Documentation of Common Cardiovascular Health Effects from Mercury from Amalgam

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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(cludication), 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 stroke 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.

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 patients’ chronic conditions such as hypertension, ulcerative colitis, or Fibromyalgia. Doctors, such as D. Klinghardt, 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 vitamin B12 and vitamin B6. Plaque buildup in arteries can cause dying of heart muscle cells, weakening of the heart muscle, irregular heartbeat, angina, etc. Vitamin C is an essential factor in building and maintaining collagen and elastin, primary factors in connective tissues, so vitamin C deficiency is a major factor in leaking veins and plaque buildup. Supplementation with vitamin C has been found to significantly reduce such plaque buildups and leaking veins. Other factors in cardiovascular disease include imbalances of lipoprotein A, C-reactive protein, homocysteine, and fibrinogen.

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 a 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 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—oxidative stress results. 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, thus 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. The primary risk factors that have been identified for cardiovascular disease are:

  • elevated C-Reactive Protein,
  • elevated fibrinogen, levated homocysteine,
  • elevated Lipoprotein(a),
  • elevated LDL cholesterol/low HDL cholesterol,
  • elevated triglycerides,
  • hyperinsulinemia (excess insulin), and
  • low testosterone levels in men.

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. 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; however, these risks 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. 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.

Mercury, Toxic Metals, and Cardiovascular Disease

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 attack. 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. 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 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.

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. 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, methylmercury, and thimerosal significantly activated pulmonary artery endothelial cells in a dose-dependent and time-dependent fashion. Metal chelators significantly attenuated mercury-induced PLD activation, suggesting that cellular mercury-ligand interaction(s) is required for the enzyme activation and 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 A(PLA) in vascular endothelial cells (ECs), causing upstream regulation of cytotoxicity. Methylmercury also induced the loss of thiols and increase of lipid peroxidation in BPAECs. Numerous studies have reported tachycardia, high blood pressure and heart palpitations after acute exposure to elemental mercury vapor. A positive correlation was found between heart palpitations and urinary Hg concentrations in workers from a chlor-alkali plant. 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. In children, tachycardia associated with the inhalation of elemental mercury vapor might be related to a non-allergenic hypersensitivity reaction to mercury. 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.

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 five years of age. Many patients with Kawasaki’s Disease have presented with elevated urine mercury levels compared to matched controls. 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.

Recent review studies found that toxic metals are a significant factor in cardiovascular disease. 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. 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. Both metals bind to metallothionein and substitute for zinc, copper, and other trace metals reducing the effectiveness of metalloenzymes. Mercury induces mitochondrial dysfunction with reduction in ATP, depletion of glutathione, and increased lipid peroxidation; increased oxidative stress is common. 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.

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 cardiovascular 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. 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. Thus, even at a level 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 in order 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 start 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.

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. A 2009 study found that inorganic mercury levels in people have been increasing rapidly in recent years. 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, the 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.

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, including methylmercury since elemental and inorganic mercury are commonly methylated in the body. But many also get significant exposure to methylmercury from fish,and ethyl mercury from vaccines. The number of amalgam surfaces has a statistically significant correlation to blood plasma mercury level. Much mercury in saliva and the brain is also organic, since mouth bacteria and other organisms in the body methylate elemental and inorganic mercury to organic mercury. Studies and clinical tests have found amalgam to be the largest source of methylmercury in most people. Bacteria also oxidize mercury vapor to the water soluble, ionic form Hg(II). 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. 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.

As is known from autopsy studies for those with chronic mercury exposure, such as amalgam fillings, mercury also bio-accumulates in the heart in addition to accumulating in the brain, CNS, and hormone glands. 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. Thus the level in the brain and heart is higher after exposure to Hg vapor than for other forms. 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 and commonly in adults with levels below 10 ug/l.

Effects of Mercury Exposure on the Cardiovascular System

A recent 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. 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, an 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.

Mercury vapor is lipid soluble and has an affinity for red blood cells and CNS cells. Both mercury and methylmercury have been shown to cause depletion of calcium from the heart muscle and to inhibit myosin ATPase activity by 50% at 30 ppb, as well as to reduce NK-cells in the blood and spleen. The interruption of the ATP energy chemistry results in high levels of porphyrins in the urine 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, and has been found to cause significant heart damage. 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. Studies have found patients with mucoid angiopathy, endomyocardial fibrosis, and syndrome X there experience as reduction in serum magnesium and RBC membrane Na(+)-K+-ATPase activity 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, and 4) defective golgi body function and protein processing dysfunction. It is documented that mercury is a cause of most of these conditions. 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, increased reactive oxygen species, and increased risk of acute myocardial infarction.

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. 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. 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.

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. Melatonin has found to have a significant protective action against methylmercury toxicity, likely from antioxidative effect of melatonin on the MMC induced toxicity. 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 night sleep in patients with many chronic conditions, which is important to both cardiovascular and neurological health.

Mercury binds to hemoglobin oxygen binding sites in the red blood cells, thus reducing oxygen carrying capacity, and adversely affects the vascular response to norepinephrine and potassium. Mercury’s effect on pituitary gland vasopressin is a factor in high blood pressure. Mercury also increases cytosolic free calcium levels in lymphocytes in a concentration-dependent manner, causing influx from the extracellular medium, and blocks entry of calcium ions into the cytoplasm. At 100 ppb mercury can destroy the membrane of red blood cells and damage blood vessels, reducing blood supply to the tissues. Amalgam fillings have been found to be related to higher blood pressure, hemoglobin irregularities, tachycardia, chest pains, etc. Mercury also accumulates in the heart and damages myocardial and heart valves. Mercury has been found to be a cause of atherosclerosis, hypertension, and tachycardia in children and adults and heart attacks in adults.

Thyroid imbalances, which are documented to be commonly caused by mercury, have been found to play a major role in chronic heart conditions, such as clogged arteries, myocardial infarction, and chronic heart failure. 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. 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. These are also known factors in developing atherosclerotic vascular disease. Homocysteine levels are significantly increased in hypothyroid patients and normalize with treatment.

Studies have also established a connection between subclinical maternal thyroid disease and babies born with heart, brain and neurological effects, 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 vitamin B12, and depresses enzyme isocitric dehydrogenase (ICD) in fetus, causing reduced iodine uptake, autoimmune thyroiditis, and hypothyroidism.

Another study 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 even more inflammatory damage. Clinical experience has found that mercury exposure increases susceptibility to pathogen infections, including those that adversely affect the heart, and that such infections cannot be controlled or 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. C-reactive protein is a known marker for increased cardiovascular damage and disease, along with fibrinogen and albumin. Researchers at Duke University Medical Center and other researchers 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. Mercury is documented to be a common cause of anger, hostility, depression, and anxiety. There are extensive documented cases 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, blood and circulatory conditions.

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. 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. 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. 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; it still requires additional CoQ10 supplementation.

Fish oil (DHA,EPA), DHEA, and vitamin K have been documented to suppress inflammatory cytokines, TNFa, Il-1b, and Il-6, reducing inflammatory effects. 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, in turn, lower cardiovascular risk levels. 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. CRP levels can be reduced by supplementing with natural vitamin E, fish oil, CoQ10, and ginger. 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. Studies have found that policosanol supplementation 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). 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. Pantethine (B5) is useful to increase the good cholesterol, HDL. Fiber from foods or psyllium binds cholesterol, but psyllium should be taken two hours away from medications.

Hyperinsulinemia is extremely common, especially in overweight individuals, and a significant factor in cardiovascular disease and type II diabetes. 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. DHEA is a precursor 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, and excess platelet aggregation. 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, EDTA chelation has been found to usually be a safe and significantly beneficial treatment. 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. Natural platelet aggregation inhibitors include ginkgo biloba, EFAs, and vitamin E (tocopherol). Anti-inflammatories that have been found beneficial include: curcumin, DHEA, and nettle leaf. Antioxidants that have been found beneficial in thrombosis prevention include: quercetin, green tea, lycopene, and grape juice. N-acetyl-L-cysteine, onions, and exercise have also been found beneficial. Other heart healthy nutrients include D-ribose, L-carnitine, flaxseed, and L-arginine.

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. These diet patterns all have been found to be significantly associated with metabolic syndrome, a cluster of cardiovascular diseases, and diabetes risk factors, including elevated waist circumference, high blood pressure, elevated triglycerides, low levels of high-density lipoprotein (HDL/“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. 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. Highly colorful vegetables and use of coconut and coconut oil are part of a heart healthy diet.

Higher levels of vitamin D reduce heart attacks and strokes, and supplementation with ginko biloba may also reduce strokes 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. 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.

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. 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. Melatonin supplementation has been found to be beneficial to promoting sleep and benefitting the heart.

References

1.    American Heart Association. www.americanheart.org

2.    Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem. 2005; 12(10): 1161-208.

3.    Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998; 71: S37-9.

4.    Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.

5.    Jay D. Glutathione inhibits SOD activity of Hg. Arch Inst Cardiol Mex. 1998; 68(6): 457-61.

6.    Hussain S, 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; 32(3): 395-409.

7.    Ott K, et al. Mercury burden due to amalgam fillings. Dtsch. Zahnarztl Z. 1984; 39(9): 199-205.

8.    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; 11(2): 87-94. http://www.lichtenberg.dk/mercury_vapour_in_the_oral_cavit.htm

9.    Abraham J, Svare C, et al. The effects of dental amalgam restorations on blood mercury  levels. J Dent Res. 1984; 63(1): 71-73.

10.    Snapp KR, Boyer DB, Peterson LC, Svare CW. The contribution of dental amalgam to mercury in blood. J Dent Res. 1989; 68(5): 780-5.

11.    Trakhtenberg IM. Chronic effects of mercury on organisms: The micromercurialism phenomenon on mercury handlers. 1974. DHEW Publ. No. (NIH) 74-473.

12.    Vimy MJ, TakahashiY, Lorscheider FL. Maternal-fetal distribution of mercury released from dental amalgam fillings. Amer. J. Physiol. 1990; 258: R939-945.

13.    Hahn L, et al. Distribution of mercury released from amalgam fillings into monkey tissues. FASEB J. 1990; 4: 5536.

14.    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; 163(2-3): 115-26.

15.    Galic N, Ferencic Z, et al. Dental amalgam mercury exposure in rats. Biometals. 1999; 12(3): 227-31.

16.    Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol. 1990; 52(3): 291-9.

17.    Fredin B. The distribution of mercury in various tissues of guinea pigs after application of dental amalgam fillings. Sci Total Environ. 1987; 66: 263-8.

18.    Hahn LJ, et al. Dental silver and tooth fillings: A source of mercury exposure revealed by whole body scan and tissue analysis. FASEB J. 1989; 3: 2641-6.

19.    Goyer RA. Toxic effects of metals. In: Caserett, Doull, ed. Toxicology: The Basic Science of Poisons. New York: McGraw-Hill; 1993.

20.    Goodman, Gillman. The Pharmacological Basis of Therapeutics. New York: Mac Millan Publishing Company; 1985.

21.    Kuhnert P, et al. Comparison of mercury levels in maternal blood fetal cord blood and placental tissue. Am. J Obstet and Gynecol. 1981; 139: 209-212.

22.    Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M. Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood. Environ Res. 2000; 84(2): 186-94.

23.    Kuntz WD. Maternal and cord blood mercury background levels: Longitudinal surveillance. Am J Obstet and Gynecol. 1982; 143(4): 440-443.

24.    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; 106(4): 774-81.

25.    Rath M. Why Animals Don’t Get Heart Attacks, and People Do. MR Publishing; 2003.

26.    Markovich, et al. Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol App Pharmacol. 1999; 154(2): 181-7.

27.    McFadden SA. Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3): 43-65.

28.    Huggins HA, Levy TE. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc.; 1999.

29.    Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

30.    Badou A, 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; 272(51): 32411-8.

31.    Veprintsev DB. Pb2+ and Hg2+ binding to alpha-lactalbumin. Biochem Mol Biol Int. 1996; 39(6): 1255-65.

32.    Sin YM, Teh WF, Wong MK, Reddy PK. Effect of mercury on glutathione and thyroid hormone. Bulletin of Environmental Contamination and Toxicology. 1990; 44(4): 616-622.

33.    Kawada J, et al. Effects of inorganic and methyl mercury on thyroidal function. J Pharmacobiodyn. 1980; 3(3): 149-59.

34.    Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci. 1992; 5(3): 236-40.

35.    Goldman, Blackburn. The effect of mercuric chloride on  thyroid function of the rat.  Toxicol App Pharmol. 1979; 48: 49-55.

36.    Kabuto M. Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress. Arch Toxicol. 1991; 65(2): 164-7.

37.    Heintze, et al. Methylation of Mercury from dental amalgam and mercuric chloride  by oral Streptococci. Scan. J. Dent. Res. 1983; 91: 150-152.

38.    Rowland, Grasso, Davies. The methylation of mercuric chloride by human intestinal bacteria. Experientia. Basel. 1975; 31:1064-1065.

39.    Hamdy MK, et al. Formation of methylmercury by bacteria. App Microbiol. 1975.

40.    Frustaci, et al. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy. J of American College of Cardiology. 1999; 33(6): 1578-83.

41.    Husten L. Trace elements linked to cardiomyopathy. Lancet. 1999; 353(9164): 1594.

42.    Vassalo DV. Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine. Toxicol Appl Pharmacol. 1999; 156(2): 113-8.

43.    Ilblack NG, et al. New aspects of murine coxsackie B3 mycocarditis: Focus on heavy metals. European Heart J. 1995; 16: 20-4.

44.    Dahhan, Orfaly. Electrocardiogrphic changes in mercury poisoning. J of American College of Cardiology. 1964.

45.    Lorscheider F, Vimy M.  Mercury and idiopathic dilated cardiomyopathy. J of American College of Cardiology. 2000; 35(3): 819-20.

46.    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; 134(3): 375-83.

47.    Bjorkman L, et al. Mercury in saliva and feces after removal of amalgam fillings. Toxicol App Pharm. 1997; 144(1): 156-62.

48.    Liang LI, et al. Mercury reactions in the human mouth with dental amalgams. Water, Air, and Soil Pollution. 1995; 80: 103-107.

49.    Veltman JC, 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.

50.    Riedl AG, et al. P450 and hemeoxygenase enzymes in the basal ganglia and their roles in Parkinson’s disease. Adv Neurol. 1999; 80: 271-86.

51.    Zamm AV. Dental mercury: A factor that aggravates and induces xenobiotic intolerance.  J. Orthmol. Med. 1991; 6(2): 67-77.

52.    Salonen JT. Excessive intake of iron and mercury in cardiovascular disease. In: Sandstrom B, Walter P, eds. Role of Trace Elements for Health Promotion and Disease Prevention. Basel Karger; 1998: 112-126.

53.    Weiner JA, et al. The relationship between mercury concentration in human organs and predictor variables. Sci Tot Environ. 1993; 138(1-3): 101-115.

54.    Franko A, Budihna MV, Dodic-Fikfak M. Long-term effects of elemental mercury on renal function in miners of the Idrija Mercury Mine. Ann Occup Hyg. 2005; 49(6): 521-7.

55.    Berglund A, Molin M. Mercury levels in plasma and urine after removal of all amalgam restorations: the effect of using rubber dams. Dent Mat. 1997; 13(5): 297-304.

56.    Molin M, et al. Kinetics of mercury in blood and urine after amalgam removal. J Dent Res. 1995; 74: 420.

57.    Molin M, et al. Mercury, selenium, and GPX before & after amalgam removal. Acta Odontol Scand. 1990; 48: 189-202.

58.    Lindqvist B, et al. Effects of removing amalgam fillings from patients with diseases affecting the immune system. Med Sci Res. 1996; 24(5): 355-356.

59.    Berglund F. Case reports spanning 150 years on the adverse effects of  dental amalgam. Orlando, FL: Bio-Probe, Inc; 1995.

60.    Tuthill JY. Mercurial neurosis resulting from amalgam fillings. The Brooklyn Medical Journal. 1988; 12(12): 725-742.

61.    Lichtenberg HJ. Elimination of symptoms by removal of dental amalgam from mercury poisoned patients. J Orthomol Med. 1993; 8: 145-148.

62.    Lichtenberg H. Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals. J Orthomol Med. 1996; 11(4): 195-203.

63.    Goyer RA.Toxic and essential metal interactions. Annu Rev Nutr. 1997; 17: 37-50.

64.    Goyer RA, et al. Environmental risk factors for osteoporosis. Envir Health Perspectives. 1994; 102(4): 390-394.

65.    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; 39(2): 134-142.

66.    Goldberg AF, et al. Effect of Amalgam restorations on whole body potassium and bone mineral content in older men. Gen Dent. 1996; 44(3): 246-8.

67.    Schirrmacher K. Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+] I in bone cells. Calcif Tissue Int. 1998; 63(2): 134-9.

68.    Quig D. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.

69.    de Ceaurriz J, et al. Role of gamma: Glutamyltraspeptidase (GGC) and extracellular glutathione in dissipation of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.

70.    Berndt WO, et al. Renal glutathione  and mercury uptake. Fundam Appl Toxicol. 1985; 5(5): 832-9.

71.    Zalups RK, Barfuss DW.  Accumulation and handling of inorganic mercury in the kidney after co-administration with glutathione. J Toxicol Environ Health. 1995; 44(4): 385-99.

72.    Clarkson TW, et al. Billiary secretion of glutathione-metal complexes. Fundam Appl Toxicol. 1985; 5(5): 816-31.

73.    National Research Council. Toxicological Effects of Methyl Mercury: Risk Characterization and Public Health Implications. Nat’l Academy Press; 2000: 304-332.
74.    Molin M, et al. Mercury in plasma in patients allegedly subject to oral galvanism. Scand J Dent Res. 1987; 95: 328-334.

75.    Contrino J, Marucha P, Bigazzi PE, et al. Effects of mercury on human polymorphonuclear leukocyte function in vitro. Am J Pathol. 1988; 132(1): 110-8.

76.    West ES, et al. Textbook of Biochemistry. MacMillan Co; 1957: 853.

77.    Danielsson BRG, et al. Ferotoxicity of inorganic mercury: Distribution and effects of nutrient uptake by placenta and fetus. Biol Res Preg Perinatal. 1984; 5(3): 102-109.

78.    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.

79.    Salonen JT, 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.

80.    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; 148(2): 265-73.

81.    Gualler E, et al. Mercury, fish oils, and the risk of myocardial infarction. New England J of Medicine. 2002: 347.

82.    Kishimoto T, et al. Methyl mercury injury of cultured human vascular endothelial cells. Journal of Trace Elements in Experimental Medicine. 1993; 6(4): 155-163.

83.    Ziff MF. Documented clinical side effects to dental amalgams. Adv. Dent. Res. 1992; 1(6): 131-134.

84.    Ziff S. Dentistry Without Mercury. 8th ed. Bio-Probe; 1996.

85.    Sellars WA, Sellars R. Methyl mercury in dental amalgams in the human mouth. Journal of Nutritional & Environmental Medicine. 1996; 6(1): 33-37.

86.    Golden R, et al. Dementia and Alzheimer’s disease. Minnesota Medicine. 1995; 78: 25-29.

87.    Yannai S, et al. Transformations of inorganic mercury by candida albicans and Saccharomyces cerevisiae. Applied Envir Microbiology. 1991; 7: 245-247.

88.    Zorn NE, et al. A relationship between Vit B-12, mercury uptake, and methylation. Life Sci. 1990; 47(2): 167-73.

89.    Ridley WP, Dizikes L, Cheh A, Wood JM.  Recent studies on biomethylation and demethylation of toxic elements. Environ Health Perspect. 1977; 19: 43-6.

90.    Yamada, Tonomura. Formation of methyl mercury compounds from inorganic mercury by clostridium cochlearium. J Ferment Technol. 1972; 50: 159-1660.

91.    Woods JS, et al. Urinary porphyrin profiles as biomarker of mercury exposure: Studies on dentists. J Toxicol Environ Health. 1993; 40(2-3): 235.

92.    Woods JS. Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity. Physiol Pharmocol. 1996; 74(2): 210-15.

93.    Martin MD, et al. Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion rates. J Pharmacol Exp Ther. 1996.

94.    Woods JS, et al. Effects of porphyrinogenic metals on coproporphrinogen oxidase in liver and kidney. Toxicol App Pharm. 1989; 97:  183-190.

95.    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; 47(3): 267-83.

96.    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; 66(1): 77-82.

97.    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; 15(1): 51-7.

98.    Kumar A, Kurup PA. Digoxin and membrane sodium potassium ATPase inhibition in cardiovascular disease. Indian Heart J. 2000; 52(3): 315-8.

99.    Danielsson BR, et al. Behavioral effects of prenatal metallic mercury inhalation exposure in rats. Neurotoxicol Teratol. 1993; 15(6): 391-6.

100.    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.

101.    Tan XX, Tang C, Castoldi AF, Costa Lg.  Effects of inorganic and organic mercury on intracellular calcium levels in rat T lymphocytes. J Toxico Environ Health. 1993; 38(2): 159-70.

102.    Shenker BJ. Induction of apoptosis in human T-cells by methylmercury. Toxicol Appl Pharmacol. 1999; 157(1): 23-35.

103.    Coccini T, et al. Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction. Environ Res. 1998; 77(2): 149-159.

104.    Insug O, 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.

105.    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; 79(3): 1336-45.

106.    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; 10(3): 157-62.

107.    Anner BM, Moosmayer M, Imesch E.  Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992; 262(5.2): F830-6.

108.    Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.

109.    Wagner CA, Waldegger S, et al. Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopu oocytes. Am J Physiol. 1996 Oct; 271(4.2): F926-30.

110.    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.

111.    Echeverria D, et al. Neurobehavioral effects from exposure to dental amalgam: New distinctions between recent exposure and Hg body burden. FASEB J. 1998; 12(11): 971-980.

112.    Klinghard D, Mercola J. Mercury toxicity and systemic elimination agents. J of Nutritional and Environmental Medicine. 2001; 11: 53-62.

113.    Merchant RE. Dietary supplementation with chlorella pyrenoidosa produces positive results in patients with cancer or suffering from certain common chronic illnesses. Townsend Letter for Doctors. 2001.

114.    Oliveira EM, et al. Mercury effects on the contractile activity of the heart muscle. Toxicol Appl Pharmacol. 1994; 1: 86-91.

115.    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; 10(4): 370-5.

116.    Marsh DO, et al. Fetal methyl mercury poisoning. Ann Neurol. 1980; 7: 348-55.

117.    Weihe P, Debes F, White RF, et al. Environmental epidemiology research leads to a decrease of the exposure limit for mercury. Ugeskr Laeger. 2003; 165(2): 107-11.

118.    Siblerud RL. The relationship between mercury from dental amalgam and the cardiovascular system. Science of the Total Envir. 1990; 99(1-2): 23-35.

119.    Trepka MJ, Heinrich J, Krause C, et al. Factors affecting internal mercury burdens among German children. Arch Environ Health. 1997; 52(2): 134-8.

120.    Soleo L, et al. Influence of amalgam fillings on urinary mercury excretion. G Ital Med Lav Ergon.1998; 20(2): 75-81.

121.    Freitas AJ, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Research. 1996; 738(2): 257-64.

122.    Yallapragoda PR, et al. Inhibition of calcium transport by Hg salts; in rat cerebellum and cerebral cortex. J Appl Toxicol. 1996; 164(4): 325-30.

123.    Chavez E, et al. Mitochondrial calcium release by Hg+2. J Biol Chem. 1988; 263(8): 3582.

124.    Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.

125.    Rossi AD, et al. Modifications of Ca2+ signaling by inorganic mercury in PC12 cells.  FASEB J. 1993; 7: 1507-14.

126.    Boadi WY, et al.  In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res. 1992; 57(1): 96-106.

127.    Boadi WY. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity. Pharmacol. 1992; 116(1): 17-23.

128.    Urbach J, et al.  Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Reprod Toxicol. 1992; 6(1): 69-75.

129.    Karp W, Gale TF, et al. Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters. Environmental Research. 1985; 36: 351-358.

130.    Karp W, et al. Correlation of human placental enzymatic activity with trace     metal concentration in placenta. Environmental Research. 1997; 13: 470-477.

131.    Boot JH.  Effects of SH-blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes.  Cell Struct Funct. 1995; 20(3): 233-8.

132.    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; 7(2): 332-340.

133.    Iioka H, et al. The effect of inorganic mercury on placental amino acid transport. Nippon Sanka Fujinka Gakkai Zasshi. 1987; 39(2): 202-6.

134.    Drexler H, et al. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Environmental Research. 1998; 77(2): 124-9.

135.    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; 137(3): 169-84.

136.    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; 56(2): 143-52.

137.    Benga G. Water exchange through erythrocyte membranes. Neurol Neurochir Pol. 1997; 31(5): 905-13.

138.    Kistner A. Amalgam: Diagnose und therapie. ZWR. 1995; 104(5): 412-417.

139.    Placidi GF, et al. Distribution of inhaled mercury (203Hg) in various organs. Int J Tiss React. 2983; 5: 193-200.

140.    Yoshida M, et al. Distribution of mercury in neonatal guinea pigs after exposure to mercury vapor. Bull Environ Contam Toxicol. 1989; 43(5): 697-704.

141.    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. 1984; 55:145-52.

142.    Halbach S, et al. Thiol chelators and mercury effects on isolated heart muscle. Plzen. Lek. Sborn. 1990; 62: 39-41.

143.    Klykov NV. Treatment of patients with myocardial infarction.  Vrach.Delo. 1979; (12): 50-3.

144.    Klykov NV. Treatment of patients with chronic circulatory insufficiency. Kardiologila. 1972; 12(1): 126-31.

145.    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.

146.    Sterzl I, Prochazkova J, Stejskal VDM et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.

147.    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.

148.    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.

149.    Sterzl I, Fucikova T, Zamrazil V.  The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.

150.    Sterzl I, Hrda P, Prochazkova J, Bartova J. Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitrni Lekarstvi. 1999; 45(9): 527-31.

151.    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.

152.    Smith T, Pitts K, Mc Garvey JA, Summers AO. Bacterial oxidation of mercury metal vapor. Appl Environ Microbiol. 1998; 64(4): 1328-32.

153.    Ashe W, Largent E, Dutra F, et al. Behavior of mercury in the animal organism following inhalation. Arch. Ind. Hyg. Occup. Med. 1953; 17:19-43.

154.    Rupp, Paffenberger. Significance to health of mercury used in dental practice: Reports of Councils and Bureaus. JADA. 1971; 182.

155.    Leistevuo J, Pyy L, Osterblad M. Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res. 2001; 35(3): 163-6.

156.    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.

157.    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.

158.    Haddow JE, et al. Babies born to mothers with untreated hypothyroidism have lower I.Q.’s. New England Journal of Medicine. 1999.

159.    Lavado-Autric, et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. JCI. 2003; 111: 1073-1082.

160.    Pop VJ, Vader HL, et al. Low maternal free thyroxine during early pregnancy is associated with impaired psychomotor development in infancy. Clin Endocrinol(Oxf). 1999; 50:149-55.

161.    Asami T, Suzuki H. Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid. 2001; 11: 765-8.

162.    Kumar R, Chaudhuri BN. Altered maternal thyroid function: fetal and neonatal heart cholesterol and phospholipids. Indian J Physiol Pharmacol. 1993; 37(3): 176-82.

163.    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.

164.    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.

165.    Hak AE, et al. The Rotterdam Study: Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women. Ann Int Med. 2000; 132: 270-278.

166.    Biondi B, Palmieri EA, Lombardi G, Fazio S.  Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med. 2002; 137(11): 904-14.

167.    Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med. 1999; 131: 348.

168.    Asami T, Suzuki H. Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid. 2001; 11: 765-8.

169.    Novembrino C, Bamonti F, Minoia C, Guzzi G, Pigatto PD. Homocysteine and mercury dental amalgam. Paper & presentation at 8th International Conference on Mercury Global. Madison, WI. 2006.

170.    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; 60(4): 838-46.

171.    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; 36(5): 687-97.

172.    Piikivi L, Tolonen U. EEG findings in chlor-alkali workers subjected to low long term exposure to mercury vapour. Br J Ind Med. 1989; 46(6): 370-5.

173.    Boffeta P, Sallsten G. Mortality from cardiovascular diseases and inorganic mercury exposure. Occup Environ Med. 2001; 58: 461-465.

174.    Wossmann W, et al. Mercury intoxication presenting with hypertension and tachycardia. Arch Dis Child. 1999; 80(6): 556-7.

175.    Gattineni J, Weiser S, Becker AM, Baum M. Mercury intoxication: Lack of correlation between symptoms and levels. Clin Pediatr. 2007; 46(9): 844-6.

176.    Henningsson C, et al.  Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent. J Pediatr. 1993; 122(2): 252-3.

177.    Florentine MJ, et al. Elemental mercury poisoning. Clin Pharm. 1991; 10(3): 213-21.

178.    Warkeny J, Hubbard CH. Acrodynia and mercury. Journal of Pediatrics. 1953; 42(3):  365-386.

179.    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.

180.    Hightower J. Methylmercury contaminmation in fish: Human exposures and case reports. Environ Health Perspect. 2002.

181.    Chang XZ, Lu HM, Zhang YH, Qin J. Hypertension and erythromelalgia as prominent manifestations of mercury intoxication. Beijing Da Xue Xue Bao. 2007; 39(4): 377-80.

182.    Cloarec S, et al. Arterial hypertension due to mercury poisoning: Diagnostic value of  captopril. Arch Pediatr. 1995; 2(1): 43-6.

183.    Michaeli-Yossef Y, Berkovitch M, Goldman M. Mercury intoxication in a 2-year-old girl: A diagnostic challenge for the physician. Pediatr Nephrol. 2007; 22(6): 903-6.

184.    Torres AD, Rai AN, Hardiek ML. Mercury intoxication and arterial hypertension: report of two patients and review of the literature. Pediatrics. 2000; 105(3): E34.

185.    De Oliveira J, Silva SR. Arterial hypertension due to mercury intoxication with clinico-laboratorial syndrome simulating pheochromocytoma. Arg Bras Cardiol. 1996; 66(1): 29-31.

186.    Mutter J, Yeter D. Kawasaki’s disease, acrodynia, and mercury. Curr Med Chem. 2008; 15(28): 3000-10.

187.    Orlowski JP, Mercer RD. Urine mercury ;evels in Kawasaki Disease: Myocardial infarction, abnormal EKG, A-V block, PVC, myocarditis, aneurysms by mercury. Pediatrics. 1980; 66(4): 633-6.

188.    Dan R. Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999-2006. Biometals. 2009.

189.    Laks DR, et al. Mercury has an affinity for pituitary hormones. Med Hypotheses. 2009.

190.    J Danesh, R Collins, P Appleby, Richard Peto. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease. 1998; 279: 1477-1482.

191.    Suarez E.  A good mood equals a healthy heart. Journal Psychosomatic Medicine. 2004.
192.    McIntyre IM, Judd FK, Marriott PM, et al. Plasma melatonin levels in affective states. Int J Clin Pharmacol Res. 1989; 9(2): 159-64.

193.    Riemann D, Klein T, Rodenbeck A, et al. Nocturnal cortisol and melatonin secretion in primary insomnia. Psychiatry Res. 2002; 113(1-2): 17-27.

194.    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; 23(10) :2597-605.

195.    Siblerud RL, et al. Psychometric evidence that mercury from dental fillings may be a factor in depression, anger, and anxiety. Psychol Rep. 1994; 74(1).

196.    Kim CY, Satoh H, et al. Protective effect of melatonin on methylmercury-induced mortality in mice. Tohoku J Exp Med. 2000; 191(4): 241-6.

197.    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; 74(1): 231-6.

198.    Baccarelli A, Pesatori AC, Bertazzi PA. Occupational and environmental agents as endocrine disruptors: experimental and human evidence. J Endocrinol Invest. 2000; 23(11): 771-81.

199.    Wagstaff J. Effects of a low dose of melatonin on sleep in children with Angelman syndrome. J Pediatr Endocrinol Metab. 1999; 12(1): 57-67.

200.    Brusco L, et al. Effect of melatonin in selected populations of sleep-disturbed patients.  Biol Signals Recept. 1999; 8(1-2): 126-31.

201.    Houston MC. The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. Altern Ther Health Med. 2007; 13(2): S128-33.

202.    Luoma P. Antioxidants, infections and environmental factors in health and disease in northern Finland. Int J Circumpolar Health. 1998; 57(2-3): 109-13.

203.    Hagele TJ, Mazerik JN, Parinandi NL, et al. Mercury activates vascular endothelial cell phospholipase D through thiols and oxidative stress. Int J Toxicol. 2007; 26(1): 57-69.

204.    Mazerik JN, et al.  Phospholipase A activation regulates cytotoxicity of methylmercury in vascular endothelial cells. Int J Toxicol. 2007; 26(6): 553-569.

205.    Watt R. Periodontal disease and heart disease risk. BMJ. 2010.

206.    Houston M. Role of mercury toxicity in hypertension, cardiovascular disease, and stroke. The Journal of Clinical Hypertension. 2011; 13(8).

207.    Langsjoen P, Langsjoen P, Willis R, et al. Coenzyme Q10 in essential hypertension. Mol Aspects Med. 1994; 15: S257-S263.

208.    Molyneux SL, Florkowski CM, George PM, et al. Coenzyme Q10: An independent predictor of mortality in chronic heart failure. J Am Coll Cardiol. 2008; 52(18): 1435-41.

209.    Greenberg SM, Frishman WH. Coenzyme Q10: A new drug for myocardial ischemia? Med Clin North Am. 1988; 72(1): 243-58.

210.    Bahorun T, Trotin F, Pommery J, et al. Antioxidant activities of crataegus monogyna extracts (hawthorn). Planta Med. 1994; 60: 323-8.

211.    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.

212.    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.

213.    Fujita T, Ando K, Noda H, et al. Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension. Circulation. 1987; 75(3): 525-32.

214.    Miglis M, Wilder D, Reid T, et al. Effect of taurine on platelets and the plasma coagulation system. Platelets. 2002; 13(1): 5-10.

215.    Kidd PM. Integrative cardiac revitalization: Bypass surgery, angioplasty, and chelation. Benefits, risks, and limitations. Altern Med Rev. 1998; 3(1): 4-17.

216.    Hancke C. Benefits of EDTA chelation therapy in arteriosclerosis: A retrospective study of 470 patients. J Adv Med. 1993; 6(3): 161-71.

217.    McDonagh EW. Non-invasive treatment for sequelae of failed coronary blood circulation. J Neuro Ortho Med Surg. 1993; 14: 169-73.

218.    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.

219.    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.

220.    Hancke C, Flytlie K. Benefits of EDTA chelation therapy in arteriosclerosis. J Adv Med. 1993; 6(3): 161.

221.    Lutsey PL, Steffen L, et al. Dietary intake and the development of the metabolic syndrome. The Atherosclerosis Risk in Communities Study. Circulation. 2008.

222.    Dandona P. Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein.  Mayo Clin Proc. 2008; 83(3): 333-42.

223.    Vasdev S, Gill V, Singal P. Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007; 49(1): 48-63.

 

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