Mercury Poisoning, Candida Yeast, or is it both?

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    I wanted to share an article with you all concerning the possible connection between mercury poisoning and candida.

    Some excerpts:

    At Michael Biamonte’s health clinic, testing the mercury levels in his patients with various illnesses, Michael found that 84% of his patients with candida had elevated mercury levels. The exact same number held for patients with parasites. 86% of his patients with Epstein Barr Virus also had elevated mercury levels. For those with chemical sensitivities, 85% were elevated and with chronic urinary tract infections 82% were elevated.

    Dr. J. Trowbridge has written in his book “The Yeast Syndrome,” that some doctors specializing in candida treatment have reported to him that they have discovered clinically that 98% of their patients with chronic candida also had mercury toxicity.

    Mercury poisoning disrupts the pituitary, thyroid, hypothalamus and adrenal gland. These disruptions help bring on fatigue, mind fog, short term memory loss, concentration problems, headaches and people can lose their sense of balance.

    Mercury catalyzes oxidation of important parts of your body, the worst area being the membranes around and inside the cells. It sticks to the sulhydryl groups present on the membranes and destroys the essential fatty acids that your body can’t replace. It also destroys the phospholipids that hold the membrane together.

    It oxidizes the proteins inside the cells that hold the cell together keeping things like your dna in place. It kicks out the appropriate metal from the enzyme receptor sites and renders these sites inactive.

    The significance of the above two paragraphs has a lot to do with cell to cell communication and the immune system. Your cells talk to one another and relay information so they all work together as a whole system. When cells are in danger for instance, they send out cytokines, which is a type of hormone signal asking for help from the immune system. If mercury has damaged the outer membranes it is unable to send out the required signal for help. Viruses, bad bacteria and yeast have a field day because the cells are defenseless by themselves.


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    Here’s my contribution. Dont ever stop learning-

    The Methylation Cycle

    Rich van Konynenburg’s idea is that ineffective methylation is a major cause of fatigue. There are many possible reasons but those that he’s identified for which methylation is essential to are:

    To produce vital molecules such as Co Q-10 and carnitine.

    To switch on DNA and switch off DNA. This is achieved by activating and deactivating genes by methylation. This is essential for gene expression and protein synthesis. Proteins of course make up the hormones, neurotransmitters, enzymes, immune factors and are fundamental to good health. When viruses attack our bodies, they take over our own DNA in order to replicate themselves. If we can’t switch DNA/RNA replication off then we will become more susceptible to viral infection.

    To produce myelin for the brain and nervous system.

    To determine the rate of synthesis of glutathione which is essential for detoxification.

    To determine the rate of synthesis of glutathione which is an essential anti-oxidant as glutathione-peroxidase. Furthermore oxidative stress blocks glutathione synthesis – yet another vicious cycle!

    To control sulphur metabolism of the body, not just glutathione but also cysteine, taurine and sulphate. This is an important process for detoxification.

    As part of folic acid metabolism. This also switches on synthesis of new DNA and RNA.

    For normal immune function. The methylation cycle is essential for cell mediated immune function and blockages here will mean that infections will not be adequately dealt with. I know this clinically because many patients tell me that once they get on to their B12 injections (an essential co-factor for methylation) this seems to protect them from getting infections.

    The overall effect here is that if the methylation cycle doesn’t work, the immune system mal-functions, the detoxification system mal-functions, our ability to heal and repair is reduced and the anti-oxidant system mal-functions.

    Molecular Aspects of Thimerosal-induced Autism

    Molecular Aspects of Thimerosal-induced Autism
    Richard C. Deth, Ph.D.
    Professor of Pharmacology
    Northeastern University
    Boston, Massachusetts

    The developmental disorder autism has both genetic and environmental origins, and its forty-fold increase during the past two decades reflects an increased role for environmental factors. It has been proposed that increased use of vaccines containing the ethylmercury derivative thimerasol is the major contributing factor. Published research from my laboratory has revealed that thimerosal is an exceptionally potent inhibitor of biochemical pathways that transfer single carbon atoms between molecules. These “methylation” pathways are critically involved in several important functions including the regulation of gene expression and the molecular mechanism of attention. Recent studies from my lab indicate that thimerosal exerts its toxic effect on methylation by interfering with formation of the active form of vitamin B12, also known as cobalamin. Dietary B12 must be converted to methylB12 (methylcobalamin) in order to assist in the transfer of single-carbon methyl groups from the folic acid pathway by the enzyme known as methionine synthase. By reducing methylB12 formation, thimerosal inhibits this enzyme and thereby interferes with methylation events. Autistic children have abnormal plasma levels of methylation-related metabolites and exhibit higher frequencies of genetic mutations that affect this pathway. These genetic risk factors make them less able to detoxify thimerosal and also increase their sensitivity to its mechanism of toxicity. In many cases, autism can be effectively treated by the administration of methylB12 along with other agents that augment methylation capacity. Taken together, these facts indicate that increased exposure to thimerosal has combined with genetic risk factors in a sensitive subpopulation to cause the recent rise in autism.

    1. The Puzzle of Autism
    2. Physiological and Biochemical Roles of Methylation
    3. Activity of Methionine Synthase
    4. Effects of Thimerosal and Heavy Metals
    5. Autism-associated Metabolic and Genetic Abnormalities
    6. Methylation-related Treatments for Autism
    7. Conclusions

    1. The Puzzle of Autism
    Autism is a pervasive developmental disorder characterized by deficits in language, attention, cognition and learning, frequently accompanied by abnormal behavior including social isolation, repetitive activity and emotional lability. Severe deficits may be recognized at birth, but a failure to achieve standard milestones during initial years of life remains the primary basis of diagnosis in most cases. While the underlying cause(s) remains obscure for many developmental disorders, metabolic abnormalities (e.g. Lesch-Nyhan Syndrome and adenylsuccinate lyase deficiency) or impaired methylation-dependent gene silencing and/or imprinting (Rett and Fragile-X Syndromes) (1-4) suggest biochemical mechanisms that may be involved. Development disorders can also be caused by exposure to toxins (e.g. ethanol, in fetal alcohol syndrome; heavy metals, in lead poisoning) (5,6), although the precise molecular mechanisms underlying their toxicity are not known. The recent increase in the incidence of autism has led to speculation that environmental exposures including vaccine additives (i.e. aluminum and the ethylmercury-containing preservative thimerosal) might contribute to the triggering of this developmental disorder (7).

    Based upon a high concordance in twin studies, genetic factors are thought to play an important role in causing autism. However, it is clear that the recent dramatic rise in autism rates is not caused by a genetic phenomenon. The more likely scenario is that autism is caused by the interaction of genetic risk factors with environmental risk factors and the importance of the environmental factors has increased during the past twenty years. As illustrated in Fig. 1, the “Puzzle of Autism” therefore is the challenge of understanding exactly which genes provide the inborn risk, and which environmental factor(s) is serving as the trigger. The molecular mechanism at the intersection of genetic and environmental factors should be capable of accounting for the observed symptoms of autism, and knowledge of this mechanism should help identify effective treatments for autism. The findings summarized in this report indicate that impairment in the biochemical pathways that allow for the transfer of single carbon groups (i.e. methylaion) is a major factor contributing to the cause(s) of autism.

    2. Physiological and Biochemical Roles of Methylation
    Methylation is the process by which a single carbon atom is transferred from a methyl donor to another molecule, commonly resulting in a change in the functionality of the recipient molecule. This seemingly mundane biochemical event is vital to life and to the normal capacities of developed organisms, including man. Perhaps the most important example of methylation is the epigenetic regulation of gene expression by DNA methylation. When DNA is methylated, gene expression is suppressed, and at any one time only a portion of genes are “on” with the others being turned “off”. Since all cells possess the same DNA, differences between cell types (e.g. neurons vs. heart muscle vs. liver cells) are due to specific patterns of DNA methylation that characterize each type. Development begins with undifferentiated cells (i.e. stem cells) that gradually assume the characteristics of their final destiny as guided by sequential shifts in their
    DNA methylation. Based upon this perspective, it is easy to see how abnormal methylation could alter the pathway of normal development and could contribute to neurodevelopmental disorders such as autism. Indeed, abnormal DNA methylation has previously been implicated as an important causative factor in Rett and Fragile-X syndromes (3,4)

    As illustrated in Fig. 2, the major methyl donor in biological reactions is S-adenosylmethionine (SAM), an activated form of the essential, sulfur-containing, amino acid methionine. After donating its methyl group, the residual portion of SAM, S-adenosylhomocysteine (SAH), serves as a regulator of methylation by competing with SAM and inhibiting its methyl donation. The concentration ratio of [SAM]/[SAH] therefore reflects the potential for methylation, and any increase in [SAH] or decrease in [SAM] will lower methylation. As described below, children with autism have low levels of SAM and elevated levels of SAH, indicating an impaired potential for methylation. Methylation of neurotransmitters such as dopamine and serotonin terminates their signaling activity, which may also play a role in autism

    Figure 2: DNA methylation is carried with S-adenosylmethionine (SAM) serving as the methyl donor. The resulting S-adenosylhomocysteine (SAH) inhibits methylation by competing with SAM.

    Availability of the methyl donor SAM is critical for methylation. SAM is formed by addition of an adenosyl group from the high energy molecule ATP to methionine, as a part of the methionine cycle illustrated in Fig.
    3. After methyl donation the adenosyl group is removed from SAH, in a reversible reaction yielding homocysteine (HCY) and adenosine. Any unusual build-up of adenosine can shift this reaction backwards toward SAH formation, while lowering HCY levels. As described below, this occurs in many children with autism. Activity of the vitamin B12-dependent enzyme methionine synthase converts HCY back to methionine, using a methyl group from the folate pathway.

    Figure 3: The four-step methionine cycle involves activation of methionine (MET) by ATP-dependent adenosylation, methyl donation by SAM, reversible dissociation of SAH, and remethylation of homocysteine (HCY) to MET by the vitamin B12-dependent enzyme methionine synthase, using methylfolate (5-methylTHF) as the methyl donor. HCY can alternatively be converted to cysteine and glutathione.

    The methionine cycle is also involved in the ability of the neurotransmitter dopamine to stimulate methylation of phospholipids in the neuronal membrane. This unique process was only discovered several years ago and its precise function remains unclear at this time. However, dopamine-stimulated phospholipid methylation (PLM) appears to be involved in the molecular origins of attention. Genetic variations in the D4 subtype of dopamine receptor that carries out PLM have been linked to attention-deficit hyperactivity disorder (ADHD) (8), and the ADHD-linked variant form is weak in its ability to carry out methylation (9). Impaired attention is a cardinal symptom of autism, and it is possible that this reflects reduced activity of dopamine-stimulated PLM. During dopamine-stimulated PLM, a methionine that is an integral part of the D4 receptor protein is converted to SAM, then SAH, then HCY and back to methionine again, as in the methionine cycle of Fig. 3. Thus enzymes in the methionine cycle, such as methionine synthase, actually have two substrates, one being a small individual amino acid, and the other being the large D4 dopamine receptor protein.

    3. Activity of Methionine Synthase
    Methionine synthase is situated at the intersection of the single-carbon folate pathway and the methionine cycle (Fig. 3), and is therefore well-positioned to regulate methylation. Its activity serves to maintain a low level of HCY, limiting its backward conversion to SAH and thereby promoting methylation. In a recently published study (10), we showed that methionine synthase activity in cultured human neuronal cells is substantially stimulated by both dopamine and insulin-like growth factor-1 (IGF-1) (Table 1). IGF-1 mediates many of the effects of growth hormone and is a key regulator of development, as well promoting neuronal myelination.
    The mechanism of methionine synthase activation involves an intracellular signaling pathway, the PI3-kinase pathway, commonly activated by many different
    cellular growth factors, including those that promote cellular differentiation and development. In subsequent investigations we found that methionine synthase activity in neuronal cells is absolutely dependent upon the ability of this signaling pathway to promote the formation of the biologically active form of vitamin B12 (i.e. methylB12 or methylcobalamin). It is pathway that is inhibited by thimerosal.

    Table 1: Effects of various agents on methionine synthase activity in neuronal cells. IGF-1 and dopamine stimulate activity, while the PI3-kinase inhibitor wortmannin, ethanol, mercury (HgCl2), lead (PbNO3) and thimerosal inhibit activity.

    In the diet we take in vitamin B12 as its hydroxyl derivative, hydroxycobalamin, which must be subsequently converted to methylcobalamin before it can function. Dietary vitamin supplements provide cyanocobalamin, which again must be converted to methylcobalamin. Conversion to methylcobalamin can occur either directly in the enzyme methionine synthase itself, or via the pathway outlined in Fig. 4. As illustrated, methylcobalamin synthesis requires glutathione (GSH) and SAM, and levels of each of these metabolites are reduced in autistic children (see below). Although additional studies are needed to clarify details, growth factors apparently augment synthesis of the intermediate glutathionylcobalamin, which is subsequently converted to methylcobalamin. The resultant higher level of methylcobalamin increases methionine synthase activity, lowering HCY and SAH levels and increasing methylation. In support of this mechanism, our published study showed that IGF-1 and dopamine increase the methylation of both DNA and membrane phospholipids in conjunction with their activation of methionine synthase.

    Figure 4: Dietary or multivitamin forms of vitamin B12 (cobalamin) must be converted to the active methylcobalamin form via a two-step process requiring glutathione (GSH) and SAM.
    As illustrated in Fig. 5 (left), methionine synthase normally contains four domains:
    1. A cobalamin-containing catalytic domain.
    2. A methylfolate-binding domain.
    3. A HCY-binding domain.
    4. A SAM-binding domain. During the catalytic cycle, folate and HCY domains alternatively interact with the cobalt ion in cobalamin, which alternates between Cob(I) and methylated Cob(III) states. Cob(I) is, however, extremely unstable, and occasionally it oxidizes to the Cob(II) state, interrupting folate-dependent HCY methylation. Oxidation is especially likely when levels of methylfolate are low and the Cob(I) state has to wait too long to receive a methyl group. Under this circumstance, the SAM-binding domain, when present, carries out a reductive methylation of Cob(II), with the auxiliary assistance of methionine synthase reductase. Thus the SAM-binding domain rescues oxidized cobalamin, allowing methionine synthase activity to resume. Alternatively, oxidized Cob(II) can be replaced with a new molecule of methylcobalamin to restart the enzyme. Thus oxidized cobalamin can either be repaired or replaced, but replacement places a high demand on methylcobalamin synthesis.

    Figure 5: Methionine synthase can exist in both four-domain and three-domain forms. In the three-domain form, the SAM-binding domain that rescues oxidized Cob(II) is missing. In cells containing only the three-domain form, oxidized B12 must be replaced with methylB12 to resume enzyme activity.

    In very recent and as yet unpublished studies, we have found evidence indicating that methionine synthase also exists with only three domains, with the SAM-binding domain being absent (Fig. 5, right). This form of the enzyme lacks the ability to rescue oxidized cobalamin, and therefore is highly dependent upon the availability of methylcobalamin to sustain activity. As such, this form of the enzyme is subject to regulation by growth factors and the PI3-kinase signaling pathway, since they control the level of methylcobalamin synthesis. The particular human neuronal cell line we utilized contained only the three-domain enzyme. As a consequence, its methionine synthase activity and its methylation activity were tightly and completely under the control of the growth factors signaling pathway. What would be the advantage to a cell of having a form of methionine synthase that could not repair its oxidized cobalamin co-factor? While we do not conclusively know the answer to this question, we hypothesize that the absence of the SAM-binding domain may improve the ability of the enzyme to utilize the D4 dopamine receptor as a substrate, since it is a larger, more bulky substrate than HCY, and the three-domain form is more prominent in cells expressing the D4 receptor. If correct, this would imply that the synthesis of methylcobalamin is of particular importance in those neuronal cells that express the D4 receptor. Moreover, toxic agents that impair methylcobalamin synthesis would particularly affect the methylation function of D4 receptors, and would therefore cause impaired attention.

    4. Effects of Thimerosal and Heavy Metals
    As described in our published study, a number of neurodevelopmental toxins share the ability to potently inhibit methionine synthase activity and methylation. These include ethanol, which causes fetal alcohol syndrome, heavy metals such as lead, which causes lead poisoning, as well as mercury and thimerosal. Fig. 6 illustrates the dose-dependent inhibition of phospholipid methylation (PLM) by lead and mercury. It is of particular note that concentrations of lead that reduce cognitive function (IQ) (6)
    significantly inhibit PLM. Thimerosal, which releases ethylmercury, was more than 100-fold more potent than inorganic mercury at inhibiting methylation (Fig. 7). Ten days after vaccination with a thimerosal-containing vaccine, the concentration of ethylmercury in blood is reported to be approximately 8 nM (11). In our study, this concentration produced greater than 50% inhibition of methylation. Assuming that these blood levels are also present in the brain, one could reasonably expect that vaccine-derived doses of thimerosal inhibit methylation in the brain.

    Figure 6: Mercury and lead potently inhibit the ability of IGF-1 to stimulate phospholipid methylation in human neuroblastoma cells.

    Figure 7: Thimerosal potently inhibits IGF-1-induced phospholipid methylation. Blood levels found in children ten days after vaccination produced approximately 50% inhibition.

    Thimerosal, ethanol, mercury and lead also inhibited methionine synthase activity. As shown in Table 1, enzyme activity (i.e. methylation of HCY) was undetectable after a 30 min pretreatment with a thimerosal concentration close to the blood level found after vaccination (10 nM). Thus inhibition of methionine synthase accounts for the inhibitory effect of thimerosal on methylation. The toxic effect of thimerosal was also evident simply by observing the shape of cells, which changed from their usual spindle shape to a condensed, round shape (Fig. 8).

    Figure 8: Thimerosal induces a dramatic change in the morphology of human neuroblastoma cells.
    We further investigated the mechanism by which thimerosal inhibits methionine synthase. As shown in Fig. 9 (bottom), when enzyme activity was measured in the presence of either hydroxycobalamin or cyanocobalamin, thimerosal caused almost complete inhibition, however in the presence of methylcobalamin, thimerosal caused no inhibition. Furthermore, when activity was measured in the presence of glutathionylcobalamin and SAM, thimerosal inhibition was again absent, although when SAM was not added, inhibition was observed. This pattern indicates that thimerosal inhibits the availability of glutathionylcobalamin, and that this action is responsible for its inhibition of methionine synthase and methylation.

    Figure 9: The PI3-kinase inhibitor wortmannin and thimerosaleliminate the ability of hydroxo- and cyanocobalamin to support methionine synthase activity. The presence of SAM is indicated by (+).

    We also examined the ability of different cobalamins to support methionine synthase activity after inhibition of PI3-kinase. Treatment with the selective PI3-kinase inhibitor wortmannin caused a pattern of absolute dependence on methylcobalamin or its synthesis (gluthionylcobalamin + SAM) that was identical to the effect of thimerosal (Fig. 9, top). Since thimerosal and wortmannin produce identical effects, this data strongly suggests that thimerosal acts by inhibiting the PI3-kinase signaling pathway. This is the likely mechanism by which thimerosal causes autism, and may also be the molecular basis for its toxic effect on bacteria, fungi that makes it an effective preservative.

    5. Autism-associated Metabolic and Genetic Abnormalities
    Metabolic and genetic studies of autistic subjects provide a more complete view of how thimerosal, as an environmental insult, causes autism. Some of the most compelling information has only recently been obtained, and we are all indebted to the ongoing work of Jill James, Jeff Bradstreet, Marvin Boris, Alan Goldblatt, Ted Page, Gene Stubbs and others.

    As described in a recent study by Dr. Jill James (12), the concentration of each of the individual metabolites in the methionine cycle and the trans-sulfuration pathway leading to glutathione synthesis is significantly abnormal in autistic children as compared to normal controls (Table 2). Notably, methionine and SAM levels are low, consistent with lower activity of methionine synthase. While a low HCY level might not be expected, the elevated levels of both SAH adenosine indicate that HCY is being drawn backwards toward SAH via the reversible activity of the enzyme SAH hydrolase. Thus an elevated level of adenosine restricts the availability of HCY for both methionine (and SAM) synthesis and for the formation of cysteine and glutathione.

    Table 2: Metabolites in the methionine cycle and transsulfuration pathway are abnormal in autism (data from Dr. Jill James).

    The 20% lower levels of cysteine and 54% lower levels of glutathione in autistic children will adversely affect their ability to detoxify and excrete heavy metals and thimerosal. These two compounds directly bind inorganic and organic mercury and help direct them to the kidneys for excretion. As a result, these toxic materials will reach a higher free concentration in the bloodstream of autistic children, will have an increased potential for transfer to tissue compartments such as the brain, and will remain in the body for a significantly longer period of time, as compared to their counterparts who have normal levels of cysteine and glutathione. These differences begin to define the subpopulation of children who are more vulnerable to thimerosal and heavy metal exposure.

    Earlier metabolic and genetic studies provide clues to the cause of the increased adenosine level in autism. Page and co-workers found 8 to10-fold higher activity of the enzyme that makes adenosine (5′-nucleotidase) in subgroup of children (13), while Stubbs and co-workers found that the enzyme that degrades adenosine (adenosine deaminase) has lower activity in autistic subjects (14). Genetic studies have also shown that a polymorphism in the adenosine deaminase that weakens the enzyme is more common among autistic subjects (15). Impairment of adenosine deaminase, may result from dysfunctional interactions with its binding partner, enzyme dipeptidyl peptidase IV. As illustrated in Fig. 10, these metabolic defects can combine with thimerosal exposure and other genetic risk factors to inhibit methylation and cause autism.

    There is recent evidence that polymorphisms in genes for methionine synthase and closely-related enzymes are another source of risk for autism. For example, there are two well-characterized disabling polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene, the enzyme that makes methylfolate available to methionine synthase, and these polymorphisms are more common in autism (16). MTHFR polymorphisms reduce methylfolate levels, which slows the methylation of Cob(I) and increases the probability that it will oxidize to Cob (II). As a consequence, MTHFR polymorphisms increase methylcobalamin demand for the three-domain form of methionine synthase. A disabling polymorphism in methionine synthase, in a location that can affect the proportion of three- vs. four-domain enzyme forms, is reported to be six-fold more prevalent in autistic children (17). Finally, a polymorphism in the enzyme methionine synthase reductase, which assists in the rescue of cobalamin, may also be more frequent in autism (18). While other polymorphisms remain to be discovered, these examples serve as examples of genetic risks that characterize autistic children, making them more sensitive to the toxic effect of thimerosal and more prone to develop autism.

    Figure 10: Decreased activity of adenosine deaminase or increased activity of 5′-nucleotidase (5′-NTase) can increase adenosine levels, resulting in lower levels of HCY, cysteine and glutathione.

    6. Methylation-related Treatments for Autism
    If impaired methylation is important in causing autism, metabolic interventions that augment methylation should be effective treatments. More specifically, if thimerosal’s inhibition of methylcobalamin synthesis is important in causing autism, then the administration of methylcobalamin should significantly improve autism. Indeed, this has proved to be the case. As first reported by Dr. James Neubrander (19), injections of methylcobalamin, given once every three days, has brought about significant improvement in approximately 80% of children with autism. While the degree of improvement varies, a significant number of children have improved to the point that they are no longer considered to be “on the autism spectrum”. Areas of particular improvement include language, attention and social skills, which are hallmark symptoms of autism. Within the next few months, the M.I.N.D. Institute at the University of California at Davis School of Medicine is slated to carry out a controlled study of methylcobalamin effectiveness in autism.

    Other methylation-promoting treatments are also proving helpful in autism. In the metabolic study carried out by Dr. Jill James and colleagues (12), autistic subjects were treated with folinic acid (leucovorin), a folic acid derivative that augments levels of 5-methylTHF, along with betaine (trimethylglycine), which feeds methyl groups to the folate pathway. These two agents normalized most of the abnormal metabolites listed in Table 2, and this was accompanied by clinical improvement in autism symptoms. Subsequent addition of methylcobalamin to this regimen brought about further improvement.

    While encouraging, these metabolic interventions do not help many autistic children, and there is a need for additional treatment approaches. Moreover, improving methylation capacity is only one component of the multi-dimensional approach to treating autism. Other elements such as a gluten-free/casein-free diet, chelation of heavy metals and intensive behavioral therapy are also important. Additional metabolic interventions, particularly interventions directed at normalizing adenosine metabolism may prove fruitful. Clearly further research is needed, building upon the framework of knowledge about how genetic and environmental factors can synergize to cause autism.

    7. Conclusions
    Autism is a neurological disorder caused by dysfunctional metabolic control over methylation reactions, and thimerosal appears to be a precipitating causative factor in many cases. The methionione cycle and the trans-sulfuration pathway leading to cysteine and glutathione synthesis are abnormal in autism. Genetic polymorphisms, present in only a small subpopulation, represent risk factors for autism. As illustrated in Fig. 11, some of these genetic factors impair detoxification and clearance of heavy metals, including thimerosal, and also impair the capacity for methylation. Delayed clearance of thimerosal further impairs methylation, including both DNA methylation and dopamine-stimulated phospholipid methylation, adversely affecting growth factor-directed development and the capacity for attention, respectively. Autism can be treated, and some of the most effective treatments, such as methylcobalamin, act by improving methylation. This encouraging therapeutic development reinforces the conclusion that thimerosal does indeed cause autism, and it does this by interfering with methylcobalamin synthesis. Thismolecular understanding should lead to new and improved treatments for autism and should provide a scientifically sound basis for the removal of thimerosal from all vaccines.

    So…What causes autism?
    Genetic FactorsFactors that affect the capacity for methylation
    The ability to detoxify and excrete metals
    Environmental Factors
    The Vaccine Additive Thimerosal
    Environmental Exposure To Heavy Metals

    Figure 11: Genetic and environmental factors combine to cause autism.



    Topics: 16
    Replies: 606

    bumpity bump


    Topics: 9
    Replies: 375

    Well I don’t think I’ll be able to top that post, lol. Rich Van Konynenburg seems like a real smart guy and the perspective laid out there is golden, imo. I hope people take notice.

    Everyone should check out this blog post that goes further into the methylation-mercury connection. I take no credit, just passing on some information and a perspective that I think is extremely pertinent to those on this forum:


    Topics: 9
    Replies: 375

    Just found this article:

    Some snippets

    “The CDC has been shunning the correlations between thimerosal and neurological disorders for a very long time. Although the FDA gave a two year deadline to remove the mercury based preservative from vaccines after the neurotoxin was banned in 1999, it still remains to this day in 60 percent of flu vaccines.”

    “There are dozens of scientific inquiries and studies on the adverse effects of thimerosal, including gastrointestinal abnormalities and immune system irregularities.”


    Topics: 18
    Replies: 108

    The connection between candida, mercury and immune suppression definitely catches my eye. I was diagnosed through stool test last spring with a fairly high candida overgrowth, did the strict diet and protocol from summer through December (and started to relax the diet then because I was feeling pretty close to normal.) In late December I went in to my physician b/c I had a sore on my leg that hadn’t been healing for almost 3 months and I thought it was perhaps an infection. It was squamous cell carcinoma, though it took them two months and two biopsies to actually confirm it. I’ve just had it removed and I’m on a course of antibiotics because leg surgeries heal poorly and are prone to infection.
    I’m less worried about the antibiotics than I once would have been (it’s the first time I’ve taken antibiotics in… a decade?), partly because I know the drill for recolonizing my gut, but mostly because I’m thinking there’s another disease mechanism here at work, that candida maybe wasn’t the root but yet another symptom, in the same way that the GERD, dizziness, brain fog and fatigue weren’t the root problems but part of the candida infestation.
    I’ve sent off my genetic testing kit in hopes that will give me a direction to go in next. I also hope that I can jump start the methylation cycle and have my body clear whatever toxins or viruses are wearing my systems down (my health issues began 4 years ago with a virus I couldn’t fully recover from, and have cycled from bad to nearly normal repeatedly. I think low Vit D levels have been critical b/c in most of those years I’ve felt my worst/had my biggest crashes in late winter/spring.)
    I’d really hoped that candida was the final thing I had to deal with, but I don’t really think that now. Clearly my immune system is suppressed. I hope the 23andMe data will be helpful.


    Topics: 9
    Replies: 375

    Just found another success story:

    My Battle with Candida and Mercury Poisoning…The Connection

    I am writing this story with the hope that I can help someone who may be suffering from the same illness as
    me. In April of 2007, I was in the throws of breaking off a relationship that was very stressful. One night
    we had gone out to have sushi and I cracked a tooth with a “silver filling”. I didn’t think much of it at the
    time and didn’t get it fixed right away since the part of the tooth that had broken off had been small and I
    couldn’t afford a new crown. So, each night I would brush really well at that tooth to make sure I didn’t
    get any food caught up there. Several months later, I had gotten a sinus infection and had taken a round of
    antibiotics. I then developed a strange sort of diaper rash. I went back to the doctors and they said it
    looked like a fungal rash and sent me home with an antifungal. During this time, I had been experiencing
    vicious mood swings and horrible depression. I normally didn’t experience these emotions, but I attributed
    it to the bad relationship I was involved in. The rash wouldn’t go away. I then noticed I had a yeast
    infection that kept coming back even though I had finished a round of monistat. My thinking started to
    become anxiety riddled with what I could only call brain fog. One night I was convinced I was dying and
    took myself to the emergency room. By then I had done some research and stumbled across candida and
    convinced myself I had it and thought it was from the antibiotics I had taken.

    I finally found a doctor to put me on a months worth of diflucan but the candida wouldn’t go way. I was on
    the most stringent form of anti yeast diet you can imagine. No sugar, no carbs, no fruit, no alcohol,
    nothing. I was getting so thin. Each time I killed the yeast, I was experiencing horrible die off. Dizziness,
    chronic fatigue, headaches, burning toes, persistant yeast infections. I finally found Karen’s website and
    out of desperation, I called Dr. Piller and flew out to Idaho. I had been battling this for a year on my own
    and needed real help. Before I flew out, I decided to get that tooth fixed because I had read somewhere that
    people were saying that those “silver fillings” contained 50% mercury and would keep the yeast around
    until you got rid of the mercury. I didn’t take it seriously, but decided to get the tooth fixed just in case.
    When I saw Dr. Piller, he told me I had a dairy allergy. I thought, Yay! I have a reason for my yeast not
    going away. Long story short, it didn’t go away, and cut to another year, and I was miserable. Then I ran
    across a post from someone who said that her candida die off symptoms were the same symptoms as
    mercury poisoning and when she removed all her mercury fillings her yeast went away. The light bulb
    moment came and I finally figured out it was that cracked tooth that poisoned me! I was so happy to
    finally figure it out. Dr. Piller ordered me a hair test and sure enough I was very high in mercury,
    aluminum, tin and cadmium. Mercury poisoning makes you retain other metals. I then found a mercury
    free dentist who removed another filling and two crowns since there was mercury under the crowns. Once
    I was mercury free, I followed the protocol of Dr. Andrew Cutler. He is a chemist who wrote a book called
    “Amalgam Illness”. That book changed my life and I took the appropriate meds to chelate the mercury. I
    also did saunas, massage and took Lecithin, which Dr. Piller recommended to remove metals. NOTE: IT
    YOU CHELATE, OTHERWISE YOU WILL GET SEVERELY ILL. Once I chelated the mercury to the
    point my body could handle it, my yeast went away, almost over night!! It took me about 5 months of
    chelation to get to the point I am now. My candida and mercury are under control. I will continue to
    chelate a couple of times a year to remove any remaining metals, but at this point, I am healthy, eat what I
    want and live normally. I still don’t eat milk products, but heck, after what I went through, it’s well worth
    it to stay healthy. NOTE: The mercury vapor emits from the tooth anytime you drink hot beverages, brush
    your teeth or grind your teeth at night. There is no safe level of mercury in the body, it lowers your
    immune system horribly. Some symptoms of mercury poisoning are:

    Dizziness, chronic fatigue, yeast syndrome, tingling in extremities, hormone imbalance, burning toes, night
    sweats, a feeling of electricity under skin, mood swings, depression, anxiety, brain fog, ringing in ears…to
    name a few. These are not caused by candida which I thought, they are mercury poisoning symptoms!!!
    Very important. Left unchecked it can lead to parkinsons, MS, altzheimers, fibromyalgia.

    I hope I have shed some light and given someone that light bulb moment. God bless….


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    Found some more success stories:

    Some excerpts:

    “I also regained my health by addressing dental mercury poisoning. Between March 2011 and March 2012 I became increasingly ill, and saw a dozen specialists who could not diagnose what was wrong. After six months, I basically gave up hope. Then one of my doctors heard a presentation that symptoms like mine could be caused by dental amalgam mercury poisoning. I had an elevated mercury level.

    Working with a biologic dentist and my doctor I was able to get healthy again. Not only did I lose my escalating acute symptoms, I lost my fibromyalgia of 20 years, and am regaining my short term memory and sense of well being.”

    “My doctor treated me for mercury toxicity based on my symptoms, knowing I had just been to the dentist and had been exposed to mercury vapor. He did this even though my mercury scores were not high on that particular test.

    I later went to an Integrative health neurologist who said I had MS but to use natural methods to keep down the inflammation. So that is what I am doing. He told me the MS drugs were not that effective.

    I had my fillings safely removed by a holistic biological dentist and starting using an oral chelator along with many natural anti inflammatories, anti oxidants and minerals. Many of my symptoms cleared up immediately after amalgam removal, while others slowly went away. I improved tremendously with an oral chelator or detox agent.”

    “My 30 yr migraines finally cured along with many other ailments when I exchanged my 30 yr old silvery amalgam fillings (8 plus few “buckle” dots) for non-allergenic white composite.

    Been diagnosed with ailments for 30 yrs: migraines, hypoglycemia, Reynaud’s syndrome (blue nails), insomnia. Don’t like strong meds and gravitated toward healthy eating, reducing toxins, etc. The last 10 yrs during perimenopause the symptoms just continued to increase. By chance and due to my fillings, I was given a heavy metal challenge by my doctor (DMPS). My mercury level was extremely high. I made appt with a Biologic Dentist who would use special procedures to exchange the fillings with minimal further exposure. No suggestions were made about health benefits by either practioner. After seeing my results, I just wanted it out, hoping for future benefits in the long run. I had entered the office with a migraine, brain fog, some nausea, typical being the beginning of my cycle. After 2 hours of work and driving home with a swollen mouth after having half my fillings exchanged, I realized that I did not have any headache, no brain fog, my thinking was clear. Days went by, then months and no symptoms at all.

    Gone were my debilitating migraines, hypoglycemia which had been a daily battle, brain fog, insomnia, blue nails with the slightest chill, extreme sensitivies to smells of perfume, chemicals, detergents, silent distracting hearing disturbances, slow digestion, stiff ankles upon rest, heavy painful menses, teeth grinding, overactive salivary glands “spraying it vs. saying it”, weak thighs that had me considering an elevated toilet before age 50, skin blotches faded and more.”


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    Another proof of the extreme power of imagination.


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    Floggi;55782 wrote: Another proof of the extreme power of imagination.

    Strong argument. Surely that’s enough to get desperate sick people to look the other way.


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    Are you not only denying the life-saving effects of vaccination, but also the very existence of the placebo effect?

    I can dig up some well-documented examples, if you like. For example, the man who was dying – his body functions deteriorated by the minute, he was getting weaker and weaker. The cause seemed to be an enormous overdose of some experimentel medicine which he had deliberately taken, until he decided that he didn’t want to die after all – but then it was too late, he was already dying.

    Until… the doctor revealed to him that he was in the test group of an RCT. The overdose he had taken was an overdose of a do-nothing placebo…

    When he heard this news, he started crying like he had never cried before, he fell asleep, and he fully recovered.

    If you like, I can dig up the reference to this story. I can also find some equally astonishing stories for you.

    Are you really denying the very existence of this well-known effect?


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    Floggi;55931 wrote: Are you really denying the very existence of this well-known [placebo] effect?

    To the point where someone completely recovers from all of their chronic health problems due to it? Yes… I am.

    Like I stated previously, good luck getting desperate sick people to buy that argument.


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    ThomasJoel2;56013 wrote:

    Are you really denying the very existence of this well-known [placebo] effect?

    To the point where someone completely recovers from all of their chronic health problems due to it? Yes… I am.

    You are actually denying a proven fact that is well established, both in medicine and in the alternative world…? How can you be so blind?

    • Do you deny that even fake surgery has been proven to help lots of patients?
      This has been shown in back surgery at the famous Mayo Clinic. It has also proven effective in knee operations, even in heart-artery operations. Are you really denying this?
    • Do you deny that voodoo affects susceptible people?
      Then you would probably even deny the case of Mr. Vanders, who was actually dying after he met a voodoo witch. Luckily, Mr. Vanders completely recovered after his doctor used a trick that relies on the placebo effect. Are you actually denying this well-reported case?
    • Do you deny the miraculous recovery of terminal cancer after treatment with Krebiozen?
      Then please educate yourself and read about the Krebiozen case. In summary, a patient who had terminal cancer with metastatic tumors was treated with the then-experimental drug Krebiozen. The tumors melted away and the patient recovered completely. This only lasted until the patient read about Krebiozen being a fraud. Then the tumors returned. The doctor resorted to a trick: he fooled the patient into believing that a new, improved version of Krebiozen was discovered. After treatment, the patient fully recovered again – until, that is, he read in an newspaper that Krebiozen was totally ineffective. He died shortly after.
      How can you be so shortsighted to deny this?
    • Do you deny that medical research must use RCT trials because of the placebo effect?
      In medical research, a randomized controlled trial (RCT) is the “gold standard” to study a medication or a treatment. One way to perform an RCT is by means of a placebo-controlled study. Are you really denying the existence of this well-established practice? Are you really denouncing the reasons why these methods were introduced? Are you actually asking researchers to forget the lessons that were learned the hard way?
    • Do you deny that the causes of the placebo effect are actively being studied?
      There is a lot of research going on. Not into the extent of the placebo effect, because that is a known fact, even if you choose to deny it. No, not into the large extent of the placebo effect – but into the mechanisms by which it works. Are you actually saying that all these professionals are studying an effect that doesn’t exist?

    I never thought I’d have to say this – but by denying a fact that is so well established, that has been experienced by so many persons, and that has been observed by so many knowledgeable professionals in so many fields, you are really making a caricature of yourself.


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    Well shit. If it’s all placebo like you say, then why not try and help me convince this forum about this mercury chelation thing, and then we can cure all these sick people through the power of the mind alone! Who cares why they recover as long as they do actually get better? I’m not sure your alleged motivation for arguing against mercury chelation makes much sense here.

    In all seriousness, let’s look at this placebo argument for a minute as I present a scenario for you and the readers out there: Two groups of people are convinced that they are mercury toxic. One of the groups goes to an IV chelation clinic and receives IV infusions of chelating agents. The other group goes with frequent, low-dose chelation, as advised by Andrew Cutler.

    Now, as I have brought to the attention of this forum on multiple occasions, many people report tremendous improvement and even to have been completely cured with enough frequent, low-dose chelation. On the flip side, many report extremely negative and adverse reactions after following an IV chelation protocol. How do we make sense of this within the context of the placebo argument? Both groups believed that they were mercury toxic. Both groups underwent treatment to detox heavy metals. If the placebo effect were as strong as you claim, one would assume both groups to have similar responses. This type of thinking runs contrary to what actually happens when treatment is given.

    As I have mentioned previously, IV chelation is an incredibly risky protocol. Conversely, frequent, low-dose chelation is both safe and effective. For readers who want better insight into the IV chelation vs. frequent, low-dose chelation issue, check out this thread:

    For negative reactions following IV DMPS chelation check out this site:

    For positive reactions following frequent, low-dose chelation just wade through my post history. I have posted many success stories.


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    So you keep denying the very existence of the placebo effect.

    You keep denying the lessons we learned, often the hard way, from over 150 years of solid research.

    Of course you are welcome to believe anything you want.

    But please don’t try to persuade others in following your personal beliefs. Allow others to come to their own conclusions. Based on all viewpoints.

    You presented your denial of the placebo effect. I added some broad scientific knowledge, including the very reasons for coming to these conclusions. Please do not underestimate the readers of this forum. They now have your viewpoint and mine. That’s all they need. Continuing to present your (or my) viewpoints only distracts from the subject. Unless that’s what you’re after, please stop saying the same thing over and over again. All information is already available to the readers to make their own choice.

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