984; 5(6): 1139-47.

82. Horvath K, Graaf L, Walcz E, Bodanszky H, Schuler D. Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Lancet. 1985; 2(8448): 184-5.

83. Willemsen-Swinkels SH, Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H. Plasma beta-endorphin concentrations in people with learning disability and self-injurious and/or autistic behavior. Br J Psychiary. 1996; 168(1): 105-9.

84. Leboyer M, Launay JM, et al. Difference between plasma N- and C-terminally directed beta-endorphin immunoreactivity in infantile autism. Am J Psychiatry. 1994; 151(12): 1797-1801.

85. Scifo R, Marchetti B, et al. Opioid-immune interactions in autism: Behavioral and immunological assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita. 1996; 32(3): 351-9.

86. Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J Prosthet Dent. 1990; 63(5): 593-6.

87. Yonk LJ, et al. CD+4 helper T-cell depression in autism. Immunol Lett. 1990; 25(4): 341-5.

88. Edelson SB, Cantor DS. Autism: Xenobiotic influences. Toxicol Ind Health. 1998; 14(4): 553-63.

89. Liska DJ. The detoxification enzyme systems. Altern Med Rev. 1998; 3(3):187-98.

90. Sayers LG, Brown GR, Michell RH, Michelangeli F. The effects of thimerosal on calcium uptake and inositol1,4,5-trisphosphate-induced calcium release in cerebellar microsomes. Biochem J. 1993; 289(3): 883-7.

91. Ueha-Ishibashi T, et al. Effect of thimerosal on intracellular Ca+ concentration of rat cerebellar neurons. Toxicology. 2004; 195: 77-84

92. Elferink JG. Thimerosal: A versatile sulfhydryl reagent, calcium mobilizer, and cell function-modulating agent. Gen Pharmacol. 1999; 33(1): 1-6.

93. Lewis RN, Bowler K. Rat brain (Na-K+) ATPase: Modulation of its ouabain-sensitive K+-PNPPase activity by thimerosal. Int J Biochem. 1983; 15(1): 5-7.

94. Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.

95. Silva VS, Duarte AI, Rego AC, Oliveira CR, Gonalves PP. Effect of chronic exposure to aluminum on isoform expression and activity of rat (Na+/K+)ATPase. Toxicological Sciences. 2005; 88(2): 485-494.

96. Yokel RA. Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. J Alzheimer’s Dis. 2006; 10(2-3): 223.

97. Halsey NA. Limiting infant exposure to thimerosal in vaccines. JAMA. 1999; 282: 1763-66.

98. Wecker L, Miller SB, Cochran SR, Dugger DL, Johnson WD. Trace element concentrations in hair from autistic children. Defic Res. 1985; 29(1): 15-22.

99. Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A, et al. Metal-specific memory lymphocytes: Biomarkers of sensitivity in man. Neuroendocrinology Letters. 1999.

100. Stejskal VDM, et al. Mercury-specific Lymphocytes: An indication of mercury allergy in man. J. of Clinical Immunology. 1996; 16(1): 31-40.

101. Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry. 1999; 46(3): 420-4.

102. Wakefield A, et al. Ileal-lymphoid-nodular hyperplasia and pervasive developmental disorder in children. Lancet. 1998; 351(9103): 637-41.

103. Kawashima H, Mori T, Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A. Detection and sequencing of measles virus from peripheral mononuclear cells from patients with inflammatory bowel and autism. Dig Dis Sci. 2000; 45(4):723-9.

104. Wakefield A, et al. Inflammatory bowel disease syndrome and autism. Lancet. 2000.

105. Jyonouchi H, Agnes LG, Zimmerman-Bier RB. Dysregulated innate immune responses in young children with autism spectrum disorders: Their relationship to gastrointestinal symptoms and dietary intervention. Neuropsychobiology. 2005; 51: 77-85.

106. McGinnis WR. Mercury and autistic gut disease. Environ Health Perspect. 2001; 109(7): A303-4.

107. Furlano RI, Anthony A, Day R, et al. Colonic CD8 and gamma delta T-cell infiltration with epithelial damage in children with autism. J Pediatr. 2001; 138: 366-372.

108. Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT. Gastrointestinal abnormalities in children with autistic disorder. J Pediatr. 1999;135: 559-563.

109. D’Eufemia P, Celli M, Finocchiaro R, et al. Abnormal intestinal permeability in children with autism. Acta Paediatr. 1996; 85:1076-1079.

110. Goodwin MS, Cowen MA, Goodwin TC. Malabsorption and cerebral dysfunction: a multivariate and comparative study of autistic children. J Autism Child Schizophr. 1971; 1: 48-62.

111. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability. Immunopharmacol Immunotoxicol. 1993; 15(1): 87-112.

112. Daum JR. Immunotoxicology of mercury and cadmium on B-lymphocytes. Int J Immunopharmacol. 1993; 15(3): 383-94.

113. Pfieffer SI, Norton J, Nelson L, Shott S. Efficacy of vitamin B6 and magnesium in the treatment of autism. J Autism Dev Disord. 1995; 25(5): 481-93.

114. Eppright TD, Sanfacon JA, Horwitz EA. ADHD, infantile autism, and elevated blood-lead: a possible relationship. Mod Med. 1996; 93(3):136-8.

115. Stajich GV, Lopez GP, Harry SW, Sexson WR. Iatrogenic exposure to mercury after hepatitis B vaccination in preterm infants. Journal of Pediatrics. 2000; 136(5): 679-81.

116. Hewitson L, et al. Delayed acquisition of neonatal reflexes in newborn primates receiving a thimerosal-containing Hepatitis B vaccine: Influence of gestational age and birth weight. Neurotoxicology. 2009.

117. Rodier PM. Developing brain as a target of toxicity. Environ Health Perspect. 1995; 103(6): 73-76.

118. Rice DC, Barone S. Critical periods of vulnerability for the developing nervous system: Evidence from human and animal models. Environ Health Perspect. 2000; 108(3): 511-533.

119. Grandjean P, Jurgensen PJ, Weihe P. Milk as a source of methylmercury exposure in infants. Environ Health Perspect. 1994; 102(1): 74-7.

120. Methylmercury’s toxic toll. Science News. 2000; 158(5): 77.

121. CDC. Blood and hair mercury levels in young children and women of childbearing age—United States, 1999. MMWR. 2001; 50(8): 140-3.

122. Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V. Plasma excitatory amino acids in autism. Invest Clin. 1996; 37(2): 113-28.

123. Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of autistic children. Acta Psychiatr Scand. 1993; 87(5): 312-6.

124. Naruse H, Hayashi T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment. No To Hattatsu. 1989; 21(2): 181-9.

125. Carlsson ML. Is infantile autism a hypoglutamatergic disorder? J Neural Transm. 1998; 105(4-5): 525-35.

126. Reichrtova E, et al. Cord serum immunoglobulin E related to environmental contamination of human placentas with oganochlorine compounds. Environ Health Perspect. 1999; 107(11): 895-99.

127. Gavett SH, et al. Residual oil fly ash amplifies allergic cytokines, airway responsiveness, and inflammation in mice. Am J Respir Crit Care Med. 1999; 160(6):1897-1904.

128. Kramer U, et al. Traffic-related air pollution is associated with atopy in children living in urban areas. Epidemiology. 2000; 11(1): 64-70.

129. Megson’s Pediatric and Adolescent Ability Center.

130. Holmes A. Autism: Treatments.

131. Mercola J. The deliberate lies they tell about diabetes.

132. Coulter H. Vaccination debate: Do vaccines cause cot deaths? 1996.

133. Furlano RI, Anthony A, Day R, Murch SH, et al. Colonic CD8 and gamma delta T-cell infiltration with epithelial damage in children with autism. J Pediatr. 2011; 138: 366-72.

134. Eufemia P, Celli M, Giardini O, et al. Abnormal intestinal permeability in children with autism. Acta Paediatr. 1996; 85:1076-9.

135. Goodwin MS, Cowen MA, Goodwin TC. Malabsorption and cerebral dysfunction: a multivariate and comparative sutudy of autistic children. J Austism Child Schizophr. 1971; 1: 48-52.

136. Bamerjee S, Bhattacharya S. Histopathological changes induced by chronic nonlethal levels of mercury and ammonia in the small intestine of channa puntatus. Ecol Environ Safety. 1995; 31: 62-8.

137. Bohme M, Diener M, Mestres P, Rummel W. Direct and indirect actions of HgCl2 and methyl mercury chloride on permeability and chloride secretion across the rat colonic mucosa. Toxicol App Pharmacol. 1992; 114: 285-94.

138. Andres P. IgA-IgG disease in the intestine of Brown-Norway rats ingesting mercuric chloride. Clin Immunol and Immunopath. 1984; 30: 488-494.

139. Sasser LB, Jarboe GE, Walter BK, Kelman BJ. Absorption of mercury from ligated segments of the rat gastrointestinal tract. Proc Soc Exp Biol Med. 1978; 157: 57-60.

140. Kostial K, Kargacin B, Landeka M. Gut retention of metals in rats. Biol Trace Elem 1989; 21: 213-218.

141. Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine: Part III-purification and properties of monkey intestinal pyridoxal kinase. Indian J of Biochem. 1970; 7:151-156.

142. Chen W, Body RL, Mottet NK. Biochemical and morphological studies of monkeys chronically exposed to methylmercury. J Toxicol Environ Hlth. 1983; 12: 407-416.

143. Mathieson PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995.

144. Odent MR, Culpin EE, Kimmel T. Pertussis vaccination and asthma: Is there a link? JAMA. 1994; 272: 592-30.

146. Odent MR. Pertusiss vaccine associated with increased asthma and allergies. Archives of Pediatrics and Adolescent Medicine. 1998; 152: 734-738.

147. Fine JM, Chen LC. Confounding in studies of adverse reactions to vaccines. Amer J Epidemiology. 1992; 136: 121-35.

148. Scheibner V, Karlsson L. Association between DPT injections and Cot Deat. 2nd Immuniztion Conference. Canberra, Australia. 1991.

149. Phillips A. Dispelling vaccination myths. 2001.

150. Blaylock R. The truth behind the vaccine cover-up. Vaccine Choice Canada. 2008.

151. Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998; 71: S37-9.

152. Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.

153. Spivey-Fox MR. Nutritional influences on metal toxicity. Environ Health Perspect. 1979; 29: 95-104.

154. Pfeiffer SI, et al. Efficacy of vitamin B6 and magnesium in the treatment of autism. J Autism Dev Disord. 1995; 25(5): 481-93.

155. Singhal R, Thomas J, eds. Lead Toxicity. Baltimore: Urban & Schwarzenberg, Inc; 1980.

156. Govani S, Memo M. Chronic lead treatment differentially affects dopamine synthesis. Toxicology. 1979; 12: 343-49.

157. Scheuhammer AM, Cherian MG. Effects of heavy metal cations and sulfhydyl reagents on striatal D2 dopamine receptors. Biochem Pharmacol. 1985; 34(19): 3405-13.

158. Landner L, Lindestrom L. Copper in Society and the Environment. 2nd ed. Swedish Environmental Research Group; 1999.

159. Veltman JC, et al. Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland. Arch Biochem Biophys. 1986; 248(2): 467-78.

160. Riedl AG, et al. P-450 and hemeoxygenase enzymes in the basal ganglia and their roles in Parkinson’s disease. Adv Neurol. 1999; 80: 271-86.

161. Mata L, Sanchez L, Calvo M. Interaction of mercury with human and bovine milk proteins. Biosci Biotechnol Biochem. 1997; 61(10): 1641-5.

162. Kostial K, Rabar I, Ciganovic M, Simonovic I. Effect of milk on mercury absorption and gut retention in rats. Bull Environ Contam Toxicol. 1979; 23(4-5): 566-7.

163. Rowland IR, Robinson RD, Doherty RA. Effects of diet on mercury metabolism and excretion in mice given methylmercury: Role of gut flora. Arch Environ Health. 1984; 39(6): 401-8.

164. Lutz E, et al. Concentrations of mercury in brain and kidney of fetuses and infants. Journal of Trace Elements in Medicine and Biology. 1996; 10: 61-67.

165. Drasch G, et al. Mercury burden of human fetal and infant tissues. Eur J Pediatr. 1994; 153: 607-610.

166. Oskarsson A, et al. Mercury in breast milk in relation to fish consumption and amalgam. Arch Environ Health. 1996; 51(3): 234-41.

167. Drasch, et al. Mercury in human colostrum and early breast milk. Journal of Trace Elements in Medicine and Biology. 1998; 12: 23-27.

168. Kravchenko AT, Dzagurov SG, Chervonskaia GP III. The detection of toxic properties in medical biological preparations by the degree of cell damage in the L132 continuous cell line. Zh Mikrobiol Epidemiol Immunobiol. 1983; (3): 87-92.

169. HultmanP, Johansson U, Turley SJ. Adverse immunological effects and autoimmunity induced by dental amalgam in mice. FASEB J. 1994; 8: 1183-90.

170. Pollard KM, Lee DK, Casiano CA. The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure ad antigenic properties. J Immunol. 1997; 158: 3421-8.

171. Bigazzi PL. Autoimmunity induced by metals. In: Chang L, ed. Toxicology of Metals. Lewis Publishers, CRC Press Inc.; 1996: 835-52.

172. Hu H, Moller G, Abedi-Valugerdi M. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J Autoimmun. 1997; 10(5): 441-6.

173. Robinson CJG, et al. Mercuric chloride induced anti-nuclear antibodies in mice. Toxicol App Pharmacol. 1986; 86: 159-169.

174. El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral assessment of neurotoxicity and autoimmune mechanisms. Contact Dermatitis. 1999; 41(1): 60-1.

175. Hu H, Moller G, Abedi-Valugerdi M. Mechanism of mercury-induced autoimmunity: Both T helper 1- and T helper 2-type responses are involved. Immunology. 1999; 96(3): 348-57.

176. Earl C, Chantry A, Mohammad N. Zinc ions stabilize the association of basic protein with brain myelin membranes. J Neurochem. 1988; 51: 718-24.

177. Ricco P, Giovanneli S, Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res. 1995; 20: 1107-13.

178. LeFever GB, et al. The extent of drug therapy for attention deficit-hyperactivity disorder among children in public schools. American Journal of Public Health. 1999; 89(9): 1359-64.

179. Omura, Yoshiaki. Abnormal deposits of Al, Pb, and Hg in the brain, particularly in the hippocampus, as one of the main causes of decreased cerebral acetylcholine, electromagnetic field hypersensitivity, pre-Alzheimer’s disease, and autism in children. Acupuncture & Electro-Therapeutics Research. 2000; 25(3/4): 230-3.

180. Razagui IB, Haswell SJ. Mercury and selenium concentrations in maternal and neonatal scalp hair: Relationship to amalgam-based dental treatment received during pregnancy. Biol Trace Elem Res. 2001; 81(1): 1-19.

181. Cernichiari E, Brewer R, Myers GJ, Marsh DO, Berlin M, Clarkson TW. Monitoring methyl mercury during pregnancy: maternal hair predicts fetal brain exposure. Neurotoxicology. 1995; 16(4):729005-10.

182. Magos L, Brown AW, Sparrow S, Bailey E, Snowden RT, Skipp WR. The comparative toxicology of ethyl- and methylmercury. Arch Toxicol. 1985; 57(4): 260-7.

183. Suda I, Totoki S, Uchida T, Takahashi H. Degradation of methyl and ethyl mercury into inorganic mercury by various phagocytic cells. Arch Toxicol. 1992; 66(1): 40-4.

184. Geier MR, Geier DA. Neurodevelopmental disorders following thimerosal-containing vaccines. Ex Biol Med. 2003.

185. Geier MR, Geier DA. A comparative evaluation of the effects of MMR immunization and mercury doses from thimerosal-containing childhood vaccines on the population prevalence of autism. Med Sci Monit. 2004; 10(3): PI33-9.

186. Geier MR, Geier DA. Thimerosal in childhood vaccines, neurodevelopmental disorders, and heart disease in the U.S. J of Amer Physicians and Surgeons. 2003; 8(1).

187. Bradstreet J, Geier DA, et al, A case control study of mercury burden in children with autistic spectrum disorders. J of Amer Physicians and Surgeons. 2003; 8(3).

188. Bradstreet J, Geier DA. A case series of children with apparent mercury toxic encephalopathies manifesting with clinical symptoms of regressive autistic disorders. J Toxicol Environ Health A. 2007; 70(10): 837-51.

189. Geier DA, Geier MR, et al. Neurodevelopmental disorders, maternal Rh-negativity, and Rho(D) immune globulins: A multi-center assessment. Neuroendocrinology Letters. 2008; 29(2).

190. Stratton KR, et al. Adverse Events Associated with Childhood Vaccines. Evidence Bearing on Causality. IOM. Washington, DC: National Academy Press; 1994.

191. Szucs, et al. Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol. Neruobiol. 1997; 17(3): 273-282.

A. Badou, et al. HgCl2-induced interleukin-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels. J. Biol Chem. 1997; 272(51): 32411-8.

192. Klinghardt D. Migraines, Seizures, and Mercury Toxicity. Future Medicine Publishing; 1997.

193. Szasz A, Barna B, Gajda Z, Galbacs G, Kirsch-Volders M, Szente M. Effects of continuous low-dose exposure to organic and inorganic mercury during development on epileptogenicity in rats. Neurotoxicology. 2002; 23(2):197-206.

194. Holmes AS, Blaxill MF, Haley BE. Reduced levels of mercury in first baby haircuts of autistic children. International Journal of Toxicology. 2003.

195. Grether J, Croen L, Theis C, Blaxill M, Haley B, Holmes A. Baby hair, mercury toxicity and autism. International Journal of Toxicology. 2004; 23(4): 275-6.

196. Godfrey ME, Wojcik DP, Krone CA. Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003; 5(3):189-95.

197. Waly M, Olteanu H, Banerjee R, et al. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: A target for neurodevelopmental toxins and thimerosal. Mol Psychiatry. 2004; 9(4): 358-70.

198. Mutter J, Naumann J, Schneider R, Walach H, Haley B. Mercury and autism: Accelerating evidence? Neuroendocrinology Letters. 2005; 26(5): 439-46.

199. Hornig M, Chian D, Lipkin WI., Neurotoxic effects of postnatal thimerosal are mouse strain dependent. Mol Psychiatry. 2004.

200. Makani A, Gollapudi S, Yel L, Chiplunkar S, Gupta S. Biochemical and molecular basis for thimerosal-induced apoptosi in T-cells; a major role of mitochondrial pathway. Genes and Immunity. 2002, 3: 270-278.

201. James SJ, Slikker W, Melnyk S, New E, Pogribna M, Jernigan S. Thimerosal neurotoxicity is associated with glutathione depletion: Protection with nutritional supplementation. Neurotoxicology Conference. Hawaii. 2004.

202. Adams JB, Romdalvik J, Ramanujam VM, Legator MS. Mercury, lead, and zinc in baby teeth of children with autism versus controls. J Toxicol Environ Health A. 2007; 70(12):1046-51.
203. Geier DA, Geier MR. A prospective study of mercury toxicity biomarkers in autistic spectrum disorders. J Toxicol Environ Health A. 2007; 70(20): 1723-30.

204. Geier DA, Geier MR. A prospective assessment of porphyrins in autistic disorders: a potential marker for heavy metal exposure. Neurotox Res. 2006; 10(1): 57-64.

205. Sun Z, Zhang Z, et al. Relation of beta-casomorphin to apnea in sudden infant death syndrome. Peptides. 2003; 24(6): 937-43.

206. Palmer RF, et al. Environmental mercury release, special education rates, and autism disorder: An ecological study of Texas. Health and Place. 2005.

207. Trasande L, Schechter CB, Haynes KA, Landrigan PJ. Mental retardation and prenatal methylmercury toxicity. Am J Ind Med. 2006; 49(3):153-8,

208. Geier DA, Geier MR. A clinical trial of combined anti-androgen and anti-heavy metal therapy in autistic disorders. Neuroendocrinology Letters. 2006; 27(6): 833-8.

209. Geier DA, Geier MR. A prospective assessment of androgen levels in patients with autistic spectrum disorders: Biochemical underpinnings and suggested therapies. Neuroendocrinology Letters. 2007; 28(5): 565-73.

210. Yao Y, Walsh WJ, McGinnis WR, Praticograve D. Altered vascular phenotype in autism: correlation with oxidative stress. Arch Neurol. 2006; 63(8): 1161-4.

211. McGinnis WR. Oxidative stress in autism. Altern Ther Health Med. 2004;10(6): 22-36.

212. James SJ, Cutler P, Melnyk S, et al. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr. 2004; 80: 1611-7.

213. Chauhan A, Chauhan V. Oxidative stress in autism. Pathophysiology. 2006; 13(3): 171-181.

214. Vojdani A, Pangborn JB, et al. Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism. Int J Immunopathol Pharmacol. 2003; 16(3): 189-99.

215. Bransfield R, et al. Autism and Lyme disease connection. Med Hypoth. 2008.

216. Kidd PM. Autism, an extreme challenge to integrative medicine. Part 2: medical management. Altern Med Rev. 2002; 7(6): 472-99.

217. Conner D. Autism treatment gaining acceptance. Jacksonville. 2007.” target=”_blank”>

218. Olmsted D, ed. Age of Autism website.

219. Desoto MC, Hitlan RT. Blood levels of mercury are related to diagnosis of autism. Journal of Child Neurology. 2007; 22(11): 1308-1311.

220. Kamintildeski1 S, Cieoeliska1 A, Kostyra E. Polymorphism of bovine beta-casein and its potential effect on human health. J Appl Genet. 2007; 48(3): 189-198.

221. Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE, Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999; 42(8): 1032.

222. Kost NV, et al. Regulatory peptides and psychomotor development in infants. Vestn Ross Akad Med Nauk. 2007; 3: 33-9.

223. Oleg YS, et al. Influence of human B-casomorphin-7 on specific binding of 3H-spiperone to the 5-HT2-receptors of rat brain frontal cortex. Protein Pept Lett. 2006; 13(2):169-70.

224. Dubynin VA, Malinovskaia IV, et al. Delayed effect of exorphins on learning of albino rat pups. Izv Akad Nauk Ser Biol. 2008; 1: 53-60.

225. Sun Z, Cade R. Findings in normal rats following administration of gliadorphin-7 (GD-7). Peptides. 2003; 24(2): 321-3.

226. Roman GC. Autism: Transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007; 262(1-2): 15-26.

227. Carvalho MC, Franco JL, Ghizoni H, et al. Effects of 2,3-dimercapto-1-propanesulfonic acid (DMPS) on methylmercury-induced locomotor deficits and cerebellar toxicity in mice. Toxicology. 2007; 239(3): 195-203.

228. Hua J, Brun A, Berlin M. Pathological changes in the Brown Norway rat cerebellum after mercury vapour exposure. Toxicology. 1995; 104(1-3): 83-90.

229. Zarate A, Basurto L, Hernandez M. Thyroid malfunction in women. Ginecol Obstet Mex. 2001; 69: 200-5.

230. Wier FA, Farley CL. Clinical controversies in screening women for thyroid disorders during pregnancy. J Midwifery Women’s Health. 2006; 51(3): 152-8.

231. Stagnaro-Green A. Postpartum thyroiditis. Best Pract Res Clin Endocrinol Metab. 2004; 18(2): 303-16.

232. Stagnaro-Green A. Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab Clin North Am. 2000; 29(2): 417-30.

233. Harris B. Postpartum depression and thyroid antibody status. Thyroid. 1999; 9(7): 699-703.

234. Aszaols Z. Some neurologic and psychiatric complications in endocrine disorders: the thyroid gland. Orv Hetil. 2007; 148(7): 303-10.

235. Kooistra L, Crawford S, van Baar AL, Brouwers EP, Pop VJ. Neonatal effects of maternal hypothyroxinemia during early pregnancy. Pediatrics. 2006; 117(1): 161-7.

236. Menif O, Omar S, Feki M, Kaabachi N. Hypothyroidism and pregnancy: Impact on mother and child health. Ann Biol Clin (Paris). 2008; 66(1): 43-51.

237. Culter. Chelation: The real story behind the misleading headlines. Autism Research Review International. 2005; 19(3): 3.

238. Davis JD, Tremont G. Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrine. 2007; 32(1): 49-65.

239. Almeida C, Brasil MA, Costa AJ, et al. Subclinical hypothyroidism: Psychiatric disorders and symptoms. Rev Bras Psiquiatr. 2007; 29(2):157-9.

240. Singh VK, Lin SX, Yang VC. Serological association of measles virus and human herpesvirus-6 with brain autoantibodies in autism. Clin Immunol Immunopathol. 1998; 89(1): 105-8.

241. Mercola J. Hepatitis B vaccine triples the risk of autism in infant boys. 2009.

242. Drasch G, Schupp I, Houfl H, Reinke R, Roider G. Mercury burden of human fetal and infant tissues. Eur J Pediatr. 1994; 153(8): 607-10.

243. Guzzi G, Grandi M, Severi G, et al. Dental amalgam and mercury levels in autopsy tissues: Food for thought. Am J Forensic Med Pathol. 2006; 27(1): 42-5.

244. Bjourkman L, Lundekvam BF, Vahter M. Mercury in human brain, blood, muscle and toenails in relation to exposure: An autopsy study. Environ Health. 2007: 6:30.

245. Vimy MJ, Takahashi,Y, Lorscheider FL. Maternal-fetal distribution of mercury released from dental amalgam fillings. Amer. J. Physiol. 1990; 258: R939-945.

246. Hahn LJ, Kloiber R, Leininger RW, Vimy MJ, Lorscheider FL. Distribution of mercury released from amalgam fillings into monkey tissues. FASEB J. 1990; 4: 5536.

247. Vimy MJ, Hooper DE, King WW, Lorscheider FL. Mercury from maternal “silver” tooth fillings in sheep and human breast milk: A source of neonatal exposure. Biol Trace Elem Res. 1997; 56(2): 143-52.

248. Oskarsson A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Mercury in breast milk in relation to fish consumption and amalgam. Arch Environ Health. 1996; 51(3): 234-41.

249. Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G. Mercury in human colostrum and early breast milk. J Trace Elem Med Biol. 1998; 12: 23-27.

250. Paccagnella B, Riolfatti M. Total mercury levels in human milk from Italian mothers. Ann Ig. 1989: 1(3-4): 661-71.

251. Yang J, Jiang Z, Wang Y, Qureshi IA, Wu XD. Maternal-fetal transfer of metallic mercury via placenta and milk. Ann Clin Lab Sci. 1997; 27(2): 135-141.

252. Sundberg J, Ersson B, Lonnerdal B, Oskarsson A. Protein binding of mercury in milk and plasma from mice and man—a comparison between methylmercury and inorganic mercury. Toxicology. 1999; 137(3): 169-84.

253. Kuhnert PM, Kuhnert BR, Erhard P. Comparison of mercury levels in maternal blood, fetal blood, fetal cord blood, and placental tissues. Am J Obstet Gynecol. 1981; 139(2): 209-13.

254. Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M. Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood. Environ Res. 2000; 84(2): 186-94.

255. Kuntz WD, Pitkin RM, Bostrom AW, Hughes MS. Maternal and cord blood mercury background levels: A longitudinal surveillance. Am J Obstet and Gynecol. 1982; 143(4): 440-443.

256. Ramirez GB, Cruz MC, Pagulayan O, Ostrea E, Dalisay C. The Tagum study I: Analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants’ hair. Pediatrics. 2000; 106(4): 774-81.

257. Ramirez GB, Pagulayan O, Akagi H, et al. Tagum study II: Follow-up study at two years of age after prenatal exposure to mercury. Pediatrics. 2003; 111(3): 289-95.

258. Warfvinge K, Berlin M, Logdberg B. The effect on pregnancy outcome and fetal brain development of prenatal exposure to mercury vapour. Neurotoxicology. 1994; 15(4).

259. Drexler H, Schaller KH. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Environ Res. 1998; 77(2): 124-9.

260. Mottet NK, Shaw CM, Burbacher TM. Health risks from increases in methylmercury exposure. Health Perspect. 1985; 63: 133-140.

261. Grandjean P, et al. MeHg and neurotoxicity in children. Am J Epidemiol. 1999.

262. Sorensen N, et al. Prenatal mercury exposure raises blood pressure. Am J Epidemiol. 1999; 10: 370-375.

263. Ronnback L, et al. Chronic encephalopaties induced by low doses of mercury or lead. Br J Ind Med. 1992; 49: 233-240.

264. Langauer-Lewowicka H. Chronic toxic encephalopathies. Med Pr. 1982; 33(1-3): 113-7.

265. Adventures in Autism.

266. Huggins HA, Levy TE. Uniformed Consent: The Hidden Dangers in Dental Care. Bio-Probe; 1999.

267. Knapp LT, Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem. 2000.

268. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

269. Sin YM, The WF, Wong MK, Reddy PK. Effect of mercury on glutathione and thyroid hormones. Bulletin of Environmental Contamination and Toxicology. 1990; 44(4): 616-622.

270. Kawada J, et al. Effects of inorganic and methyl mercury on thyroidal function. J Pharmacobiodyn. 1980; 3(3): 149-59.

271. Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci. 1992; 5(3): 236-40.

272. Kabuto M. Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress. Arch Toxicol. 1991; 65(2): 164-7.

273. Lee YW, Ha MS, Kim YK. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001; 26(11): 1187-93.

274. Sin YM, Teh WF, Wong MK, Reddy PK. Effect of mercury on glutathione and thyroid hormones. Bulletin of Environmental Contamination and Toxicology. 1990; 44(4): 616-622.

275. Hussain S, et al. Mercuric chloride-induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain. J Environ Sci Health B. 1997; 32(3): 395-409.

276. Nicole A, et al. Direct evidence for glutathione as mediator of apoptosis in neuronal cells. Biomed Pharmacother. 1998; 52(9): 349-55.

277. Bains JS, et al. Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death. Brain Res Rev. 1997; 25(3): 335-58.

278. Gawryluk JW, Wang J, Andreazza AC, Shao L, Young LT. Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders. Int J Neuropsychopharm. 2010.

279. Lutz E, et al. Concentrations of mercury in brain and kidney of fetuses and infants, J Trace Elem Med Biol. 1996; 10: 61-67.

280. Drasch G, et al. Mercury burden of human fetal and infant tissues. Eur J Pediatr. 1994; 153: 607-610.

281. Geier DA, Geier M. Toxic levels of mercury in Chinese infants eating fish congee. Medical Journal of Australia. 2008.

282. Melillo R. Disconnected Kids: The Groundbreaking Brain Balance Program for Children with Autism, ADHD, Dyslexia, and Other Neurological Disorders. Perigree Trade; 2009.

283. Veltman JC, et al. Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland. Arch Biochem Biophys. 1986; 248(2): 467-78.

284. Zamm AV. Dental mercury: A factor that aggravates and induces xenobiotic intolerance. J. Orthmol. Med. 1991; 6(2): 67-77.

285. Nishida M, Muraoka K, et al. Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells. J Histochem Cytochem. 1989; 37(5): 723-7.

286. Weiner JA, Nylander M. The relationship between mercury concentration in human organs and different predictor variables. Sci Total Environ. 1993; 138(1-3): 101-15.

287. Goldberg AF, et al. Effect of amalgam restorations on whole body potassium and bone mineral content in older men. Gen Dent. 1996; 44(3): 246-8.

288. Schirrmacher K. Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells. Calcif Tissue Int. 1998; 63(2): 134-9.

289. Danielsson BRG, et al. Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus. Biol Res Preg Perinatal. 1984; 5(3): 102-109.

290. Nylander M, et al. Mercury accumulation in tissues from dental staff and controls. Swedish Dental Journal. 1989; 13: 235-243.

291. Nylander M. Mercury in pituitary glands of dentists. Lancet. 1986: 442.

292. Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders. J Assoc Physicians India. 2002; 50: 400-6

293. Danielsson BR, et al. Behavioral effects of prenatal metallic mercury inhalation exposure in rats. Neurotoxicol Teratol. 1993; 15(6): 391-6.

294. Fredriksson, et al. Prenatal exposure to metallic mercury vapor and methyl mercury produce interactive behavioral changes in adult rats. Neurotoxicol Teratol. 1996; 18(2): 129-34.

295. Aposhian HV. Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). Environ Health Perspect. 1998; 4: 1017-1025.

296. Friberg L, et al. Mercury in the brain and CNS in relation to amalgam fillings. Lakartidningen. 1986; 83(7): 519-521.

297. Freitas, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Res. 1996; 738(2): 257-64.

298. Yallapragoda PR, et al. Inhibition of calcium transport by Hg salts in rat cerebellum and cerebral cortex. J Appl Toxicol. 1996; 164(4): 325-30.

299. Chavez B, et al. Mitochondrial calcium release by Hg+2. J Biol Chem. 1988; 263(8): 3582.

300. Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.

301. Rossi AD, et al. Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J. 1993; 7: 1507-14.

302. Boadi WY, et al. In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res. 1992; 57(1): 96-106.

303. Boadi WY. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity. Pharmacol. 1992; 116(1): 17-23.

304. Urbach J, et al. Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Reprod Toxicol. 1992; 6(1): 69-75.

305. Karp W, Gale TF, et al. Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters. Environ Res. 1985; 36: 351-358.

306. Karp WB, et al. Correlation of human placental enzymatic activity with trace metal concentration in placenta. Environ Res. 1977; 13: 470-477.

307. Boot JH. Effects of SH-blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct. 1995; 20(3): 233-8.

308. Semczuk M, Semczuk-Sikora A. New data on toxic metal intoxication (Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit. 2001; 7(2): 332-340.

309. Sterzl I, Prochazkova J, Stejskal VDM, et al. Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters.1999; 20: 221-228.

310. Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.

311. Sterzl I, Hrda P, Prochazkova J, Bartova J. Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitrni Lekarstvi. 1999; 45(9): 527-31.

312. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuroendocrinology Letters. 2004; 25(3): 211-8.

313. Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI. Effects of low mercury vapour exposure on the thyroid function in chloralkali workers. J Appl Toxicol. 2000; 20(6): 483-9.

314. Barregard L, Lindstedt G, Schutz A, Sallsten G. Endocrine function in mercury exposed chloralkali workers. Occup Environ Med. 1994; 51(8): 536-40.

315. Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H. In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain. Environ Res. 1999; 80(3): 208-14.

316. Roman GC. Autism: Transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007; 262(1-2): 15-26.

317. Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes. Yonsei Med J. 1995; 36(3): 299-305.

318. Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology. 1992; 76(3): 245-56.

319. Albrecht J, Matyja E. Glutamate: A potential mediator of inorganic mercury toxicity. Metab Brain Dis. 1996; 11: 175-84.

320. Tirosh O, Sen CK, Roy S, Packer L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death. Neuroscience. 2000; 97(3): 531-41.

321. Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Biochem. 1990; 98(5): 261-7.

322. Bara M, Guiet-Bara A, Durlach J. Comparison of the effects of taurine and magnesium on electrical characteristics of artificial and natural membranes. V. Study on the human amnion of the antagonism between magnesium, taurine and polluting metals. Magnesium. 1985; 4(5-6): 325-32.

323. Doble A. The role of excitotoxicity in neurodegenerative disease: Implications for therapy. Pharmacol Ther. 1999; 81(3): 163-221.

324. Bonar DB, McColgan B, Smith DR, Darke C, Guttridge MG, Williams H, Smyth PPA. Hypothyroidism and aging: The Rosses’ Survey. Thyroid. 2000; 10(9): 821-827.

325. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Tntern Med. 2000; 160(4): 526-34.

326. Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE, Mitchell ML. Relation of severity of maternal hypothyroidism to cognitive development of offspring. J Med Screen. 2001; 8:18-20.

327. de Escobar DM, Orbregon MF, del Rey FE. Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? J Clin Endocrin Metab. 2000: 3975-3987.

328. Haddow JE, et al. Babies born to mothers with untreated hypothyroidism have lower I.Q.’s. New England Journal of Medicine. 1999.

329. Lavado-Autric, et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. JCI. 2003; 111: 1073-1082.

330. Pop VJ, Vader HL, et al. Low maternal free thyroxine during early pregnancy is associated with impaired psychomotor development in infancy. Clin Endocrinol(Oxf). 1999; 50: 149-55.

331. Man EB, Brown JF, Serunian SA. Maternal hypothyroxinemia: psychoneurological deficits of progeny. Ann Clin Lab Sci. 1991; 21(4): 227-39.

332. Pharoah POD, Connolly KJ, et al. Maternal thyroid hormone levels in pregnancy and cognitive and motor performance of the children. Clin Endocrinol(Oxf). 1984; 21: 265-70.

333. Pop VJ, de Vries E, et al. Maternal thyroid peroxidase antibodies during pregnancy: and impaired child development. J Clin Endocrinol Metab. 1995; 80: 3561-3566.

334. Connors MH, Styne DM. Neonatal athyreosis resulting from thyrotropin-binding inhibitory immonoglobulins. Pediatrics. 1986; 78: 287-290.

335. Asami T, Suzuki H. Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid. 2001; 11: 765-8.

336. Kumar R, Chaudhuri BN. Altered maternal thyroid function: fetal and neonatal heart cholesterol and phospholipids. Indian J Physiol Pharmacol. 1993; 37(3): 176-82.

337. Morris MS, Bostom AG, Jacques PJ, Selhub J, Rosenberg IH. Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination Survey. Artherosclerosis. 2001; 155: 195-200.

338. Shanoudy H. Soliman A, Moe S, et al. Early manifestations of sick eythyroid syndrome in patients with compensated chronic heart failure. J Card Fail. 2001; 7(2): 146-52.

339. Hak AE, Pols HAP, Visser TJ, et al. The Rotterdam Study: Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women. Ann Int Med. 2000; 132: 270-278.

340. Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med. 2002; 137(11): 904-14.

341. Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med. 1999; 131: 348.

342. Abramson J, Stagnaro-Green A. Thyroid antibodies and fetal loss. Thyroid. 2001; 11(1): 57-63.

343. Allan W. Maternal hypothyroidism during pregnancy linked to increased risk for miscarriage. Journal of Medical Screening. 2000.

344. Man EB, Jones WS. Thyroid function in human pregnancy: Retardation in 8-month old infants. Am J Obstet Gynecol. 1969; 104: 898-908.

345. Brent GA, Maternal hyrothyroidism: Recognition and management. Thyroid. 1999, 9: 661-5.

346. Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol. 2001; 60(4): 838-46.

347. Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury. J Environ Sci Health B. 2001; 36(5): 687-97.

348. Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: The role of peroxynitrite. Brain Res Brain Res Rev. 1999; 30(2): 153-63.

349. Aoyama K, Matsubara K, Kobayashi S. Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases. Ann Neurol. 2000; 47(4): 524-7.

350. Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol. 2001; 60(4): 838-46.

351. Lewis RN, Bowler K. Rat brain (Na+-K+)ATPase: Modulation of its ouabain-sensitive K+-PNPPase activity by thimerosal. Int J Biochem. 1983; 15(1): 5-7.

352. Bellabarba D, Tremblay R. Effect of thimerosal on serum binding of thyroid hormones, Can J Physsiol Pharmacol. 1973; 51: 156-159.

353. Hokkfen B, Kodding R, Hesch RD. Regulation of thyroid hormone metabolism in rat liver fractions. Biochim Biophys Acta. 1978; 539(1): 114-24.

354. American Assoc. of Clinical Endocrinologists and American College of Endocrinolog. AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 1995; 1: 54-62.

355. Stevenson, et al. Common Food Additives found to cause and increase ADHD behavior problems in some children. Lancet. 2007.

356. Geier DA, Carmody T, Kern JK, King PG, Geier MR. A dose-dependent relationship between mercury exposure from dental amalgams and urinary mercury levels: A further assessment of the Casa Pia Children’s Dental Amalgam Trial. Hum Exp Toxicol. 2011.

357. Cave S, Mitchell D. What Your Doctor May Not Tell You About Children’s Vaccinations. Warner Books; 2001.

358. Waly, M, et al. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: A target for neurodevelopmental toxins and thimerosal. Mol Psych. 2004: 1-13.

359. Mariea TJ, Carlo GL. Wireless radiation in the etiology and treatment of autism: Clinical observations and mechanisms. J. Aust. Coll. Nutr. & Env. Med. 2007; 26(2): 3-7.

360. Authier FJ, Cherin P, et al. Central nervous system disease in patients with macrophagic myofasciitis. Brain Res. 2001; 124: 974-983.

361. Blaylock RL. Immunoexcitotoxicity and autism. Alt Ther Health Med. 2008; 14: 46-53.

362. Dandona P. Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008; 83(3): 333-42.

363. Taylor P, et al. Misfolded neural proteins linked to some autism disorders. Journal of Biological Chemistry. 2010.

364. Barnes DM, Kircher EA. Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005; 19(2): 207-14.

365. Barnes DM, Hanlon PR, Kircher EA. Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003; 75(2): 368-77.
366. Iturri SJ, Pentildea A. Heavy metal-induced inhibition of active transport in the rat small intestine in vitro. Interaction with other ions. Comp Biochem Physiol C. 1986; 84(2): 363-8.

367. Klip A, Grinstein S, Biber J, Semenza G. Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980; 598(1): 100-14.

368. Blaylock Report.

369. Rayssiguier Y, Gueux E, et al. High fructose consumption combined with low dietary magnes: The danger of excessive vaccination during brain development. Magnes Res. 2006; 19(4): 237-43.

370. Bo S, Durazzo M, Pagano G, et al. Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006; 84(5):1062-9.

371. Guerrero-Romero F, Rodriguez-Moran. Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev. 2006; 22(6): 471-6.

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