Documentation of Common Cardiovascular
Health Effects from Mercury from Amalgam B. Windham (Ed)
Introduction.
Inflammation and inflammatory cytokines
have been found to be major factors in most cardiovascular conditions (598).
Measures of inflammation such as C-reactive protein and level of immune
cytokines have been found to be the best guides to assessing cardiovascular
health since these generate high levels of free radicals and lipid peroxidation chemicals.
Both organic and ionic mercury accumulates in the
heart and has been associated with elevated blood pressure, abnormal heart
rhythms such as, tachycardia and ventricular heart rhythms, and increased heart
attacks (125,276,10,19,20,59,205,348,539)(125,NAS,p.168 & 276,U.S.EPA,p.3-20). It is unknown to what extent cardiovascular
effects of mercury are due to direct cardiac toxicity or to indirect toxicity
caused by effects on the neural control of cardiac function (276). The
researchers believe that mercury promotes heart disease in several ways:
mercury promotes free radical generation; it inactivates the body's natural
antioxidant glutathione; and it binds with selenium thus making it unavailable
as an antioxidant and component of glutathione peroxidase;
it also affects All these mechanisms
would lead to an increased level of lipid peroxidation
and subsequent heart disease. The researchers also point out that earlier
studies have discovered a clear correlation between the number of amalgam tooth
fillings and the risk of heart attack. Selenium and vitamin E have both been
found to have a protective effect against mercury toxicity.
Numerous studies have reported tachycardia, high
blood pressure and heart palpitations after acute exposure to elemental mercury
vapor (19,571,etc.) A positive correlation was found
between heart palpitations and urinary Hg concentrations in workers from a chlor-alkali plant(538,276). In addition, tachycardia and
elevated blood pressure have been reported in numerous instances after children
were exposed to a broken thermometer or treated with medicines containing mercurous chloride, such as calomel containing teething
powder, worm medicine, or ammoniated mercury ointments used for diaper rash
(539). In children,
tachycardia associated with the inhalation of elemental mercury vapor might be
related to a non-allergenic hypersensitivity reaction to mercury(ATSDR,539f). It should be noted that
both blood and urine measure very recent exposures and are not reliable indicators
of mercury body burden or mercury toxicity, as in (539b).
A
recent review study found that toxic metals are a significant factor in
cardiovascular disease(571). Mercury, cadmium, and
other heavy metals have a high affinity for sulfhydryl
(-SH) groups, inactivating numerous enzymatic reactions, amino acids, and
sulfur-containing antioxidants (NAC, ALA, GSH), with subsequent decreased
oxidant defense and increased oxidative stress(13,571,581).
Oxidative stress and lipid peroxidation have been found to be factors in metabolic
syndrome and causes of inflammation(596,598). Both metals bind to metallothionein
and substitute for zinc, copper, and other trace metals reducing the
effectiveness of metalloenzymes(571,581). Mercury induces mitochondrial dysfunction with
reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common(13,571,581,303). Selenium antagonizes mercury
toxicity. The overall vascular effects of mercury include oxidative stress,
inflammation, thrombosis, vascular smooth muscle dysfunction, endothelial
dysfunction, dyslipidemia, immune dysfunction, and
mitochondrial dysfunction(571). The clinical
consequences of mercury toxicity include hypertension, CHD, MI, increased
carotid IMT and obstruction, CVA, generalized atherosclerosis, and renal
dysfunction with proteinuria. Pathological,
biochemical, and functional medicine correlations are significant and logical.
Mercury diminishes the protective effect of fish and omega-3 fatty acids.
Mercury, cadmium, and other heavy metals inactivate COMT, which increases serum
and urinary epinephrine, norepinephrine, and
dopamine. This effect will increase blood pressure and may be a clinical clue
to heavy metal toxicity. Cadmium concentrates in the kidney, particularly
inducing proteinuria and renal dysfunction; it is
associated with hypertension, but less so with CHD. Renal cadmium reduces
CYP4A11 and PPARs, which may be related to
hypertension, sodium retention, glucose intolerance, dyslipidemia,
and zinc deficiency. Dietary calcium may mitigate some of the toxicity of
cadmium.
Adverse cardivascular
effects have been associated with exposure to MeHg. A
retrospective study of cord-blood levels on 1000 children in the Faeroe Islands
at age seven who had been exposed prenatally to MeHg was conducted. After body weight adjustments, as the
cord-blood levels of MeHg increased from 1-10
micrograms/ liter, the diastolic and systolic pressures increased by 13.9 and
14.6 mm Hg. In boys, as cord-blood levels increased from 1-10 micrograms/liter
their heart rate variability decreased by 47%. Heart rate variability is a
reflection of cardiac autonomic control (308).
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(d).
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.
A cohort of 1833 Finnish men were followed over 7
years (201), to compare dietary intake of fish, and MeHg
concentrations in hair and urine with the incidence of cardiovascular disease.
All participants were free of clinical heart disease, stroke, claudication, and cancer at the onset of the study. Fish
intake correlated with hair Hg and daily urinary Hg excretions. Men who
consumed at least 30 grams of fish per day had a 2.1 fold greater risk of acute
myocardial infarction. For each additional 10 grams of fish consumed there was
an incremental 5% increase in the five-year risk of acute myocardial
infarction. The fish consumed by this
population was mostly fresh water fish, as differentiated from populations that
eat mostly fatty fish like salmon and tuna and may factors that factors that
partially counteract the effects of mercury(201c).
II. Mercury
Exposure from Amalgam
Amalgam has been well documented by peer-reviewed
studies, government studies, and scientific panels to be the largest source of
mercury in most people(580), including methyl mercury since
elemental and inorganic mercury are commonly methylated
in the body. But many also get
significant exposure to methyl mercury from fish, and ethyl mercury from
vaccines. The number of amalgam
surfaces has a statistically significant correlation to blood plasma mercury
level (17,22,23,49,79,89,133, 211) .
Much mercury in saliva and the brain is also organic (220,272,506),
since mouth bacteria and other organisms in the body methylate
elemental and inorganic mercury to organic mercury
(51,81,225,503b,506,512). Studies and
clinical tests have found amalgam to be the largest source of methyl mercury in
most people (506,220,79,386,580). Bacteria
also oxidize mercury vapor to the
water soluble, ionic form Hg(II) (431).
A clinical study found that methyl mercury in saliva is significantly
higher in those with amalgam fillings than those without, and correlated with
the number of amalgam fillings(506).
The average level of methyl mercury in the blood of a group with amalgam
was more than 4 times that of groups without amalgam or that had amalgam
replaced. Total mercury in those with
amalgams was over 10 times that of those without amalgam. Other studies have
found similar results(512,580).
As is known
from autopsy studies for those with chronic mercury exposure such as amalgam
fillings, in addition to accumulating in the brain, CNS, and hormone glands, mercury also bioaccumulates in the heart(59,85,205,348). Significant levels are able to cross the
blood brain barrier, placenta, and also cellular membranes into major organs
such as the heart since the oxidation rate of Hg0 though relatively fast is
slower than the time required by pumped blood to reach these organs(290,370).
Thus the level in the brain and heart is higher after exposure to Hg vapor than
for other forms(360,370). The upper level of
mercury exposure recommended by the German Commission on Human Biomonitoring is 10 micrograms per liter in the blood, but
adverse effects such as increases in
blood pressure and cognitive effects have been documented as low as 1 ug/L cord blood, with impacts higher in low birth weight
babies(308) and commonly in adults with
levels below 10 ug/l(540).
Effects of Mercury Exposure
Mercury vapor is lipid soluble and has an affinity
for red blood cells and CNS cells(21a).
Both
mercury and methyl mercury have been shown to cause depletion of calcium from
the heart muscle and to inhibit myosin ATPase
activity by 50% at 30 ppb(59), as well as reducing NK-cells in the blood and
spleen. The interruption of the
ATP energy chemistry results in high levels of porphyrins
in the urine(260) and stresses the major organs. The fractionated porphyrin test is approved by the FDA for diagnosis of mercury
toxicity. Mercury also inhibits aquaporin‑mediated
water transport in red blood cells(479a), and has been found to cause
significant heart damage(479b). Mercury
accumulates in all hormone glands and adversely affects hormonal function,
which controls all bodily processes, at very low levels of exposure.
Na(+),K(+)-ATPase is a transmembrane protein
that transports sodium and potassium ions across cell membranes during an
activity cycle that uses the energy released by ATP hydrolysis. Mercury is documented to inhibit Na(+),K(+)-ATPase function at very low levels of exposure(288).
Studies have found that in patients with mucoid angiopathy, endomyocardial
fibrosis and syndrome X there was a reduction in serum magnesium and
RBC membrane Na(+)-K+ ATPase activity (263,260d) and an elevation in plasma serum digoxin. This
inhibition leads to depletion of intracellular magnesium and an increase in
intracellular calcium load. This underlying magnesium-related insulin
resistance and the consequence of this intracellular magnesium and calcium
alteration in the pathogenesis of these disorders along with the inhibition of
Na+-K+ ATPase can result in 1) defective
neurotransmitter transport mechanism, 2) neuronal degeneration and apoptosis,
3) mitochondrial dysfunction, 4) defective golgi body
function and protein processing dysfunction.
It
is documented that mercury is a cause of most of these conditions
(13a,43,111,288,521b,263, etc.)
Mercury causes cardiovascular damage and disease:
including damage to vascular endothelial cells, damage to sarcoplasmic
reticula, sarcolemma, and
contractile proteins, increased white cell count, decreased oxyhemoglobin
level, high blood pressure, tachycardia, inhibits cytochrome
P450/heme synthesis(84,35,201,538,539), increased reactive oxygen
species(13,137), and increased risk of
acute myocardial infarction
(35,59,201,202,205,212,232,306,310,351,510,50/201,308).
Studies have demonstrated
that low concentrations of mercury(HgCl2,ie, 10(-9)-10(-15) M) significantly
enhanced chemiluminescence, as well as stimulated
H2O2 production by polymorphonuclear leukocytes(137).
These studies clearly demonstrate the ability of extremely low levels of HgCl2
not only to suppress various PMN
leukocyte functions involved in host defense, but also to stimulate
oxygen metabolism(137,13). In vivo, these HgCl2 effects would not only
compromise host defense but also promote tissue injury via the local production
of oxygen metabolites. This has been
demonstrated increase effects of factors in cardiovascular disease and
neurological disease. Melatonin, vitamin
E, and vitamin C have been found to partially alleviate these conditions(13a).
Mercury
has been found to accumulate in the pineal gland and reduce melatonin levels, which is thought to be
a significant factor in mercury’s toxic effects(569). Melatonin has found to
have a significant protective action against methyl mercury toxicity, likely
from antioxidative effect of melatonin on the MMC
induced toxicity(567).
Melatonin is documented to be effective at prevention of stroke and
cardiovascular damage, as well as seizures and other neurological damage in
patients that are prone to such conditions, and to be important in getting a
good nights sleep in patients with many chronic conditions, which is important
to both cardiovascular and neurological health(570).
Mercury
binds to hemoglobin oxygen binding sites in the red blood cells thus reducing
oxygen carrying capacity(232,35) and adversely affects the vascular response to norepinephrine and potassium. Mercury’s effect on pituitary
gland vasopressin is a factor in high blood pressure(35,201). Mercury also
increases cytosolic free calcium levels in
lymphocytes in a concentration-dependant manner causing influx from the extracellular medium(270c), and blocks entry of calcium
ions into the cytoplasm (16,17,21,33,35,333), and at 100 ppb can destroy the
membrane of red blood cells(35,22,17,270c) and damage blood vessels- reducing
blood supply to the tissues (34,202,306).
Amalgam fillings have been found to be related to higher blood pressure,
hemoglobin irregularities, tachycardia, chest pains, etc.
(201,202,205,212,222,306,310,35,59).
Mercury also accumulates in the heart and damages myocardial and heart
valves (Turpayev,in (35) & 59,201,205,306,351,370).
Mercury has been found to be a cause of
atherosclerosis, hypertension, and tachycardia in children and
adults(539,59,201, 205,306,308,538,539,35) and heart attacks in
adults(59,201,310).
Thyroid imbalances,
which are documented to be commonly caused by mercury
(369,382,459,35,50,91,212,10b), have been found to play a major role in chronic heart conditions such as
clogged arteries, myocardial infarction, and chronic heart failure(510). In a recent study, published in the Annals of
Internal Medicine, researchers reported that subclinical
hypothyroidism is highly prevalent in elderly women and is strongly and
independently associated with cardiac atherosclerosis and myocardial infarction(510c). People who tested hypothyroid usually have
significantly higher levels of homocysteine and
cholesterol, which are documented factors in heart disease. 50% of those testing hypothyroid, also had
high levels of homocysteine (hyperhomocysteinenic)
and 90% were either hyperhomocystemic or hypercholesterolemic(510a). These are also known factors in
developing atherosclerotic vascular disease. Homocysteine
levels are significantly increased in
hypothyroid patients and normalize with treatment(510efg).
Studies have also established a connection between subclinical maternal thyroid disease and babies born with
heart(509g), brain and neurological effects(509a-f), kidney defects,etc. Mercury reduces the bloods ability to
transport oxygen to fetus and transport of essential nutrients including amino
acids, glucose, magnesium, zinc and Vit B12 (43,55,96,198,263,264,338,339,
347,427); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake
, autoimmune thyroiditis, & hypothyroidism. (50,91,212,222,369,382,459,35).
Another study(59) found
such impairment of neutrophils decreases the body’s
ability to combat viruses such as those that cause heart damage, resulting in
more inflammatory damage. Another way
that mercury may cause cardiovascular conditions is through its adverse effects
on gum disease, which is known to cause inflammation and increased levels of
C-reactive protein(581). C-reactive protein is a known
marker for increased cardiovascular damage and disease(561),
along with fibrinogen and albumin. Researchers at Duke University Medical Center have discovered that otherwise healthy
people who are prone to anger, hostility and mild to moderate depressive
symptoms produce higher levels of C-reactive protein, a substance that promotes
cardiovascular
disease and stroke(562).
Mercury is documented to be a common cause of anger, hostility,
depression, and anxiety(564).
There are extensive documented cases (many
thousands) where removal of amalgam fillings led to cure or significant
improvement of serious health problems such as
tachycardia and heart problems
(205,35,59,94,115,212,222,232,233,271,306,310) ,blood and circulatory
conditions (212,222,232,233,271,523,35,95).
Other factors that have
been found to be significantly associated with cardiovascular disease include
daily consumption of soda drinks, diet drinks, fried foods, or a “Western Diet”
high in fried
foods, refined grains, fast foods, soda, etc. and low in fruits and
vegetables(590). These diet patterns all have been found to be significantly
associated with metabolic syndrome, a cluster of
cardiovascular disease and diabetes risk factors including elevated waist
circumference, high blood pressure, elevated triglycerides, low
levels of high-density lipoprotein (HDL or "good") cholesterol,
clogged arteries, and high fasting glucose levels. The presence of three or
more of the factors increases a person's risk of developing diabetes and
cardiovascular disease.
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