How Mercury Can Cause CFS & FMS
Not only can mercury cause CFS and FMS, it can weaken the immune system, provoke a leaky gut and Irritable Bowel Syndrome, fatigue, depression, and sleeplessness.
1) Low Level Mercury Enters Body
The little mercury molecule is close to the bottom of the periodic table, which means it is very heavy, with 80 protons and neutrons in it's nucleus. This molecule is considered a poison by the Center for Disease Control and by the FDA. It is poisonous because it binds to other things in the body, and then inactivates or changes what they were doing. This molecule enters the body from 2 sources. One is dental amalgam (metal cavity filling in teeth), and the other is from saltwater fish, which absorb it from water pollution.1
The mercury dental amalgam is 200,000 ppm (parts per million) mercury, whereas the FDA says that more than 1 ppm mercury in food is no good. And the dental amalgam wears out and disappears over time, therefore requiring refilling of the cavity. And since our oceans are full of mercury from dumping waste products into the ocean, mercury is known to be in fish. Mercury can easily be measured using scientific instruments, and can therefore be detected in tissues, liquids, and solids; including things like urine, and organs from dead bodies. And this instrumentation can easily measure levels of mercury in fish (i.e. number of micrograms of mercury for each gram of fish), and is more often than not seen in saltwater fish (freshwater is ok).
An interesting study was done by Dr. Lorscheider who placed mercury fillings in sheep and in monkey, and then let them chew on them for several weeks. He then ground up the organs of these sheep and some control sheep that did not receive the amalgam (after sacrificing the animals), and found mercury molecules in almost every organ. He proved to the world that mercury molecules to can enter the organs from dental fillings.1
2) Mercury Impairs The Immune System
Mercury molecules inactivates a part of the immune system called Neutrophils. These are responsible for killing fungi inside the body (i.e. blood and soft tissues) that originate from places like the small intestine.2 Measuring Neutrophils function is very difficult, since a blood sample must be analyzed several hours after being drawn. Subsequently, very few Docs measure this. (reference 3) shows how mercury can impair leukocytes, another part of the immune system that fights fungi. In our example case involving George, an immune test showed decrease leukocytes function.
3) With an Impaired Immune System, Fungi Grow Internally
It is well known in medicine that fungi cannot activate unless the immune system is impaired in some way (e.g. leukemia), and if someone does not have an obviously impaired immune system, then the traditional Doc will not think fungi. This is why Docs have not focused more on fungi. They are taught, if the patient does not have obvious external signs of fungi or does not have an impaired immune system (e.g. low white blood cell count, AIDS), then they should not think fungi.
One way to see fungi internally is a fungi antibody test, which shows soldiers in the blood that attack a specific type of fungi. Antibody tests have many false negatives, since they only test for a handful of specific fungi, and there are many possible types of fungi that can enter a body. This compounds the difficulty in implicating fungi in disease. In our example case, George had a very high antibody level to a fungi called Pullaria Pullans.
4) Fungi Affix to Tissues And are Attacked By Immune System
Fungi, once in the blood, can go anywhere including soft tissues and joints. They can then be attacked by the immune system causing inflammation and pain. A good way to test for internal inflammation is a Sedimentation blood test.
5) Mercury Encourages Leaky Gut
Mercury can also inactivate enzymes in the liver, inhibiting it's ability to filter the blood. When this occurs, more waste products build within the body (the liver's job is to filter the natural waste products secreted by the body's cells), and the immune system becomes more sensitive, causing it to attack things which are not harmful (i.e. allergies). And when allergies develop to foods, the gut can be attacked by the immune system, and the person can develop Irritable Bowel Syndrome (IBS). And then the small intestine wall inflames and becomes permeable to the large bacteria and fungi molecules in the gut, which leak into the blood, challenging the immune system further, making one more allergic, and inducing Fibromyalgia pain after they affix to joints and soft tissues.
6) Mercury Impairs The Manufacture of Blood
A study by Dr. James Woods published in the Journal of Toxicology 1993 showed that mercury can inactivate the liver enzymes that are used in the manufacture of a precursor to blood called HEME, and this disrupts one's ability to generate energy. More specifically he showed that mercury can disrupt the Coproporphyrin III Porphyrin step. In our example case, George's Coproporphyrin III level was out of range. There are very few things that cause this abnormal range yet do not affect other porphyrins (there are a total of 9 of them); therefore, this test is sometimes viewed as a biomarker for mercury. In other words, one an run this test and see if mercury had been in the body in the past, to the extent that it was able to disrupt this enzyme. If so, it probably did other deeds as well.4
7) Mercury Impairs DBH, used to make Noradrenaline
There is evidence that mercury can block the dopamine-beta-hydroxylase (DBH) enzyme. DBH is used to make the noradrenaline (NA) neurotransmitter and low NA can cause fatigue and depression. Mercury molecules can block all copper catalyzed dithiolane oxidases, such as coproporphyrin oxidase (resulting in low copro III seen w/ Porphyrin Analysis) and dopamine-beta-hydroxylase (DBH). Low VMA, a by-product of NA, can be seen with a 24hr Organic Acids test. A low VMA level implicates low NA, which implicates low DBH, which implicates mercury (just implications, not conclusions, since other things can cause problems here as well). In our example case, George's VMA was close to 0. Mercury can also clog the NA alpha-1 receptors, which reduces NA communication, and results in fatigue. Additionally, mercury can clog seratonin 5-HT2 receptors, impair astrocytic dopamine uptake, impair acetylcholine estererase, and impair cholinergic metabolism.5
8) Heavy Metals Can Disrupt The Sleep Cycle
The Melatonin hormone controls the sleep/no sleep states. If Melatonin is on in the day, one will feels tired. If it is off at night, one cannot sleep (it should be the other way around). Too much noradrenaline (NA) at night can also inhibit the sleep state. A chemical called SAMe reduces the level of NA at night; yet mercury, lead, arsenic, cadmium and a variety of other chemicals can bind to SAMe and make it less affective at reducing the night-time NA. If this is the case, supplementing with SAMe, available from health food stores, can help one sleep. In our example case, George's Melatonin was off at night, and on during the day, which is the opposite of what one would want. Those with mercury induced autoimmune problems can worsen from Melatonin supplements, and therefore Melatonin supplementation is not recommended for people with mercury issues.
If you have teeth that contain mercury fillings, your body has experienced long-term poisoning and requires special attention!
Answer: You must remove all sources of mercury and go through a mercury detox treatment to remove all the mercury from your body.
Read the true CFS recovery story of someone who didn't know he had been mercury poisoned because of mercury fillings.
Title: Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues [see comments]
Author: Hahn LJ; Kloiber R; Leininger RW; Vimy MJ; Lorscheider FL
Address: Department of Radiology, University of Calgary, Faculty of Medicine, Alberta, Canada.
Source: FASEB J, 4(14):3256-60 1990 Nov
Abstract: The fate of mercury (Hg) released from dental "silver amalgam tooth fillings into human mouth air is uncertain. A previous report about sheep revealed uptake routes and distribution of amalgam Hg among body tissues. The present investigation demonstrates the bodily distribution of amalgam Hg in a monkey whose dentition, diet, feeding regimen, and chewing pattern closely resemble those of humans. When amalgam fillings, which normally contain 50% Hg, are made with a tracer of radioactive 203Hg and then placed into monkey teeth, the isotope appears in high concentration in various organs and tissues within 4 wk. Whole-body images of the monkey revealed that the highest levels of Hg were located in the kidney, gastrointestinal tract, and jaw. The dental profession's advocacy of silver amalgam as a stable tooth restorative material is not supported by these findings.
Unique Identifier: 91032709
MESH Headings: Animal ; Comparative Study ; Dental Amalgam * ; Diagnostic Imaging ; Gastrointestinal System ME ; Jaw ME ; Kidney ME ; Macaca fascicularis ; Male ; Mercury *PK ; Mercury Radioisotopes ; Support, Non-U.S. Gov't ; Tissue Distribution ; Tomography, Emission-Computed, Single-Photon
Publication Type: JOURNAL ARTICLE
Country of Publication: UNITED STATES
CAS Registry Number: 0 (Mercury Radioisotopes); 7439-97-6 (Mercury); 8049-85-2 (Dental Amalgam)
Title: Polymorphonuclear phagocytosis and killing workers exposed to inorganic mercury.
Perlingeiro RC; Queiroz ML
Department of Pharmacology and Hemocentre, State University of Campinas, Faculty of Medical Sciences, UNICAMP, SP, Brazil.
Int J Immunopharmacol, 1994 Dec, 16:12, 1011-7
The ability of neutrophils to phagocytose and kill Candida species as well as the splenic phagocytic function were investigated in workers from a mercury-producing plant. In the neutrophil phagocytosis study, two species of Candida were used since in individuals with myeloperoxidase deficiency neutrophils are unable to kill Candida albicans, while Candida pseudotropicalis can be effectively lysed. Phagocytosis of both antigens and splenic phagocytic function were normal in all the workers studied. However, following ingestion of the organisms there was considerable reduction in the ability of neutrophils from exposed workers to kill both species of Candida, and this was not explained by a mild impairment of phagocytosis. After improvement in the hygiene conditions in the factory, a new evaluation was performed, 6 months later, in the same workers and urinary mercury concentrations were determined monthly in each worker. Despite a significant reduction in urinary mercury concentrations, a greater impairment in the ability of neutrophils to kill C. albicans was observed. The killing of C. pseudotropicalis presented no further impairment when compared to the previous evaluation. These results suggest that impairment of the lytic activity of neutrophils from workers with urinary mercury concentrations within the safe level for exposed population is due, at least in part, to some interference with myeloperoxidase activity. In addition, the mercury-NADPH complex, once formed, could limit the utilization of reduced pyridine nucleotides by NADPH-dependent enzymes such as NADPH oxidase, thereby inhibiting the PMN respiratory burst.
Title : Effects of mercury on human polymorphonuclear leukocyte function in vitro.
Author: Contrino J; Marucha P; Ribaudo R; Ference R; Bigazzi PE; Kreutzer DL
Address: Department of Pathology, University of Connecticut Health Center, Farmington 06032.
Source: Am J Pathol, 1988 Jul, 132:1, 110-8
Abstract: A variety of heavy metals are recognized as environmental pollutants, and although a significant body of literature exists on the acute toxicity of these metals in various tissues, little is known about the effects of metals such as mercury on host defense. Therefore, the effect of mercuric chloride (HgCl2) on human polymorphonuclear leukocytes (PMN) function in vitro was evaluated. The acute toxicity of HgCl2 for human PMN was calculated initially using vital dye exclusion (trypan blue), and lactate dehydrogenase (LDH) release. Concentrations of HgCl2 less than or equal to 10(-6) M did not induce significant LDH release, or uptake of trypan blue. Additionally, HgCl2 at less than or equal to 10(-7) M produced no ultrastructural alterations in the PMN. The effects of HgCl2 on human PMN functions involved in host defense were evaluated next. HgCl2 consistently suppressed human PMN adherence, polarization, chemotaxis, and erythrophagocytosis at concentrations between 10(-6) and 10(-17) M. Because of the established role of oxygen metabolites in host defense, the effects of HgCl2 on human PMN chemiluminescence and H2O2 production were evaluated next. These studies demonstrated that low concentrations of HgCl2 (ie, 10(-9)-10(-15) M) significantly enhanced chemiluminescence, as well as stimulated H2O2 production by the PMN. These studies clearly demonstrate the ability of extremely low levels of HgCl2 not only to suppress various PMN 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.
Title: Altered porphyrin metabolism as a biomarker of mercury exposure and toxicity.
Author: Woods JS
Address: Department of Environmental Health, University of Washington, Seattle, USA.
Source: Can J Physiol Pharmacol, 74(2):210-5 1996 Feb
Abstract: Changes in urinary porphyrin excretion patterns (porphyrin profiles) have been described in response to a variety of drugs and chemicals. The present studies were conducted to define the specific changes in the urinary porphyrin profile associated with prolonged exposure to mercury and mercury compounds. In rats, exposure for a prolonged period to mercury as methyl mercury hydroxide was associated with urinary porphyrin changes, which were uniquely characterized by highly elevated levels of 4- and 5-carboxyl porphyrins and by the expression of an atypical porphyrin ("precoproporphyrin") not found in urine of unexposed animals. These distinct changes in urinary porphyrin concentrations were observed as early as 1-2 weeks after initiation of mercury exposure, and increased in a dose- and time-related fashion with the concentration of mercury in the kidney, a principal target organ of mercury compounds. Following cessation of mercury exposure, urinary porphyrin concentrations reverted to normal levels, consistent with renal mercury clearance. In human studies, a comparable change in the urinary porphyrin profile was observed among subjects with occupational exposure to mercury as mercury vapor sufficient to elicit urinary mercury levels greater than 20 micrograms/L. Urinary porphyrin profiles were also shown to correlate significantly with mercury body burden and with specific neurobehavioral deficits associated with low level mercury exposure. These findings support the utility of urinary porphyrin profiles as a useful biomarker of mercury exposure and potential health effects in human subjects.
Unique Identifier: 96303184
MESH Headings: Adult ; Animal ; Biological Markers UR ; Central Nervous System Diseases CI/UR ; Chelating Agents PD ; Comparative Study ; Dentistry ; Environmental Monitoring ; Human ; Male ; Mercury *AE/*TO/UR ; Methylmercury Compounds TO ; Occupational Exposure *AE ; Porphyrins *UR ; Rats ; Support, U.S. Gov't, P.H.S. ; United States ; Unithiol PD
Re: Dopamine beta hydroxylase and poisons ( lead, mercury, manganese etc. )
Title: Biochemical markers of neurotoxicity. A review of mechanistic studies and applications.
Author ": Manzo L; Artigas F; Martínez E; Mutti A; Bergamaschi E; Nicotera P; Tonini M; Candura SM; Ray DE; Costa LG
Address: Toxicology Unit, University of Pavia, Italy.
Source: Hum Exp Toxicol, 1996 Mar, 15 Suppl 1:, S20-35
Abstract: Neurotoxicology presents major challenges to the development of biological markers in accordance to conventional research strategies. Because of the inaccessibility of the nervous system, one of the proposed alternatives is the study of biochemical signals in peripheral tissues which can easily and ethically be obtained in humans, and which could represent surrogate indicators of equivalent parameters in the nervous tissue. Considerable scientific support to this approach is provided by the results of recent investigations in major areas of pharmacology and psychobiology. Studies examining parameters of neurotransmission and second messenger systems in peripheral blood cells, and variations in the peripheral body fluid content of endogenous substances reflecting nervous tissue dysfunction or damage are presented in this paper as examples of efforts toward rational development and validation of novel indicators of nervous system toxicity. Cholinergic muscarinic receptors and calcium signalling in peripheral blood lymphocytes, myelin basic protein in cerebrospinal fluid, and blood polyamines are discussed as potential surrogate indicators based on the results of in vitro or in vivo animal studies of neurotoxic metals (mercury, triethyltin), pesticides (disulfoton), drugs of abuse (d-fenfluramine) and model epileptogenic compounds (kainic acid). Data from investigations examining serum prolactin, type B monoamine oxidase (MAO-B) and dopamine beta-hydroxylase (DBH) in workers occupationally exposed to manganese, lead or styrene are also presented. Although research in this field is still at its very early stage, current evidence suggests that (i) certain neurochemical markers may be valuably used in animal studies as a complement to conventional laboratory tests to augment their sensitivity or predictivity; (ii) a mechanistic research approach is required to establish which markers offer the greatest promise for application in human biomonitoring.