Documentation of Common Cardiovascular Health Effects from Mercury from Amalgam B. Windham (Ed)
Cardiovascular disease affects more people and causes more deaths each year than any other chronic condition. Atherosclerosis (buildup of plaque deposits in arteries) is the most common type of heart disease. Atherosclerosis is a significant factor in many types of cardiovascular disease: coronary heart disease (CHD), myocardial infarction (MI), angina pectoris, cerebral vascular disease (CVD), peripheral artery disease (PAD), thrombotic stroke, transient ishcmic attacks (TIAs), insufficient blood supply to lower limbs (claudication), organ damage, and vascular complications of diabetes.
Stroke is the third leading cause of death in the U.S. but millions also suffer silent strokes (TIAs) each year that cause memory loss, neurologic disorders, etc. Ischemic stoke is where a blood clot blocks the flow of oxygenated blood to a portion of the brain (83% of all strokes). The majority of these are related to atherosclerosis. Hemorrhagic stroke is where a blood vessel in the brain ruptures (17%). Irregular heartbeat and tachycardia is another common type of heart disease that has become more common. (580,584)
Other types of cardiovascular problems include hypertension, thrombosis, thrombocytopenia, peripheral artery disease (PAD), anemia, and Leukopenia. Hypertension is high blood pressure and may be caused by atherosclerosis or other factors including mercury toxicity. Supplementation with chlorella has been found to result in beneficial effects when used in patient’s chronic conditions such as hypertension, ulcerative colitis, or Fibromyalgia (304). Doctors such as D. Klinghardt (303) have suggested that the mechanism by which chlorella improves treatment of such conditions is metals detoxification, which is the main mechanism of action of chlorella and has been found to greatly improve intestinal function.
Factors underlying atherosclerosis include inflammation, free-radical assault, nutrient deficiency, “thick blood”, and ability to activate B vitamins such as vit B12 and vit B6. (30) Plaque buildup in arteries can cause dying of heart muscle cells, weakening of the heart muscle, irregular heartbeat, angina, etc. Vit C is an essential factor in building and maintaining collagen and elastin, primary factors in connective tissues, so Vit C deficiency is a major factor in leaking veins and plaque buildup. Supplementation with vit C has been found to significantly reduce such plaque buildups and leaking veins(30ab). Other factors in cardiovascular disease include imbalances of Lipoprotein A, C-reactive protein, Homocysteine, and Fibrinogen. See the section on treatment of cardiovascular conditions for more factors and tests to determine which factors need consideration.
Anemia is a decrease in the number of red blood cells. Anemia can be related to iron deficiency, Vitamin B12 deficiency, folate deficiency, etc. When one of these factors is present, supplementation can often resolve the problem, though B12 deficiency can also be related to reduced ability to absorb B12. In this case weekly injections may be required. Methylcobalamin is the preferred form of B12. Thrombosis is an abnormal blood clot inside a blood vessel, causing an obstruction of blood flow. Thrombocytopenia is usually microvascular leakage with platelet aggregation, often induced by drugs. Leukopenia is an abnormal decrease in the number of white blood cells. Chronic mercury exposure such as from amalgam dental fillings commonly has significant effects on levels and function of both red and white blood cells(35,303) and reduction of mercury exposure often results in improvement of these conditions. Peripheral artery disease (PAD) is a lesser-known condition marked by blockages in the arteries leading to your extremities, most commonly your feet and legs. The damaging process begins when low-density lipoprotein cholesterol (commonly known as LDL or “bad cholesterol”) encounters free radicals on the walls of your arteries. Free radicals are a factor in most chronic inflammatory process—and the development of atherosclerosis is no exception. When the production of free radicals exceeds your body’s ability to remove them—a condition that can result from stress, smoking, drugs, environmental toxins, and even extreme sports—it results in oxidative stress. Unstable free radicals meeting with LDL cholesterol in the lining of arteries, causes a reaction called lipid peroxidation. The constant inflammatory assault that takes place at the site of these lesions can eventually take its toll on the fibrous cap that the immune system forms to keep it intact. Macrophages will secrete enzymes that weaken the cap, which can cause it to rupture—and once ruptured, platelets will be activated, causing thrombosis (the formation of a clot). In cases of advanced atherosclerosis, coronary arteries have become significantly narrowed over the years, allowing a clot to block blood flow to the heart—resulting in cell death (known as myocardial infarction) and heart failure. Likewise, a clot in your neck can block blood flow to your brain, resulting in a stroke. Lastly, the potential exists for embolism, in which the clots break off to enter your circulation, where they can obstruct blood flow to any number of your vital organs. All of these risks are increased by a condition known as hyperviscosity or hypercoagulation—an innate tendency toward clotting. Certain blood markers can reveal this condition: High levels of the amino acid homocysteine or excess fibrinogen- a protein that plays a key role in your body’s clotting mechanisms , have been linked to hypercoagulation. Any of these conditions if untreated commonly lead to other degenerative conditions or can lead to death. (580)
The primary risk factors that have been identified for cardiovascular disease are: elevated inflammation, elevated oxidative stress, mitochondrial dysfunction, C-Reactive Protein, elevated fibrinogen, elevated homocysteine, elevated Lipoprotein(a), elevated LDL cholesterol/low HDL cholesterol, elevated triglycerides, hyperinsulinemia (excess insulin), low testosterone levels in men (580). Anyone concerned about cardiovascular health should periodically get a blood test to monitor the levels of these risk factors, which all can be significantly controlled or improved by avoidance of toxic exposures, diet and supplementation. As will be seen in this paper, toxic metal exposure is a significant factor in cardiovascular disease, causing inflammation and oxidative damage to the cardiovascular system and increases in the noted risk factors.
The personal risk factors of cardiovascular disease, like smoking, alcohol consumption, a diet high in saturated fat and cholesterol, sedentary life style, obesity, glucose intolerance and diabetes, and high salt intake have been extensively studied as contributors to the vascular diseases of the heart, brain and peripheral circulation but can be controlled by lifestyle decisions.
Inflammation and inflammatory cytokines such as Tumor Necrosis Factor Alpha (TNFa), interleukin 1b (Il-1b), and interleukin 6 (Il-6) have been found to be major factors in most cardiovascular conditions (580,598). Measures of inflammation such as C-reactive protein, fibrinogen, homocysteine, 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. Excess insulin levels (hyperinsulinemia) has been found to be a significant risk factor for cardiovascular disease, and causes reactive hypoglycemia due to blood glucose deficiency, causing chronic hunger feeling and is a factor in why obese people do not lose weight.
II. Mercury, toxic metals, and cardiovascular disease
Amalgam fillings, which vaporize continuously in the mouth since mercury is a vapor at room temperature, are the largest source of mercury in most people, and exposure is to mercury vapor, inorganic mercury, and organic mercury since oral bacteria methylate inorganic mercury to methylmercury. Mercury is extremely toxic, and both mercury vapor and methylmercury readily cross the blood-brain barrier. Susceptibility factors are a major reason that some are damaged much more severely by mercury exposure than others. Some examples which affect one’s toxicity protection systems are Apolopoprotein blood allele type, mutations of the protective SOD1 gene, and mutations of the MTHFR gene. Person’s with APO-4 type allele or a mutated form of SOD1 or MTHFR are affected more and more rapidly to mercury exposure. And exposures to EMF or microwaves or wi-fi cause higher exposure to mercury for those with amalgam fillings, which increases exposure and damage.
Both ionic and organic mercury accumulate in the heart and has been associated with elevated blood pressure, abnormal heart rhythms including tachycardia and ventricular heart rhythms, and increased heart attacks (125,276,10,19,20,59,205,303,348,539,571) [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; All these mechanisms would lead to an increased level of lipid peroxidation and subsequent heart disease. The researchers also point out that 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. Mercury has also been found to promote overgrowths of pathogens including bacteria and viruses that are known to damage the heart (303,577).
The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, increased carotid IMT and obstruction, cerebrovascular accident, generalized atherosclerosis, and renal dysfunction with proteinuria (539,541,571a, etc.). Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation and oxidative stress. The endothelial lipid signaling enzyme, phospholipase D (PLD), which is an important player in the endothelial cell (EC) barrier functions. All three forms of mercury (inorganic mercury, methyl mercury, and thimerosal significantly activated pulmonary artery endothelial cells in a dose-dependent and time-dependent fashion(571c). Metal chelators significantly attenuated mercury-induced PLD activation, suggesting that cellular mercury-ligand interaction(s) is required for the enzyme activation a nd that chelators are suitable blockers for mercury-induced PLD activation. Sulfhydryl (thiol-protective) agents and antioxidants also significantly attenuated the mercury-induced PLD activation. All the three different forms of mercury significantly induced the decrease of levels of total cellular thiols. Methylmercury also activates the lipid signaling enzyme phospholipase A2 (PLA2) in vascular endothelial cells (ECs), causing upstream regulation of cytotoxicity. Methylmercury also induced the loss of thiols and increase of lipid peroxidation in BPAECs. (571d)
Numerous studies have reported tachycardia, high blood pressure and heart palpitations after acute exposure to elemental mercury vapor (19,571,538,539,541, 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, elemental mercury vapor, mercury in vaccines, or treated with medicines containing mercurous chloride, such as calomel containing teething powder, worm medicine, or ammoniated mercury ointments used for diaper rash (539,541,542). 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).
KAWASAKI DISEASE IS THE LEADING CAUSE of acquired heart disease in children in the developed world. Kawasaki disease is an acute systemic vasculitis that primarily affects children under 5 years of age. Many patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls (542). Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day (542).
Recent review studies found that toxic metals are a significant factor in cardiovascular disease (571,573). 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 (13,571,576). Such metal exposures are common and have additive or synergistic effects. 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 (571,576). Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common (13,571,576,303). 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).
A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings (more mercury exposure) have significantly higher levels of chronic health conditions(543a). A 2009 study found that inorganic mercury levels in people have been increasing rapidly in recent years(543b). It used data from the U.S. Centers for Disease Control and Prevention’s National Health Nutrition Examination Survey (NHANES) finding that while inorganic mercury was detected in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006. Surveys in all states using hair tests have found dangerous levels of mercury in an average of 22 % of the population, with over 30% in some states like Florida and New York(543c).
III. High levels of Mercury Exposure from Dental Amalgam
Dental amalgam has been documented by peer-reviewed studies, government studies, and scientific panels to be the largest source of mercury in most people (575), 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 (506,220,79,386,575). 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 (512,575).
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 on the Cardiovascular System
A recent review study reviewed previous studies of mercury effects on the cardiovascular system and found mercury to be one of the most common causes of many types of cardiovascular conditions (573). Mercury has a high affinity for sulfhydryl groups, inactivating numerous enzymatic reactions, amino acids, and sulfur-containing antioxidants (N-acetyl-L-cysteine, alphalipoic acid, L-glutathione), with subsequent decreased oxidant defense and increased oxidative stress. Mercury binds to metallothionein and substitute for zinc, copper, and other trace metals, reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in adenosine triphosphate, depletion of glutathione, and increased lipid peroxidation. Increased oxidative stress and reduced oxidative defense are common. Selenium and fish containing omega-3 fatty acids antagonize mercury toxicity. The overall vascular effects of mercury include increased oxidative stress and inflammation, reduced oxidative defense, thrombosis, vascular smooth muscle dysfunction, endothelial dysfunction, dyslipidemia, and immune and mitochondrial dysfunction. The clinical consequences of mercury toxicity include hypertension, coronary heart disease, myocardial infarction, cardiac arrhythmias, reduced heart rate variability, increased carotid intima-media thickness and carotid artery obstruction, cerebrovascular accident, generalized atherosclerosis, and
renal dysfunction, insufficiency, and proteinuria. Pathological, biochemical, and functional medicine correlations are significant and logical. Mercury diminishes the protective effect of fish and omega-3 fatty acids. Mercury inactivates catecholaminei-0-methyl transferase, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to mercury-induced heavy metal toxicity. Mercury toxicity should be evaluated in any patient with hypertension, coronary heart disease, cerebral vascular disease, cerebrovascular accident, or other vascular disease. Specific testing for acute and chronic toxicity and total body burden using hair, toenail, urine, and serum should be performed.(573)
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(539,541), tachycardia(539), 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 (539,541), hemoglobin irregularities, tachycardia (539), 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 (539,541), and tachycardia (539) in children and adults (59,201, 205, 306,308,538,571,35) 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,511).
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 by mercury decreases the body’s ability to combat viruses or bacteria such as those that cause heart damage, resulting in more inflammatory damage. Clinical experience has found that mercury exposure increases susceptibility to pathogen infections, including those that adversely affect the heart(303), and that such infections cannot be controlled of eliminated without reducing mercury levels. 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(572,576). 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 and other research 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 and/or mercury detoxification led to cure or significant improvement of serious health problems such as tachycardia and heart problems (205,35,59,94,115,212,222,232,233,271,306,310,539,541,571), blood and circulatory conditions (212,222,232,233,271,523,35,95).
V. Other factors in Cardiovascular Disease and Beneficial Treatments
Some drugs that can cause cardiac arrest include codeine, hydrocodone, oxycodone, viagra, triptan drugs for migraine, and diuretics. S
Inflammation, free-radical assault, nutrient deficiency, and “thick blood” are factors underlying cardiovascular disease, affecting levels of Lipoprotein A, “high sensitivity C-reactive protein, homocysteine, and fibrinogen- which are factors/indicators of heart disease that can be tested for through blood tests. (30) High cholesterol is the body’s defense against some of these other factors, and reducing cholesterol without dealing with the real underlying problem can be counterproductive and dangerous. (30) Statin drug use depletes the vital heart nutrient CoQ10, so anyone taking Statins should also take CoQ10. Likewise, Red Yeast Rice has similar effects as statins, but less dangerous side effects, but also requires additional CoQ10 supplementation. (30)
Fish oil (DHA, EPA), DHEA, and vitamin K have been documented to suppress inflammatory cytokines, TNFa, Il-1b, and Il-6, reducing inflammatory effects (580,30). Green tea, ginkgo biloba, garlic, vitamin E, vitamin A, lumbrokinase, nattokinase, L-carnitine, hawthorn, forskolin, and beta-carotene have been found to lower fibrinogen levels and lower cardiovascular risk levels (580,581,30). Excess homocysteine blocks the natural breakdown of fibrinogen. Elevated homocysteine can be reduced through the remethylation process [tri-methyl glycine(TMG), vitamin B12, folic acid, garlic] or the trans-sulfuration process(vitamin B6). Methionine is the only amino acid that creates homocystiene, so people who eat a lot of methionine foods such as red meat, chicken, dairy products need more vitamin B6. The level of supplementation can be determined by blood tests to see if risk factors are under control. In people with elevated fibrinogen levels, high levels of fish or olive oil and vitamin C (=>2000 mg) have been found to break down excess fibrinogen levels (580). CRP levels can be reduced by supplementing with natural vit E, fish oil, CoQ10, and ginger(30). Vitamin C, hawthorn, and CoQ10 have also been found to be effective in reducing the effects of congestive heart failure (CHF) and other types of cardiovascular conditions. Ginger appears to increase the contractile strength of the heart and to increase ATP energy production in the heart. (580) Studies have found that policosanol supplemenatation decreases LDL cholesterol and increases HDL. Choline, lecithin, and creatine have been found to have beneficial effects on cholesterol levels. L-arginine promotes vasodilation, maintaining both healthy blood pressure and regulating angina symptoms and taurine lowers the risk of abnormal clots and regulates heartbeat). (581cd) Padma Basic is a combination of many of these natural substances that has been found to be effective at reducing factors involved in cardiovascular disease (581). Pantethine (B5) is useful to increase the good cholesterol, HDL. Fiber from foods or psyllium binds cholesterol, but psyllium should be taken 2 hours away from medications (30).
Hyperinsulinemia is extremely common, especially in overweight individuals, and a significant factor in cardiovascular disease and type 2 diabetes. (580) High insulin levels deplete glucose levels in the blood, causing”reactive hypoglycemia” which prevents breakdown of fat cells . This can bring about a condition where the individual is constantly “hungry” (low in blood glucose) making it difficult to lose weight. Consuming foods high in glycemic index is a factor in this. Studies indicate that attention should be given to consuming foods primarily low in glycemic index and regular exercise. Low testosterone level in men has also been found to be a risk factor of cardiovascular disease, causing higher levels of cholesterol, fibrinogen, triglycerides, and insulin, along with abdominal fat increases, human growth hormone decreases, blood pressure increase. (580) DHEA is a precurser hormone of testosterone produced by the adrenal glands. Low levels of DHEA have been to be significantly related to heart disease.
Thrombosis causes can include atherosclerosis; injury to endothelial cells lining the heart, arteries, veins; blood hypercoagulability, excess fibrinogen, excess platelet aggregation (580,581). As previously noted, mercury and toxic metals can be a factor in some of these conditions and improvement commonly occurs after treatment for mercury toxicity. For cardiovascular conditions related to atherosclerosis, etc. EDTA chelation has been found to usually be a safe and significantly beneficial treatment (585)
Aspirin or blood thinning drugs are often used to reduce platelet aggregation to prevent thrombosis or strokes. Polycosanol, aged garlic, and niacin have been found to improve cholesterol balance safely and can be beneficial in alleviating or preventing cardiovascular disease. (580) Natural platelet aggregation inhibitors include ginkgo biloba, EFAs, Vitamin E (tocopherol). Anti-Inflammatories that have been found beneficial include: curcumin, DHEA, Nettle leaf. Antioxidants that have been found beneficial in thrombosis prevention include quercetin, green tea, lycopene, grape juice. N-acetyl-L-cysteine, onions, and exercise have also been found beneficial (580). Other heart healthy nutrients include D-ribose, L-Carnitine, Flaxseed, and L-Arginine (30).
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, excitotoxins such as MSG and aspartame, and diet low in fruits and vegetables(590,597). 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. An elevated hemoglobin HbA1c level has been found to increase risk of cardiovascular related problems and deaths, and this test can be useful in assessing risk.(580) Avoiding processed food and food cooked at high temperatures, and consuming nutrients that block damaging glycation reactions such as carnosine, benfotaine, and pridoxamine reduce A1c levels. Good dietary habits and regular exercise have been found to reduce cardiovascular problems and promote cardiovascular health. (30,580) Highly colorful vegetables and use of coconut and coconut oil are part of a heart healthy diet.
Higher levels of vit D reduce heart attacks and strokes, and supplementation with Ginko Biloba may also reduce strokes (580) and improve recovery. EGCG extract from green tea or theaflavins from black tea have also been shown to have a significant protective effect in reducing inflammation and preventing cardiovascular disease(580). Studies have shown theaflavin supplementation significantly reduces levels of inflammatory cytokines such as TNF-alpha, Il-6, Il-8, and C-reactive protein; and lowered rates of production of inflammation-generating trasnscription factor NF-kB, cytokine generating COX-2, and the adhesion molecule ICAM-1. Theaflavin supplementation or drinking multiple cups of tea has also been found to have beneficial effects to prevention of ischemia-reperfusion injury following strokes as well as in reduction of LDL cholesterol and endothelial vasomotor dysfunction in patients with coronary artery disease (580).
Normal aging usually involves calcification in soft tissues throughout the body, such as heart valves, glands, and blood vessels. A calcium deficient diet increases such calcification. Atherosclerosis is the leading cause of disability and death. Homocysteine or oxidized LDL cholesterol are two factors that increase such damage. Studies show that insufficient vitamin K2 accelerates arterial calcification and vitamin K2 supplementation can reverse such arterial calcification (580). Studies also have found that emotional factors such as chronic anxiety, anger, or depression as well as insufficient sleep promote inflammation and cardiovascular disease, and that measures that decrease these are beneficial to cardiovascular health (562). Melatonin supplementation has been found to be beneficial to promoting sleep and benefitting the heart (563).
(1)American Heart Association. Women and Coronary Heart Disease, www.americanheart.org/presenter.jhtml?identifier=2859 ?
(10) Maine Dept. of Environmental Protection, 2006, www.maine.gov/dep/air/toxics/mercury.htm;? & Dr Klaus Toepfer, executive director, United Nations Environment Programme(UNEP), Mercury Health Effects More Widespread than Previously Believed, 4 February, 2003, http://news.bbc.co.uk/2/hi/science/nature/2722629.stm ; & Univ. of Minnesota, Environmental and Occupational Health, http://www1.umn.edu/eoh/hazards/hazardssite/mercury/merchealtheffects.html
(13)(a) Metals, toxicity and oxidative stress. Valko M, Morris H, Cronin MT. Curr Med Chem. 2005;12(10):1161-208, & (b) P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & (c)Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36 ; & (d)D.Jay, “Glutathione inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998,68(6):457-61; & S.Hussain et al, “Mercuric chloride induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci Health B 1997 May;32(3):395 409;
(16) K. Ott et. al. “Mercury burden due to amalgam fillings” Dtsch. Zahnarztl Z 39(9):199 205, 1984; & Lichtenberg H, "Mercury vapor in the oral cavity in relation to number of amalgam surfaces and the classic symptoms of chronic mercury poisoning", J Orthomol Med (1996), v11, n.2, 87-94
(17) J.Abraham,C.Svare, et al. “The effects of dental amalgam restorations on Blood Mercury levels”. J. Dent.Res. 1984; 63(1):71 73; & Snapp KR, Boyer DB, Peterson LC, Svare CW, "The contribution of dental amalgam to mercury in blood", J Dent Res 1989 May;68(5):780-5
(19) Trakhtenberg, IM. Chronic Effects of Mercury on Organisms: The Micromercurialism Phenomenon on Mercury Handlers. Chap. VI:109-34, DHEW Publ. No. (NIH) 74-473, 1974, & Mercury: Cardiovascular Adverse Effects,
(20) (a)M.J.Vimy,Takahashi,Y, Lorscheider,FL Maternal Fetal Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine and Medical Physiology , faculty of Medicine, Univ. of Calgary, Calgary Alberta Canada, 1990 , Amer.J.Physiol.,1990, 258:R939-945; & (b) L.Hahn et al, Distribution of mercury released from amalgam fillings into monkey tissues”, FASEB J.,1990, 4:5536; &(c)Takahashi Y, Tsuruta S, Hasegawa J, Kameyama Y, Yoshida M. Release of mercury from dental amalgam fillings in pregnant rats and distribution of mercury in maternal and fetal tissues. Toxicology 2001 Jun 21;163(2-3):115-26; & Galic N, Ferencic Z et al, Dental amalgam mercury exposure in rats. Biometals. 1999 Sep;12(3):227-31; & Danscher G, Horsted-Bindslev P, Rungby J.,Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol. 1990 Jun;52(3):291-9 & Fredin, B. The Distribution of Mercury in Various Tissues of Guinea Pigs After Application of Dental Amalgam Fillings. Sci Total Environ., 66:263-8, 1987: & Hahn, LJ; et al. Dental "silver " tooth fillings: a source of mercury exposure revealed by whole body scan and tissue analysis. FASEB J, 3:2641-6, 1989.
(21) R.A.Goyer,”Toxic effects of metals”in: Caserett and Doull’s Toxicology- TheBasic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; &(b) Goodman, Gillman, The Pharmacological Basis of Therapeutics, Mac Millan Publishing Company, N.Y. 1985; &(c) Encyclopedia of Occumpational Health and Safety, International Labour Office, Geneva, Vol 2, 3rd Edition.;&(d) Arena, Drew, Poisoning. Fifth Edition. Toxicology-Symptoms-Treatment, Charles C. Thomas-Publisher, Springfield, Il 1986.
(22) P.Kuhnert et al, “Comparison of mercury levels in maternal blood fetal cord blood and placental tissue”. Am. J. Obstet and Gynecol.,139:209 212., 1981; & Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M, "Longitudinal study of methyl mercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood", Environ Res 2000 Oct;84(2):186-94.
(23) W.D.Kuntz “Maternal and chord blood mercury background levels; Longitudinal surveillance”. Am J Obstet and Gynecol. 143(4): 440 443., 1982; & (b) Ramirez GB, Cruz MC, Pagulayan O, Ostrea E, Dalisay C. The Tagum study I: analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants' hair. Pediatrics 2000 Oct;106(4):774 81.
(30) The 24 Hour Pharmacy, S. Cohen, R. Ph., 2008; & (b) Dr. Matthias Rath, Why Animals Don’t Get Heart Attacks, and People Do, MR Publishing, 2003.
(33) Markovich et al, "Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat 1", Toxicol Appl Pharmacol, 1999,154(2):181 7; & S.A. McFadden, “Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways”,Toxicology, 1996, 111(1-3):43-65;
(35) Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc. & autoimmune conditions (MS,arthritis, diabetes, Lupus, Parkinson’s, Alzheimer’s, Leukemia, etc. )
(43) B.Rajanna et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997 Dec 19;272(51):32411-8., & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha lactalbumin”.Biochem Mol Biol Int 1996 Aug;39(6):1255 65;
(50) Sin YM, Teh WF, Wong MK, Reddy PK - "Effect of Mercury on Glutathione and Thyroid Hormones" Bulletin of Environmental Contamination and Toxicology 44(4):616-622 (1990); & (b) J.Kawada et al, “Effects of inorganic and methyl mercury on thyroidal function”, J Pharmacobiodyn, 1980, 3(3):149-59; & (c) Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci 1992, 5(3): 236-40; &(d) Goldman, Blackburn, The Effect of Mercuric Chloride on Thyroid Function of the Rat, Toxicol and Applied Pharm 1979, 48: 49-55; &(e)Kabuto M - "Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress" Arch Toxicol 65(2):164-7 (1991) ; & Assoc. for Birth Defect Children, Birth Defect News, March 2001; (? add topic title)
(51) Heintze et al,“Methylation of Mercury from dental amalgam and mercuric chloride by oral Streptococci”.,Scan. J. Dent. Res. 1983, 91:150 152: & Rowland, Grasso, Davies “The Methylation of Mercuric Chloride by Human Intestinal Bacteria”. Experientia. Basel 1975 ,31: 1064 1065; & M.K.Hamdy et al, “Formation of methyl mercury by bacteria”, App Microbiol, 1975, Sept.; & W.Forth, “Toxikologie von Quecksilberverbindungen”, in Quecksilber in der Umwelt-Hearing zur Amalgamprolematik, Niedersachsisches Umweltministerium, 1991.
(55) Mercury and food intolerances: common causes of chronic conditions related to leaky gut and intestinal dysfunction such as ulcerative colitis, IBS, Crohn’s, eczema, psoriasis, food allergies, arthritis, ADHD, and autoimmune disease; and treatments that improve these conditions. www.flcv.com/leakyghg.html
(59) A. Frustaci et al, “Marked elevation of myocardial trace elements in Idiopathic Dilated Cardiomyopathy”, J of American College of Cardiology, 1999, 33(6):1578-83; & (b)Husten L. “Trace elements linked to cardiomyopathy”, Lancet 1999; 353(9164): 1594; &(c) D.V. Vassalo, 1999, Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine”, Toxicol Appl Pharmacol 1999 Apr 15;156(2):113 8; & (d)N.G. Ilblack et al, “New aspects of murine coxsackie B3 mycocarditis: focus on heavy metals”, European Heart J, 1995, 16: supp O: 20-4; & (e)Dahhan, Orfaly, Electrocardiogrphic Changes in Mercury Poisoning, Amer J of Cardiology, Aug, 1964; & (f)Lorscheider F, Vimy M. Mercury and idiopathic dilated cardiomyopathy. J Am Coll Cardiol 2000 Mar 1;35(3):819 20; & (g)Souza de Assis GP, et al; Effects of small concentrations of mercury on the contractile activity of the rat ventricular myocardium. Comp Biochem Physiol C Toxicol Pharmacol. 2003 Mar;134(3):375-83.
(79) L.Bjorkman et al, "Mercury in Saliva and Feces after Removal of Amalgam Fillings", Toxicology and Applied Pharmacology, 1997, 144(1), p156-62; & Eur J Oral Sci 1998 Apr;106(2 Pt 2):678-86 (b) J Dent Res 75: 38-, IADR Abstract 165, 1996.
(81) L.I.Liang et al, "Mercury reactions in the human mouth with dental amalgams" Water, Air, and Soil pollution, 80:103-107.
(84) J.C.Veltman et al, “Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland”, Arch Biochem Biophys, 1986, 248(2):467-78; & A.G.Riedl et al, Neurodegenerative Disease Research Center, King’s College, UK, “P450 and hemeoxygenase enzymes in the basal ganglia and their role’s in Parkinson’s disease”, Adv Neurol, 1999; 80:271-86; & Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance. J. Orthmol. Med. v6#2 pp67-77 (1991).; & Salonen JT. Excessive intake of iron and mercury in cardiovascular disease. In: Sandströöm B, Walter P, eds. Role of Trace Elements for Health Promotion and Disease Prevention, p. 112-126. Basel: Karger, 1998. Bibliotheca Nutritio et Dieta 54.
(85) J.A.Weiner et al,“The relationship between mercury concentration in human organs and predictor variables", Sci Tot Environ, 138(1-3):101-115,1993; & (b) Long-term effects of elemental mercury on renal function in miners of the Idrija Mercury Mine. Franko A, Budihna MV, Dodic-Fikfak M. Ann Occup Hyg. 2005 Aug;49(6):521-7.
(89) Berglund A, Molin M, "Mercury levels in plasma and urine after removal of all amalgam restorations: the effect of using rubber dams", Dent Mater 1997 Sep;13(5):297-304 ; & M.Molin et al, "Kinetics of mercury in blood and urine after amalgam removal", J Dent Res 74:420, IADR Abstract 159, 1995; & (b) M.Molin et al, “Mercury, selenium, And GPX before & after amalgam removal”, Acta Odontol Scand, 1990,48:189-202
(91) B.Lindqvist et al, "Effects of removing amalgam fillings from patients with diseases affecting the immune system", Med Sci Res 24(5): 355-356, 1996.
(94) F.Berglund, Case reports spanning 150 years on the adverse effects of dental amalgam, Bio-Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured); & Tuthill JY, "Mercurial neurosis resulting from amalgam fillings", The Brooklyn Medical Journal, December 1898, v.12, n.12, p725-742
(95) Lichtenberg, HJ "Elimination of symptoms by removal of dental amalgam from mercury poisoned patients” J Orthomol Med 8:145-148, 1993; & Lichtenberg H, "Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals", Journal of Orthomolecular Medicine,1996, 11(4): 195-203. (119 cases) www.lichtenberg.dk/experience_after_amalgam_removal.htm
(96) Goyer RA, National Institute of Environmental Health Sciences. Toxic and essential metal interactions. Annu Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity. Am J Clin Nutr 1995; 61(Suppl 3): 646S-650S; & Goyer RA et al, Environmental Risk Factors for Osteoporosis, Envir Health Perspectives, 1994, 102(4): 390-394; ; & Lindh U, Carlmark B, Gronquist SO, Lindvall A. Metal exposure from amalgam alters the distribution of trace elements in blood cells and plasma. Clin Chem Lab Med 2001 Feb;39(2):134 142. ; & A.F.Goldberg et al, “Effect of Amalgam restorations on whole body potassium and bone mineral content in older men”,Gen Dent, 1996, 44(3): 246-8; & K.Schirrmacher,1998, “Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells”, Calcif Tissue Int 1998 Aug;63(2):134 9..
(111) (a) Quig D, Doctors Data Lab,"Cysteine metabolism and metal toxicity", Altern Med Rev, 1998;3:4, p262 270, & (b) J.de Ceaurriz et al, Role of gamma glutamyltraspeptidase(GGC) and extracellular glutathione in dissipation of inorganic mercury",J Appl Toxicol,1994, 14(3): 201 ; & W.O. Berndt et al, "Renal glutathione and mercury uptake", Fundam Appl Toxicol, 1985, 5(5):832 9; & Zalups RK, Barfuss DW. Accumulation and handling of inorganic mercury in the kidney after coadministration with glutathione, J Toxicol Environ Health, 1995, 44(4): 385-99; & T.W.Clarkson et al, "Billiary secretion of glutathione metal complexes", Fundam Appl Toxicol, 1985, 5(5):816 31;
(125) National Research Council, Toxicological Effects of Methyl mercury (2000), pp. 304 332: Risk Characterization and Public Health Implications, Nat'l Academy Press 2000.; & U.S. CDC, National Center for Environmental Health , National Report on Human Exposure to Environmental Chemicals, 2001, www.cdc.gov/nceh/dls/report/Highlights.htm
(133) M.Molin et al, "Mercury in plasma in patients allegedly subject to oral galvanism", Scand J Dent Res 95:328-334, 1987.
(137) Effects of mercury on human polymorphonuclear leukocyte function in vitro. Contrino J, Marucha P, Bigazzi PE, et al, Am J Pathol. 1988 Jul;132(1):110-8.
(198) E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853;& B.R.G.Danielsson et al,”Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus”, Biol Res Preg Perinatal. 5(3):102-109,1984;
(201) Virtanen JK, Voutilainen S, Salonen Jt et al. Mercury, Fish Oils, and Risk of Acute Coronary Events and Cardiovascular Disease, Coronary Heart Disease, and All-Cause Mortality in Men in Eastern Finland. Arterioscler Thromb Vasc Biol. 2004 Nov 11; & J.T. Salonen et al, “Intake of mercury from fish and the risk of myocardial infarction and cardiovascular disease in eastern Finnish men”, Circulation, 1995; 91(3):645-55; & Salonen JT, Seppanen K, Lakka TA, Salonen R, Kaplan GA. Mercury accumulation and accelerated progression of carotid atherosclerosis: a population-based prospective 4-year follow-up study in men in eastern Finland. Atherosclerosis 2000 Feb;148(2):265-73; & Gualler E, et al; Mercury, fish oils, and the risk of myocardial infarction, New England J of Medicine, 2002, 347:
(202) T.Kishimoto et al, “Methyl mercury injury of Cultured Human Vascular Endothelial Cells”, Journal of Trace Elements in Experimental Medicine, 6(4): 155-163, 1993.
(205) M.F. Ziff et al, A Persuasive New Look at Heart Disease As It Relates to Mercury, Bio-Probe, Inc., ISBN 0-941011-08-9; & J. of American College of Cardiology V33,#6, pp1578 1583, 1999.
(211) M.J.Vimy and F.L. Lorscheider, Faculty of Medicine, Univ. Of Calgary, July 1991. (Study findings) & J. Trace Elem. Exper. Med., 1990,3, 111-123.
(212) Ziff, M.F., “Documented Clinical Side Effects to Dental Amalgams”, ADV. Dent. Res.,1992; 1(6):131-134; & S.Ziff,Dentistry without Mercury, 8th Edition, 1996, Bio-Probe, Inc., ISBN 0-941011-04-6; & Dental Mercury Detox, Bio-Probe, Inc. http://www.bioprobe.com. (cases:FDA Patient Adverse Reaction Reports-762, Dr. M.Hanson-Swedish patients-519(includes many MS), Dr. H. Lichtenberg-100 Danish patients, Dr. P.Larose- 80 Canadian patients, Dr. R.Siblerud, 86 Colorado patients, Dr. A.V.Zamm, 22 patients(see (26)
(220) Sellars WA, Sellars R. Univ. Of Texas Southwestern Medical School “Methyl mercury in dental amalgams in the human mouth”, Journal of Nutritional & Environmental Medicine 1996; 6(1): 33-37; & C Arch Environmental Health, 19,891-905, Dec 1969.
(221) R. Golden et al, Duke Univ., “Dementia and Alzheimer’s’s Disease”, Minnesota Medicine, 78:p25-29, 1995.
(222) M. Daunderer, Handbuch der Amalgamvergiftung, Ecomed Verlag, Landsberg 1998, ISBN 3 609 71750 5 (in German); & “Improvement of Nerve and Immunological Damages after Amalgam Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991; & Toxicologische erfahrungen am menchen; Quecksilber in der umwelf-hearing zum amalgamproblem”,Niedersachsiscles Umweltministerium, 1991; & “Amalgam”, Ecomed-Verlag, Landsberg, 1995; & “Amalgamtest”, Forum Prakt.Allgen.Arzt, 1990, 29(8): 213-4; & “Besserung von Nerven- und Immunschaden nach Amalgamsanierung”,Dtsch.Aschr. F. Biologische Zahnmedzin, 1990, 6(4):152-7. ( amalgam removal & DMPS, over 5,000 cases)
(225) S. Yannai et al, “Transformations of inorganic mercury by candida albicans and Saccharomyces cerevisiae”, Applied Envir Microbiology,1991, 7:245-247; & N.E.Zorn et al, “ A relationship between Vit B-12, mercury uptake, and methylation”, Life Sci, 1990, 47(2):167-73; & Ridley WP, Dizikes L, Cheh A, Wood JM. Recent studies on biomethylation and demethylation of toxic elements. Environ Health Perspect 1977 Aug;19:43 6 & R.E.DeSimone et al, Biochem Biophys Acta, 1973,May 28; & Yamada, Tonomura“Formation of methyl Mercury Compounds from inorganic Mercury by Clostridium cochlearium” J Ferment Technol1972 50:159 1660
(232) Adolph Coors Foundation, “Coors Amalgam Study: Effects of placement and removal of amalgam fillings”, 1995. (www) & International DAMS Newsletter, p17, Vol VII, Issue 2, Spring 1997. (31 cases); & (b)
Antero Danersund,"Dental Materials and Psychoneuroimmunology Conference". Danderyd Hospital, 14-16 August, 1998; www.melisa.org/archive/6th_melisa_study_group.html
(260) J.S. Woods et al, “Urinary porphyrin profiles as biomarker of mercury exposure: studies on dentists”, J Toxicol Environ Health, 40(2-3):1993, p235-; & “Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity”, Physiol Pharmocol, 1996,74(2):210-15,& M.D.Martin et al, “Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion rates”, J Pharmacol Exp Ther, Apr 1996 & J.S. Woods et al, “Effects of Porphyrinogenic Metals on Coproporphrinogen Oxidase in Liver and Kidney” Toxicology and Applied Pharmacology, Vol 97, 183-190, 1989; & (b) Strubelt O, Kremer J, et al, Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver. J Toxicol Environ Health. 1996 Feb 23;47(3):267-83; & (c)Kaliman PA, Nikitchenko IV, Sokol OA, Strel'chenko EV. Regulation of heme oxygenase activity in rat liver during oxidative stress induced by cobalt chloride and mercury chloride. Biochemistry (Mosc). 2001 Jan;66(1):77-82; &(d) Kumar SV, Maitra S, Bhattacharya S. In vitro binding of inorganic mercury to the plasma membrane of rat platelet affects Na+-K+-Atpase activity and platelet aggregation. Biometals. 2002 Mar;15(1):51-7.
(263) Ravi Kumar A, Kurup PA. Digoxin and membrane sodium potassium ATPase inhibition in cardiovascular disease.Indian Heart J. 2000 May-Jun;52(3):315-8.
(264) B.R. Danielsson et al, “ ”Behavioral effects of prenatal metallic mercury inhalation exposure in rats”, Neurotoxicol Teratol, 1993, 15(6): 391-6;& A. Fredriksson et al,”Prenatal exposure to metallic mercury vapor and methyl mercury produce interactive behavioral changes in adult rats”, Neurotoxicol Teratol, 1996, 18(2): 129-34;
(270) Tan XX, Tang C, Castoldi AF, Costa Lg. Effects of inorganic and organic mercury on intracellular calcium levels in rat T lymphocytes. J Toxicol Environ Health 1993, 38(2):159-70.
(271) B.A.Weber, “The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases) & (b) “Amalgam and Allergy”, Institute for Naturopathic Medicine, 1994; www.karlloren.com/ultrasound/p23.htm
& © “Conjunctivitis sicca(dry eye study)”,Institute for Naturopathic Medicine, 1994; & , “Alternative treatment of Multiple Schlerosis, Tumor, or Cancer”, Institute for Naturopathic Medicine 1997
(40 MS cases), http://home,t online.de/home/Institut_f._Naturheilverfahren/patinf.htm" (272) BJ Shenker, “Induction of apoptosis in human T-cells by methyl mercury”, Toxicol Appl Pharmacol, 1999,157(1):23-35; Immunopharmacol Immunotoxicol, 1992; 14(3):555-77; & Immunotoxicol, 1992, 14(3):539-53; & “Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial disfunction”, Environ Res, 1998, 77(2):149-159; & O.Insug et al, “Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species(ROS), development of mitochondrial membrane permeability, and loss of reductive reserve”, Toxicology, 1997, 124(3):211-24;
(276) Office of Air Quality Planning & Standards and Office of Research and Development. (1997, December). Mercury study report to congress volume V: Health effects of mercury and mercury compounds. Retrieved October 27, 02, from U.S. Environmental Protection Agency Web Site: www.epa.gov
(288) Hisatome I, Kurata Y, et al; Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region. Biophys J. 2000 Sep;79(3):1336-45; & Bhattacharya S, Sen S et al, Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997 Jul;10(3):157-62; & Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992 May;262(5 Pt 2):F830-6. & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308; & Wagner CA, Waldegger S,et al; Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes.. Am J Physiol. 1996 Oct;271(4 Pt 2):F926-30; & Lewis RN; Bowler K. Rat brain (Na+ K+)ATPase: modulation of its ouabain sensitive K+ PNPPase activity by thimerosal. Int J Biochem 1983;15(1):5 7
(290) D. Echeverria et al, “Neurobehavioral effects from exposure to dental amalgam: new distinctions between recent exposure and Hg body burden” FASEB J, Aug 1998, 12(11):971-980; & Amalgam and Health, Swedish Council for Planning and Coordination of Research, 1999; p297-307.
(303) Heavy Metal and Chemical Toxicity, Dietrich Klinghardt, MD, Ph.D. http://www.klinghardtacademy.com/Neural-Therapy/; & Mercury Toxicity and Systemic Elimination Agents, D. Klinghardt & J Mercola(DO), J of Nutritional and Environmental Medicine, 2001, 11:53-62; & Amalgam Detox, Klinghardt Academy of Neurobiology, 2008
(304) Dietary Supplementation with Chlorella pyrenoidosa Produces Positive Results in Patients with Cancer or Suffering from Certain Common Chronic Illnesses, R.E. Merchant and C.A. Andre, Townsend Letter for Doctors & Patients, Feb/Mar 2001
(306) E.M.Oliveira et al, “Mercury effects on the contractile activity of the heart muscle”, Toxicol Appl Pharmacol, 1:86-91,1994;
(308) Sorensen N, Murata K, Budtz-Jorgensen E, Weihe P, Grandjean P. Prenatal methylmercury exposure as a cardiovascular risk factor at seven years of age. Epidemiology 1999 Jul;10(4):370-5;& D.O.Marsh et al, “Fetal Methyl mercury Poisoning”, Ann Neurol, 1980, 7:348-55; & (c) More evidence of mercury effects in children; Environ Health Perspect. 1999 Nov;107(11):A554-5; & Epidemiology July 1999;10:370-375; & (d) [Environmental epidemiology research leads to a decrease of the exposure limit for mercury] [Article in Danish] Weihe P, Debes F, White RF, Sorensen N, Budtz-Jorgensen E, Keiding N, Grandjean P. Ugeskr Laeger. 2003 Jan 6;165(2):107-11.
(310)R.L.Siblerud, “The relationship between mercury from dental amalgam and the cardiovascular system”, Science of the Total Envir., 1990, 99(1-2): 23-35.
(332) Trepka MJ, Heinrich J, Krause C, Schulz C, Wjst M, Popescu M, Wichmann HE,, “Factors affecting internal mercury burdens among German children”, Arch Environ Health, 1997, 52(2):134-8; & L.Soleo et al, “Influence of amalgam fillings on urinary mercury excretion”(S.Italy), G Ital Med Lav Ergon,1998,20(2): 75- 81 .
(333) A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain”, Brain Research, 1996, 738(2): 257-64; & P.R.Yallapragoda et al,“Inhibition of calcium transport by Hg salts” in rat cerebellum and cerebral cortex”, J Appl toxicol, 1996, 164(4): 325-30; & E.Chavez et al, “Mitochondrial calcium release by Hg+2",J Biol Chem, 1988, 263:8, 3582-; A. Szucs et al, Cell Mol Neurobiol, 1997,17(3): 273-8; & D.Busselberg, 1995, “Calcium channels as target sites of heavy metals”,Toxicol Lett, Dec;82 83:255 61; & Cell Mol Neurobiol 1994 Dec;14(6):675 87; & Rossi AD, et al, Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J 1993, 7:1507-14.
(338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta”, Environ Res, 1992, 57(1):96-106;& “In vitro exposure to mercury and cadmium alters term human placental membrane fluidity”, Pharmacol, 1992, 116(1): 17-23; & (b)J.Urbach et al, Dept. of Obstetrics & Gynecology, Rambam Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption”, Reprod Toxicol, 1992,6(1):69-75;& © Karp W, Gale TF et al, Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters” Environmental Research, 36:351-358; & W.B. Karp et al, “Correlation of human placental enzymatic activity with trace metal concentration in placenta”, Environ Res. 13:470- 477,1977; & (d) Boot JH. Effects of SH blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct 1995 Jun;20(3):233 8; & Semczuk M, Semczuk Sikora A. New data on toxic metal intoxication (Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit 2001 Mar;7(2):332 340; & H.Iioka et al, “The effect of inorganic mercury on placental amino acid transport”, Nippon sanka Fujinka Gakkai Zasshi, 1987, 39(2): 202-6.
(339) H.Drexler et al, “The mercury concentration in breast milk resulting from amalgam fillings and dietary habits”, Environ Res, 1998, 77(2):124-9; & Sundberg J, Ersson B, Lonnerdal B, Oskarsson A. Protein binding of mercury in milk and plasma from mice and man a comparison between methyl mercury and inorganic mercury. Toxicology 1999 Oct 1;137(3):169 84; & Vimy MJ, Hooper DE, King WW, Lorscheider FL.; Mercury from maternal "silver" tooth fillings in sheep and human breast milk. A source of neonatal exposure. Biol Trace Elem Res 1997 Feb;56(2):143-52.
(347) G.Benga “Water exchange through erythrocyte membranes” Neurol Neurochir Pol 1997 Sep Oct;31(5):905 13
(348) A Kistner, “Quecksilbervergiftung durch Amalgam: Diagnose und Therapie” ZWR, 1995,104(5):412-417; & , & Placidi, GF; et al. Distribution of Inhaled Mercury (203Hg) in Various Organs. Int J Tiss React., 5:193-200, 1983; & Yoshida, M; et al. Distribution of Mercury in Neonatal Guinea Pigs After Exposure to Mercury Vapor. Bull Environ Contam Toxicol., 43(5):697-704, Nov 1989; &Khayat, A; Dencker, L. Organ and cellular distribution of inhaled metallic mercury in the rat and marmoset monkey (Callithrix jacchus): Influence of ethyl alcohol pretreatment. Acta Pharmacol Toxicol, 55:145-52, 1984:
(351) S.Halbach et al, “Thiol chelators and mercury effects on isolated heart muscle”, Plzen.Lek. Sborn, 1990,62(Supp), 39-41, 1990; & “Sulfhydryl-induced restoration of myocardial contractility after alteration by mercury”, Arch. Toxicol. 63(Supp 13) 349-352, 1989; & N.V.Klykov, “Treatment of patients with myocardial infarction”, Vrach.Delo.1979,(12):50-3; & “Treatment of patients with chronic circulatory insufficiency” Kardiologila, 1972,12(1):126-31.
(360) Buchet JP, Lauwerys RR, Influence of DMPS on the mobilization of mercury from tissues of rats pretreated with mercuric chloride, phenylmercury acetate, or mercury vapor, Toxicology 1989;54(3):323-33.
(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & & Kosuda LL, Greiner DL, Bigazzi PE. Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes prone (DP) BB rats. Autoimmunity 1997;26(3):173 87.
(370) Magos L, Clarkson TW, Hudson AR. The effects of dose of elemental mercury and first pass circulation time on organ distribution of inorganic mercury in rats. Biochem Biophys Acta 1989; 991(1):85-9.
(382) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60; & Sterzl I, Hrda P, Prochazkova J, Bartova J, Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45(9):527 31
(386) Great Smokies Diagnostic Lab, research web pages (by condition) http://www.gsdl.com; & Doctors Data Lab , http://www.doctorsdata.com , inquiries @doctors data.com, www.doctorsdata.com, & MetaMetrix Lab, www.metametrix.com; &(d) Biospectron Lab, LMI, Lennart Månsson International AB, firstname.lastname@example.org http://home.swipnet.se/misac/research11.html#biospectrons
(427) Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Arch Int Physiol Biochem 1990, 98(5):261-7;
(431) Smith T, Pitts K, Mc Garvey JA, Summers AO. Bacterial oxidation of mercury metal vapor. Appl Environ Microbiol 1998, 64(4): 1328-32.
(459) Isny Clinic(South Germany) Kurt Muller , MD, member of Editorial board for Ganzheitliches Medicine Journal. Wassertornstrasse 6 , Isny, BRD fax: 0049 7562 550 52
(479) Amphotericin B, HgCl2 and Peritoneal Transport in Rabbits, Zweers MM, Douma CE, van der Wardt AB, Krediet RT, Struijk DG. Department of Nephrology, Academic Medical Center, Amsterdam, The Netherlands. The 3rd European Peritoneal Dialysis Meeting 5 7 April 1998, Edinburgh, U.K; & (b) Ashe, W., E. Largent, F. Dutra, et al. 1953. Behavior of mercury in the animal organism following inhalation. Arch. Ind. Hyg. Occup. Med. 17: 19-43.
(503) Rupp, Paffenberger, Significance to health of mercury used in dental practice, Reports of Councils and Bureaus, JADA, Vol 182, June 1971; & Rao, Hefferen, Biocompatibility of Dental Materials, Vol III,D.C. Smith and D.F. Williams, Eds., CRC Press, Boca Raton, Fl 1982, Toxicity of Mercury; & Center for Chemical Hazard Assessment, Potential Occupational Hazards: Dentistry, Syracuse Research, Contract No.210-78-0019, 1980; & Merck Manuel, 14th Edition, p1552.
(506) Leistevuo J, Pyy L, Osterblad M, Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res 2001 May Jun;35(3):163 6
(509)(a) Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE, Mitchell ML, Relation of severity of maternal hypothyroidism to cognitive development of offspring. J Med Screen 2001: 8:18-20; &(b) de Escobar DM, Orbregon MF, del Rey FE, Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia? C Clin Endocrin Metab 2000; 3975-3987; &(c) Thyroid Imbalances in Pregnancy Linked to Poor Child Neurodelopment, Great Smokies Diagnostic Lab, www.gsdl.com/news/connections/vol11/conn20010228.html &(d) J. E. Haddow et al, Babies Born to Mothers with Untreated Hypothyroidism Have Lower I.Q.'s, New England Journal of Medicine, Aug 19, 1999; & (e) Lavado-Autric et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. JCI 111:1073-1082 (2003); & (f)Pop VJ, Vader HL et al, Low maternal free thyroxine during early pregnancy is associated with impaired psychomotor development in infancy, Clin Endocrinol(Oxf), 50:149-55, 1999; & (g) Asami T, Suzuki H, Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid 11: 765-8, 2001; & Kumar R, Chaudhuri BN. Altered maternal thyroid function: fetal and neonatal heart cholesterol and phospholipids, .Indian J Physiol Pharmacol 1993 Jul;37(3):176-82
(510) (a)Morris MS, Bostom AG, Jacques PJ, Selhub J, Rosenberg IH, Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination Survey, Artherosclerosis 2001, 155:195-200; & (b) Shanoudy H. Soliman A, Moe S, Hadian D, Veldhuis F, Iranmanesh A, Russell D, Early manifestations of “sick eythyroid syndrome” in patients with compensated chronic heart failure, J Card Fail 2001, 7(2):146-52; & (c)AE. Hak, HAP. Pols, TJ. Visser, et al., The Rotterdam Study., Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women, Ann Int Med, 2000, vol. 132, pp. 270--278 &(d)Thyroid Dysfunction Linked to Elevated Cardiac Risk, GSDL, www.gsdl.com/news/connections/vol12/conn20010411.html.; &(e) Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002 Dec 3;137(11):904-14; & (f) B.G. Nedreboe, O. Nygard, et al, Plasma Total Homocysteine of hypothyroid patients during 12 months of treatment, Haukeland Univ. Hospital, Bergen, Norway, email@example.com (references 7 other studies with similar findings); & (g) Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med 1999; 131:348; & (h) Asami T, Suzuki H, Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid 11: 765-8, 2001.
(511) Novembrino C, Bamonti F, Minoia C, Guzzi G, Pigatto PD. Homocysteine and mercury dental amalgam. Paper & presentation, 8th International Conference on Mercury Global Pollutant, Madison, WI, USA; R-103,434,2006
(512) Zeeman Mercury Spectrometer RA-915 Demonstration, Fifth International Conference on Mercury, Rio de Janeiro, Brazil, May 23-28, 1999. (methyl mercury sniffer)
(521) Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46; & Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury. J Environ Sci Health B. 2001 Sep;36(5):687-97.
(523) CBS Television Network,” 60 Minutes”, television program narrated by Morley Safer, December 12, 1990 www.vimy dentistry.com/tttoc.htm#_Toc499123411
(538) (a)Piikivi L, Tolonen U. EEG findings in chlor-alkali workers subjected to low long term exposure to mercury vapour.Br J Ind Med. 1989 Jun;46(6):370-5; & (b)P Boffeta, G Sallsten, Mortality from cardiovascular diseases and inorganic mercury exposure, Occup Environ Med, 2001, 58:461-465; & (c) Mercury: Cardiovascular Effects(Bibliography): www.bioprobe.com/reviews.asp?review_id=28
(539)(a) Wossmann W, et al, Mercury intoxication presenting with hypertension and tachycardia. Arch Dis Child 1999 Jun;80(6):556 7; & (b) Mercury intoxication: lack of correlation between symptoms and levels; Gattineni J, Weiser S, Becker AM, Baum M. Clin Pediatr (Phila). 2007 Nov;46(9):844-6;
& (c) Henningsson C, et al. Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent. J Pediatr 1993 Feb;122(2):252 3; & (d) Florentine MJ et al, Elemental mercury poisoning, Clin Pharm. 1991, 10(3):213-21; & (e)Warkeny, J., & Hubbard, CH. E. (1953). Acrodynia and mercury. Journal of Pediatrics, 42(3), 365-386; & (f) U.S. Dept. of Health, Agency for Toxic Substances and Disease Registry, Medical Management Guidelines for Mercury: Cardiovascular Effects of Mercury, www.atsdr.cdc.gov/MHMI/mmg46.html
(540) Wisconsin Bureau of Public Health, Imported seabass as a source of mercury exposure: a Wisconsin Case Study, Environ Health Perspect 1995, 103(6): 604-6; & J. Hightower, “Methylmercury Contaminmation in Fish: Human Exposures and Case Reports," Environmental Health Perspectives; Nov 1, 2002.
(541) Hypertension and erythromelalgia as prominent manifestations of mercury intoxication; Chang XZ, Lu HM, Zhang YH, Qin J. Beijing Da Xue Xue Bao. 2007 Aug 18;39(4):377-80; & (b) Cloarec S, et al, Arterial hypertension due to mercury poisoning: diagnostic value of captopril. Arch Pediatr 1995 Jan;2(1):43 6;& (c) Mercury intoxication in a 2-year-old girl: a diagnostic challenge for the physician; Michaeli-Yossef Y, Berkovitch M, Goldman M. Pediatr Nephrol. 2007 Jun;22(6):903-6; & (d) Mercury intoxication and arterial hypertension: report of two patients and review of the literature; Torres AD, Rai AN, Hardiek ML. Pediatrics. 2000 Mar;105(3):E34; & [Arterial hypertension due to mercury intoxication with clinico-laboratorial syndrome simulating pheochromocytoma] ; Joaquim de Oliveira J, Silva SR. Arq Bras Cardiol. 1996 Jan;66(1):29-31
(542) Kawasaki's disease, acrodynia, and mercury; Mutter J, Yeter D. Curr Med Chem. 2008;15(28):3000-10; & Orlowski, JP; Mercer, RD. Urine Mercury Levels in Kawasaki Disease [Myocardial infarction, abnormal EKG, A-V block, PVC, myocarditis, aneurysms by mercury]. Pediatrics, 66(4):633-6, )ct 1980.
(543) U.S. Centers for Disease Control, National Center for Health Statistics,
NHANES III study(thousands of people’s health monitored),
www.mercola.com/article/mercury/no_mercury.htm & Review: cancer related to
mercury exposure, B. Windham (Ed) http://www.myflcv.com/cancerhg.html ; & (b) Laks,
Dan R. Assessment of chronic mercury exposure within the U.S. population, National
Health and Nutrition Examination Survey, 1999–2006. Biometals. August 2009; &
Laks, D.R. et al, Mercury has an affinity for pituitary hormones, Medical Hypotheses,
Dec 2009; & (c) An Investigation of Factors Related to Levels of Mercury in Human
Hair, Environmental Quality Institute, October 01, 2005,
(561) Association of Fibrinogen, C-reactive Protein, Albumin, or Leukocyte Count With Coronary Heart Disease, J Danesh, R Collins, P Appleby, Richard Peto, JAMA. 1998;279:1477-1482.
(562) Edward Suarez, associate professor in the Duke Department of Psychiatry and Behavioral Sciences., journal Psychosomatic Medicine, September, 2004; & A Good Mood Equals a Healthy Heart, Vitamin Research Products- Review of emotional factors affecting cardiovascular disease,
(563) McIntyre IM, Judd FK, Marriott PM, et al. Plasma melatonin levels in affective states. Int J Clin Pharmacol Res. 1989;9(2):159-64; & Riemann D, Klein T, Rodenbeck A, et al. Nocturnal cortisol and melatonin secretion in primary insomnia. Psychiatry Res. 2002 Dec 15;113(1-2):17-27; & Wade AG, Ford I, Crawford G, McMahon AD, Nir T, Laudon M, Zisapel N. Efficacy of prolonged release melatonin in insomnia patients aged 55-80 years: quality of sleep and next-day alertness outcomes. Curr Med Res Opin. 2007 Oct;23(10):2597-605.
(564) R.L.Siblerud et al,”Psychometric evidence that mercury from dental fillings may be a factor in depression,anger,and anxiety", Psychol Rep, v74,n1,1994, & Mechanisms by which mercury causes depression and anxiety, annotated bibliography, B Windham(Ed), www.flcv.com/depress.html
(567) Kim CY, Satoh H, et al, Protective effect of melatonin on methylmercury-Induced mortality in mice. Tohoku J Exp Med. 2000 Aug;191(4):241-6; & Olivieri G, Hock C, et al , Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000 Jan;74(1):231-6.
(569) Baccarelli A, Pesatori AC, Bertazzi PA. Occupational and environmental agents as endocrine disruptors: experimental and human evidence. J Endocrinol Invest. 2000 Dec;23(11):771-81
(570) Melatonin in sleep rhythm disorders after cerebral stroke. Pol Merkuriusz Lek 2000 Jun;8(48):411-2; & Melatonin treatment of non-epileptic myoclonus in children., Dev Med Child Neurol 1999 Apr;41(4):255-9, & Effects of a low dose of melatonin on sleep in children with Angelman syndrome, J Pediatr Endocrinol Metab 1999 Jan-Feb;12(1):57-67, & Effect of melatonin in selected populations of sleep-disturbed patients. Biol Signals Recept 1999 Jan-Apr;8(1-2):126-31
(571) (a) The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. Altern Ther Health Med. 2007 Mar-Apr;13(2):S128-33. Houston MC; & (b)Antioxidants, infections and environmental factors in health and disease in northern Finland. Luoma P. Int J Circumpolar Health. 1998 Jul;57(2-3):109-13; www.melisa.org
& (c ) Mercury activates vascular endothelial cell phospholipase D through thiols and oxidative stress. Hagele TJ, Mazerik JN, Parinandi NL et al. , Int J Toxicol. 2007 Jan-Feb;26(1):57-69; & (d) Phospholipase A2 Activation Regulates Cytotoxicity of Methylmercury in Vascular Endothelial Cells, J. N. Mazerik, T. Hagele, N.L. Parinandi,et al; International Journal of Toxicology, Vol. 26, No. 6, 553-569 (2007)
(572) Periodontal disease and heart disease risk, Richard Watt et al, BMJ, May 2010
(573) Role of Mercury Toxicity in Hypertension, Cardiovascular Disease, and Stroke; Mark C. Houston, MD, The Journal of Clinical Hypertension Vol 13 | No 8 | August 2011
(575) Summary of Medical, Government, and Medical Lab studies and findings regarding mercury exposures from amalgam dental fillings, DAMS Intl., www.flcv.com/damspr1.html
(576) Review of exposure levels and health effects from mercury and dental amalgam; B.Windham(Ed.), www.flcv.com/amalg6.html over 4000 p.r. studies
(577) Mercury From Amalgam Fillings: A Major Factor in Periodontal Disease and Oral Health Problems, B Windham(Ed), over 100 peer-reviewed cites, www.flcv.com/periodon.html; & Evaluation of dental diseases' effect on systemic C-reactive protein levels, N. YUDINA, Byelorussian State Medical University, Minsk, Belarus, 1996, etc.
(580) 52. Life Extension, Disease Prevention and Treatment, Fifth Edition, 2013. 51. Life Extension Magazine,
&(b) Life Extension Magazine, July 2018; & (b) Langsjoen P, Langsjoen P, Willis R, et al. Coenzyme Q10 in essential hypertension. Mol Aspects Med. 1994;15(suppl):S257-S263; & Molyneux SL, Florkowski CM, George PM et al. Coenzyme Q10: an independent predictor of mortality in chronic heart failure. J Am Coll Cardiol. 2008 Oct 28;52(18):1435-41; & Greenberg SM, Frishman WH. Coenzyme Q10: a new drug for myocardial ischemia? Med Clin North Am. 1988 Jan;72(1):243-58; & (d) Bahorun T, Trotin F, Pommery J, et al. Antioxidant activities of Crataegus monogyna extracts(hawthorn). Planta Med. 1994; 60:323-8; & (e) Lindner E, Dohadwalla AN, Bhattacharya BK. Positive inotropic and blood pressure lowering activity of a diterpene derivative isolated from Coleus forskohli: Forskolin. Arzneimittelforschung. 1978;28(2):284-9
(581) Overcoming Cardiovascular Disease, Isaac Eliaz, M.D., Better Health Publishing. 2009;(b) & Anon. Monograph. L-carnitine. Altern Med Rev. 2005 Mar;10(1):42-50; & (c) Palloshi A, Fragasso G, Piatti P, et al. Effect of oral L-arginine on blood pressure and symptoms and endothelial function in patients with systemic hypertension, positive exercise tests, and normal coronary arteries. Am J Cardiol. 2004;93:933—935; & (d) Fujita T, Ando K, Noda H, et al. Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension. Circulation. 1987 Mar; 75(3):525-32; & Miglis M, Wilder D, Reid T, et al. Effect of taurine on platelets and the plasma coagulation system. Platelets. 2002 Feb;13(1):5-10.
(584) An Invitation to Health: 2009-2010 Edition, Dianne Hales, 2009.
(585) Olszewer E, Carter JP. Med Hypotheses. 1988 Sep;27(1):41-9 (2870 patients); & Integrative cardiac revitalization: bypass surgery, angioplasty, and chelation. Benefits, risks, and limitations. Kidd PM. Altern Med Rev. 1998 Feb;3(1):4-17; & Hancke C. Benefits of EDTA chelation therapy in arteriosclerosis: a retrospective study of 470 patients. J Adv Med 1993; 6; 3:161-71; & McDonagh EW. Non-invasive treatment for sequelae of failed coronary blood circulation. J Neuro Ortho Med Surg 1993; 14:169-73.;& Casdorph HR, Farr CH. EDTA chelation therapy: treatment of peripheral arterial occlusion, an alternative to amputation. J Adv Med 1989; 2; 1,2:170-80.; & Chappell LT, Stahl JP. The correlation between EDTA chelation therapy and improvements in cardiovascular function meta-analysis. J Adv Med 1993; 6;3:139-60 ; & Hancke C, Flytlie K. Benefits of EDTA chelation therapy in arteriosclerosis. J Adv Med 1993; 6; 3:161-71
(590) Dietary Intake and the Development of the Metabolic Syndrome. The Atherosclerosis Risk in Communities Study , Pamela L. Lutsey MPH, Lyn M. Steffen PhD, MPH, RD*, and June Stevens PhD, MS, RD , Circulation, Jan 2008 (Journal of the American Heart Association)
(596) Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008 Mar;83(3):333-42, Dandona P; & Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007;49(1):48-63, Vasdev S, Gill V, Singal P.
(597) Immunoexcitotoxicity, R L Blaylock, Alt Ther Health Med, 2008, 14:46-53; & (b) Sudden Cardiac Death and Excitotoxic Foods, Dr. Russell Blaylock, www.blaylockwellnesscenter.com/
(598) Overcoming Depression, Dr. Russell Blaylock, The Blaylock Wellness Report, Vol 5, No. 3, March 2008; & Beat Depression and Anxiety with Diet/Nutrition, Blaylock Report, Dec 2010; & (c ) Microglial Activation and Neurodegeneration, Dr. Russell Blaylock, www.blaylockwellnesscenter.com/
Contact person: Bernard Windham, President & Research Director, DAMS Intl 12164 Whitehouse Rd, Tallahassee, Fl 32317