Metabolic Effects of Mercury Exposure
- Dental amalgam has been documented by medical lab tests and government agencies to be the largest source of mercury in most people who have several amalgam fillings. Bacteria in the mouth and intestines and other methyl donors methylate mercury to methyl mercury, so amalgam fillings are also the largest source of methyl mercury in many people. Some people also get significant mercury exposures from fish or vaccinations, and in a large survey testing people’s mercury levels, it was found that over 22% had dangerous levels of mercury, with over 30% in some states such as Florida and New York.
- 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. Using NHANES data, it found that while inorganic mercury was detected in the blood of 2% of women aged 18 to 49 in the 1999-2000, that level rose to 30% by 2005-2006.
- Mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage to the stomach lining. It adversely alters bacterial populations in the intestines, causing leaky gut syndrome with toxic, incompletely digested complexes in the blood and accumulation of heliobacter pylori, a suspected major factor in stomach ulcers and stomach cancer, and candida albicans, as well as poor nutrient absorption. Mercury has also been found to cause ulcerative colitis.
- Mercury’s ability to bind to SH hydroxyl radicals in cell membranes alters cell permeability, which further adds to essential mineral deficiencies and imbalances. Forming strong bonds with and modification of the-SH groups of proteins causes reactive oxygen species (free radicals) and mitochondrial release of calcium, as well as altering molecular function of amino acids and damaging enzymatic processes, resulting in improper cysteine regulation, inhibited glucose transfer and uptake, damaged sulfur oxidation processes, and reduced glutathione availability (necessary for detoxification). Several other toxic metals have similar effects, as well as synergistically causing more serious effects in conjunction with mercury.
- Mercury from amalgam binds to the SH (sulfhydryl) groups, resulting in inactivation of sulfur and blocking of enzyme functions such as cysteine dioxygenase(CDO), gamma‑ glutamyltraspeptidase (GGC), and sulfite oxidase, producing sulfur metabolites with extreme toxicity that the body is unable to properly detoxify, as well as a deficiency in sulfates and other metabolites required for many body functions. Sulfur is essential in enzymes, hormones, nerve tissue, and red blood cells. These exist in almost every enzymatic process in the body. Blocked or inhibited sulfur oxidation at the cellular level has been found in most with many of the chronic degenerative diseases, including Parkinson’s, Alzheimer’s, ALS, lupus, rheumatoid arthritis, MCS, and autism. It appears to be a major factor in these conditions.
- Mercury also blocks the metabolic action of manganese and the entry of calcium ions into cytoplasm. Mercury affects the free selenium levels and superoxide dimustase function. Mercury reduces the blood’s ability to transport oxygen to organs or the fetus, as well as the transport of essential nutrients, including amino acids, glucose, magnesium, zinc and vitamin B12. It depresses enzyme isocitric dehydrogenase (ICD) in fetuses, causes reduced iodine uptake & hypothyroidism, and increased homocysteine levels.
- Mercury from amalgam thus has the potential to disturb all metabolic processes. Mercury is transported throughout the body in blood and can affect cells in the body and organs in different ways.
- Mercury blocks the immune function of magnesium and zinc, whose deficiencies are known to have significant neurological effects. The low zinc levels result in deficient CuZnSuperoxide dismustase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure. This is in addition to mercury’s effect on metallothionein and copper homeostasis. Copper is an essential trace metal which plays a fundamental role in the biochemistry of the nervous system. Several chronic neurological conditions involving copper metabolic disorders are well documented, such as Wilson’s disease and Menkes disease. Mutations in the copper/zinc enzyme superoxide dismustase (SOD) have been shown to be a major factor in the motor neuron degeneration in conditions such as familial ALS. Similar effects on Cu/Zn SOD is known to be a factor in other conditions such as autism, Alzheimer’s, Parkinson’s, and non-familial ALS. This condition can result in zinc deficient SOD and oxidative damage involving nitric oxide, peroxynitrite, and lipid peroxidation, which have been found to affect glutamate mediated excitability and apoptosis of nerve cells and effects on mitochondria.
- These effects can be reduced by zinc supplementation, as well as supplementation with antioxidants, nitric oxide-suppressing agents, and peroxynitrite scavengers such as vitamin C, vitamin E, lipoic acid, coenzyme Q10, carnosine, gingko biloba, and N-acetylcysteine, among others. Some of the antioxidants were also found to have protective effects through increasing catalase and SOD action, while reducing lipid peroxidations. Ceruloplasmin in plasma can be similarly affected by copper metabolism dysfunction, like SOD function, and is often a factor in neurodegeneration.
- Mercury causes interruption of the Cytochrome c oxidase system/ATP energy function and blocks enzymes needed to convert porphyrins to adenosine triphosphate (ATP), the body’s basic energy source, causing progressive porphyrinuria and resulting in low energy, digestive problems, and porphyrins in urine.
- Mercury binding with cell membranes interferes with sodium and potassium enzyme functions, causing excess membrane permeability, especially in terms of the blood-brain barrier. Less than 1ppm mercury in the blood stream can impair the blood-brain barrier.
- The essential mineral deficiencies and imbalances have been found to be a major factor in epilepsy, ADHD, depression, and other chronic conditions, and correcting mineral imbalances has been found to cause significant improvement in many such chronic conditions caused by mercury toxicity.
- Mercury inactivates or inhibits enzyme or coenzyme systems or hormones involving the sulfhydryl protein (SH) groups, along with OH, NH2, and Cl groups in proteins. HgCl2 also inhibits aquaporin‑mediated water transport in red blood cells, as well as oxygen transport by hemoglobin. Thus some of the main mechanisms of toxic effects of metals include cytotoxicity, changes in cellular membrane permeability, inhibition of enzymes, coenzymes, and hormones, and the generation of lipid peroxides or free radicals. This results in neurotoxicity, immuno toxicity, impaired cellular respiration, gastrointestinal/metabolic effects, hormonal effects, and immune reactivity or autoimmunity.
- The alteration of intestinal bacterial populations necessary for proper digestion, along with other damage and membrane permeability effects of mercury, are major factors in creating leaky gut conditions with poor digestion, poor absorption of nutrients, and toxic, incompletely digested compounds in the bloodstream. Some of the gastrointestinal problems caused by mercury include poor mineral absorption, diarrhea, stomatis, bloating, wasting disease, food allergies, and leaky gut syndrome.
Documentation of this information is available from DAMS at amalgam.org.
DAMS is currently working with thousands of people in the U.S. dealing with serious health effects caused by exposure to mercury from amalgam and urges everyone to find out more about this major problem and to get involved in resolving these health safety issues. DAMS can provide information and help to anyone who is interested or who thinks they might have health problems related to their amalgam fillings.