The mercury/casein/gluten factor effect
on opioid peptides as a mechanism in causing autism,
schizophrenia, ADHD, MS, and other neurological conditions
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 MS.
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(15-23,36,47,51,90). For example, mercury has been found to strongly
inhibit the activity of xanthineoxidase and dipeptyl peptidase (DPP IV) which are required in the
digestion of the milk protein casein or wheat protein gluten
(15,16,17,19,20,91,23-26,90,92), 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
(15). 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(24,25,27),
and similarly for the corresponding enzyme needed to digest wheat
gluten(24,26). 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
(92). 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 (92). 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 BCM-7 is found in the blood(24-26).
BCM-7 appears to play a significant role in the aetiology of human diseases (92). 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 (92).
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 disfunction(24,25), as well
as being a direct histamine releaser in humans and inducing skin reactions
(14,21,25c). Similarly many also had a corresponding form of gluten protein
with similar effects(24,26). Elimination
of milk and wheat products and sulfur foods from the diet has been found to
improve the condition (40,28, etc.).
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 (28). 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 (29). As noted previously,
such populations of patients have also been found to have high levels of
mercury and to recover after mercury detoxification (23,11,30,40,91). As
mercury levels are reduced the protein binding is reduced and improvement in
the enzymatic process occurs (91,11,96).
A
mechanism in multiple sclerosis (MS) 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 (31,97). 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 (31). [
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 symptoms (97).]
Studies have also found heavy metals
to 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 (39,43,45-47,
63-65,89,97,91). 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 bind
cuprous ions (66), thus allowing buildup of copper to toxic levels in many
and malfunction of the Zn/Cu SOD function. Another large study (51)
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 P‑450
enzymatic process (67,89). Another study found accelerated lipofuscin deposition--consistent
with oxidative injury to autistic brain in cortical areas serving language
and communication (97). 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.
An IRB approved study
assessing urinary levels of porphyrins found an apparent dose-response
effect between autism severity and increased urinary coproporphyrins (68).
Mercury has been well documented to cause neurological, mood and behavioral problems
for children and others(8,9, etc.) Mercury also has additive and synergistic effects
with other toxic metals and toxins so lower exposure levels of each can produce
significant damage (9). Susceptibility factors also reduce
some people’s ability to detoxify mercury and other toxins, making some more
affected by toxic exposures.The papers discussed here show some of the ways
that mercury can cause or be a factor in autism and other neurological
conditions.
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