Susceptibility
factors in mercury toxicity: immune reactivity, detoxification system function,
enzymatic blockages, synergistic exposures. B. Windham(Ed.)
It is well documented in the medical
literature that the major factors in mercury toxicity effects, in addition to
dose, are susceptibility factors like
immune reactivity(1,2), degree of other toxic exposures and synergisms (3,15,27), systemic detoxification ability based on
blood allele type(4,15,27) or metallothionein
function(5), sulfur detoxification deficiencies(6), or other inhibited
enzymatic processes related to detoxification (7-10,27) or methylation
(27,28). It has been shown that such
susceptibility factors can play a larger role in effects than dose among a
population with significant exposure to mercury and at extremely low levels of
exposure. Toxic metals such as aluminum and lead have been documented to have synergistic effects with mercury,
increasing mercury effects significantly. Aluminum has its own toxic effects
plus increasing mercury effects by depleting glutathione.
Inherited defects or differences in
the body’s ability to detoxify can contribute to heavy metal accumulation (27,4,11,15,etc.). Deficiencies of certain minerals, vitamins, and amino acids reduce
the body’s ability to excrete toxins following exposure (27). Those
with the genetic allele ApoE4 protein in the blood have been found to detoxify
metals poorly and to be much more genetically susceptible to chronic
neurological conditions than those with types ApoE2 or
E3(4,11,15). Researchers
have shown that genetic carriers of the brain protein APO E2 are protected
against Alzheimer's disease (AD) whereas genetic carriers of the APO E4
genotype are at enhanced risk factor for developing AD and other degenerative
neurological conditions. APO E proteins are synthesized in the brain with the
assigned physiological task of carrying waste material from the brain to the
cerebrospinal fluid, across the blood brain barrier into the plasma where the
material is cleared by the liver. The biochemical difference between APO E2 and
APO E4 is that APO E2 has two additional thiol
groups, capable of binding and removing mercury (and ethyl mercury) that APO E4
does not have. The second highest concentration of APO E proteins is in the
cerebrospinal fluid. Therefore, the protective effects of APO E2 is due to its
ability to protect the brain from exposure to oxidants like mercury and ethyl
mercury by binding these toxicants in the cerebrospinal fluid and keeping them
from entering the brain.
Another
study found that polymorphisms in glutamyl-cysteine ligase and glutathione S-tranferases
genes modify mercury retention in humans exposed to elemental mercury vapor. Genotypes
with decreased GSH availability for mercury conjugation affect the metabolism
of inorganic mercury, increasing mercury retention (26). Similarly, many people
lack a Metallothionene related glutathione-S-Transferase gene called GSTM1 or have a related
polymorphism that appears to be key for proper functioning of the body’s own
natural detoxification mechanisms. This may explain
at least in part why some people develop the chronic health problems linked to
heavy metals while others who are similarly exposed do not. (31)
Recent studies found that prenatal mercury exposures from
mother’s amalgams and other sources along with susceptibility factors such as
ability to excrete mercury appear to be major factors in those with chronic
neurological conditions like autism and ADHD(11,15,20,27). Infants whose mothers received prenatal Rho D
immunoglobulin injections containing mercury thimerosal for RH factor or whose
mother’s 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 mother’s 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(12). Exposure to toxics such as mercury
have been found to inhibit enzymes needed to digest wheat gluten and milk
casein, resulting in symptoms of autism,
ADHD, diabetes, etc. after chronic exposure to gluten or casein. These
conditions commonly significantly improve after avoidance of gluten and
casein. Some cases of hypothyroidism are driven by immune
reactions to gluten in celiac disease (27) Genetic or toxic exposure related impairments
in methylation function ,
detoxification, clearance
of catecholamines, or in the clearance of adrenalin may
contribute to symptoms in autism or ADD/ADHD for those subjected to stress or inadequate
nutrition to overcome impairments(27). Prenatal and neonatal toxic exposures
also can cause leaky gut in infants; ‘Leaky gut’ in autism can promote toxic
burden in the body, as well as the development of food allergies(27) which have
been found to often be factors in
autism symptoms.
Studies have documented that
prenatal mercury exposure causes lasting effects that causes increased
susceptibility to future toxic exposures. The effects of chronic, low-dose
fetal and lactational organic (MeHgCl)
and inorganic (HgCl2) mercury intoxication on epilepsy/seizures were
investigated and compared in rats and were found to have significant
correlations between seizure susceptibility and cortical mercury level(16) Inorganic mercury exposure facilitated the
duration of seizure discharges in younger animals and appeared to be more
permanent than methyl mercury exposure.
Another researcher had similar findings for infants(17).
A
study of children of mothers consuming a marine diet which exposes them to
mercury, found that there are significant cardiovascular effects as birth
mercury blood level increases from 1 microgram per liter to 10 ug/L(a), as well as effects on
ability to respond to sensory stimuli in exposed children later in life(18). Children
with lower birth weights experienced blood pressure increases about 50% higher
than normal birth weight children having similar mercury levels. At seven years of age, clear
dose-response relationships were observed for deficits in attention, language,
and memory(b). Thus a levels
of exposure below current Government health safety limits, mercury is
documented to have significant cardiovascular effects and the recommended limit
for mercury has been decreased from the former limit of 10 ug/L
in blood.
Large studies of U.S. dentists and
dental assistants have found that mercury level in urine is significantly associated
with neurological dysfunction using several different measures, but that among
a population with low level mercury exposure those with a polymorphism in blood heme (CPOX4)
or to a polymorphism in neurofactor (BDNF) or to a functional
single nucleotide polymorphism (Val158Met) in the gene encoding the
catecholamine catabolic enzyme catechol O-methyltransferase
(COMT) were more susceptible to neurological effects or deficits(19). An
association in a population with low level mercury exposure between such
polymorphisms and mood disorders was found only for female dental assistants. The associations between a
polymorphism of the serotonin transporter gene (5-HTTLPR), dental mercury
exposure, and self-reported symptoms were evaluated among 157 male dentists and
84 female dental assistants. The
findings suggest that within this restricted population of mercury exposed
workers, increased symptoms of depression, anxiety, and memory are associated
with the 5-HTTLPR polymorphism among both males and females(19d).
Inherited impairments in methylation
or toxic related inhibition of functional methylation
by toxics such as mercury can have a dramatic effect on mood regulation and depression (27,28).
Genetic related or toxic exposure
related hormone imbalances
are documented to make people more susceptible to depression and anxiety disorders(27)
. Many patients with depression suffer from thyroid hormone imbalances that may
make them more treatment-resistant, or imbalances of DHEA or cortisol(27),
which can be related to genetic susceptibility or toxic exposures to toxics such as
mercury. Thyroid imbalances can
strain the adrenal glands; or adrenal imbalances can also disrupt normal
thyroid function; either making an individual more susceptible to depression or anxiety disorders(27).
Malabsorption in genetically or toxic related celiac disease can
interfere with mood regulating neurotransmitters and nutrients such as vitamin B12(27).
Inherited defects in detoxification
of environmental chemicals (as previously documented) may promote toxicity and fatigue in CFS, and inherited
tendencies toward inflammation and methylation
defects can exacerbate the chronic pain of fibromyalgia(27).
Exposures to heavy metal toxins can impair energy production and further burden
the detoxification system. Stress can
over time cause hormonal imbalances and deficiencies and leaky gut and malabsorption of essential nutrients either genetic or
related to toxic exposures can result in inability to detoxify harmful
substances and waste products(27), enabling chronic
conditions.
Chronic
exposure to toxic substances such as mercury can facilitate overgrowths of
pathogenic bacteria, viruses, and yeast(27), leading
to chronic conditions. Thyroid
imbalances related to genetic susceptibility or toxic exposures can strain
the adrenal glands; or adrenal imbalances in similar regards can disrupt normal
thyroid function(27).
Genetic
factors or toxic exposures that weaken the immune system can
result in increased
susceptibility to allergies and biological pathogens.
Inherited impairments in detoxification
function can also interact with environmental factors to promote multiple
chemical sensitivity(MCS) (27). Defects in the body’s
ability to neutralize environmental chemicals lead directly to the accumulation
of toxins, and the body’s ability to neutralize and excrete environmental
toxins depends on the availability of key nutrients(27).
Some cases of MCS may be secondary to ‘leaky
gut’ and the passage of toxins or food particles into the system. Arthritis
is an inflammatory condition also often secondary to ‘leaky gut’,which can be caused by toxic exposures, and to the
related passage of toxins or undigested food particles into the system(27).
Individuals with asthma often have an inherited predisposition to produce
excessive inflammatory mediators(27) or increased inflammatory cytokines
related to either prenatal or
later toxic exposures to toxics such as mercury.
Inherited defects in methylation or control of inflammation in the body or similar toxic related effects can
influence the course of heart disease(27)
Inherited risks associated with cardiovascular disease, obesity,
or estrogen metabolism may exacerbate Metabolic Syndrome, for which toxic exposures are also significant
factors. Metabolic Syndrome increases cardiovascular risk by
promoting hyperlipidemia, clot formation,
inflammation, and hypertension. Imbalances or deficiencies in key nutrients can
exacerbate metabolic imbalances in Metabolic Syndrome and prevent healing(27). High insulin levels in Metabolic Syndrome
contribute to oxidative stress by unstable free radicals in the body(27). As men age, declining testosterone may trigger
metabolic imbalances that promote insulin resistance with significant
differences depending on genetic factors and cumulative toxic exposures.
Although a study of mercury in children showed that females given the
same exposure as males excrete more mercury(30) and males
are more likely to have autism, another study found that females are two to
three times more likely to develop local (e.g., lichenoid
contact stomatitis) or systemic adverse health outcomes (e.g., skin disorders)
compared with males from prolonged exposure to mercury vapor from dental
amalgams(29). Moreover, given that inorganic mercury [Hg2+] binds
mainly to thiol ligands
[–SH] as homocysteine (Bridges and Zalups 2004), the
authors suggest that future clinical trials addressing the role of sex in mercury excretion should include an evaluation
of serum homocysteine, which is higher in males than
in females and might account for an increased tissue retention of mercury(29b). Toxic exposures can
facilitate dysbiosis (digestive problems) related to leaky
gut, chronic maldigestion, exposure to gut
pathogens, and/or suppression of protective microorganisms by toxic exposures(27).
Chronic imbalances in the intestinal flora can irritate the mucosa due
to poor diet or toxic exposures, allow the passage of toxins into the system,
weaken the immune system, etc(27). Many of the same underlying environmental
factors promoting dysbiosis in the colon can
encourage bacterial overgrowth in the delicate small bowel. Parasite
infestation occurs more easily with dysbiosis and
deficiencies of protective bacteria(27). ‘Leaky gut’ from intestinal irritants can
allow bacterial toxins to enter the system and promote skin inflammation such
as eczema(27). Identifying high levels of various gluten-associated antibodies is
an important first step in the diagnosis and correction of either genetic or
toxic related celiac disease(27).
Programmed
cell death (apoptosis) is documented to be a major factor in degenerative
neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. Some of the factors documented to be involved
in apoptosis of neurons and immune cells include mitochondrial membrane
dysfunction (22bc, 24). Mitochondrial DNA mutations or dysfunction is
fairly common, found in at least 1 in every 200 people(23),
and toxicity effects affect this population more than those with less
susceptibility to mitochondrial dysfunction.
Mercury depletion of GSH and damage to cellular mitochrondria
and the increased lipid peroxidation in protein and
DNA oxidation in the brain appear to be a major factor in conditions such as
autism, Parkinson’s disease, etc. (21-25).
The mechanisms by which low level
chronic mercury exposure causes over 30
chronic health conditions such as those looked at in this review are well
documented in the literature and differences in susceptibilities are documented
in all of these; and the fact that those treated for mercury toxicity usually recover after treatment
is also well documented by many dozens of medical studies in the literature and
thousands of clinical cases(13). Some
of the autoimmune conditions commonly
caused by immune reactivity to mercury include chronic fatigue syndrome(CFS), fibromyalgia, lupus, rheumatoid
arthritis, Parkinson’s,
multiple sclerosis (MS), amyotropic lateral
sclerosis(ALS), depression, autism, ADHD, eczema, asthma, etc.
(14,1,2,hyperlinks). People are
documented to vary significantly in immune reactivity to toxic substances and
susceptibility to these conditions(see hyperlinks).
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note: underlined or
shaded statements have hyperlinks to additional documentation that can be
reached by clicking on the link.