The Mercury/Casein/Gluten Factor Effect on Peptides as a Mechanism in Causing Autism, Schizophrenia, ADHD, & Other Neurological Conditions

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Mercury and toxic metals block 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, ADHD, and other neurological conditions.

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, 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 and 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 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 is yielded by the successive gastrointestinal digestion of bovine beta-casein variants A1 and B, but this was not seen in variant A2 or in goats’ milk. In milk with variant A1 of beta-casein, -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, mother’s dental amalgams, or other sources, higher levels of -7 is found in the blood. -7 appears to play a significant role in the etiology of human diseases. Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from 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 properties including immunosuppression, which for the specificity of the relation between the consumption of some but not all beta-casein variants and diabetes incidence.

-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 -7. The studies found high levels of IgA 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 protein with similar effects. Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition.

A double blind study using a potent opiate antagonist, naltrexone, 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.

A mechanism in multiple sclerosis occurs due to a reduction in immune system activity. Specifically, it is the reduction in the number of the suppressor T-cells within the immune system that allows CD4 helper T-cells to do damage. Thus, during an acute relapse the overall number of T-cells is reduced, the normal balance of helper and suppressor T-cells is disrupted, and helper T-cells tend to predominate. This is most pronounced during an acute relapse, but a similar situation occurs although perhaps to a lesser extent, in chronic progressive MS. Low dose naltrexone (LDN) has been found to commonly be effective in reducing MS symptoms and exerbations, apparently due its opioid suppressive effects. Chronic toxic exposures to toxics, such as mercury, are one documented factor that can cause such immune effects. Reducing chronic exposures and detoxification have been documented to commonly bring improvement in these conditions and in MS.

Studies have also found heavy metals to deplete glutathione and bind to protein-bound SH groups, resulting in inhibiting SH-containing enzymes and production of reactive oxygen species such as ion, hydrogen peroxide, and hydroxyl radical. In addition to forming strong bonds with SH and other groups like OH,NH2, and Clin 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, which normally binds 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 that with proper treatment, most recover.

Mercury has also been found to play a part in neuronal problems through blockage of the enzymatic process. Another study found accelerated 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.


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