Mercury is a toxic metal with significant effects on the thyroid. There is ample evidence that mercury leaches from dental amalgam fillings and contributes to thyroid disease and anemia. While large doses of mercury can induce hyperthyroidism, smaller amounts can induce hypothyroidism by interfering with both the production of thyroxin (T4) and the conversion of T4 to T3.
Mercury disturbs the metabolism of copper and zinc which are two minerals critical to thyroid function. Gray hair can be an indication of mercury accumulation, more so in females than males.
Mercury causes disruptions to the immune system functioning and promotes the production of IgG and IgE autoantibodies which also are involved in autoimmune thyroid disease. Different forms of mercury, organic or inorganic, have different effects on the thyroid.
Milk and quite likely estrogen cause an increase in the absorption of mercury.
Mercury has a very long half-life in the body with a duration of perhaps many years and has been found in cancerous tissues.
Selenium is the key mineral which protects the body from mercury toxicity. One study showed that cilantro (Chinese parsley) helps remove mercury from the body and protects the body from pre-cancerous lesions.
As the following article indicates mercury gets into our bodies in a variety of ways including vaccinations. Perhaps the negative effects we see from vaccines are at least partially the result of toxic metals. The association of autism with vaccinations may be related to mercury toxicity. Thimerosal is the mercury-containing preservative that was used in contact lens solutions. Hopefully there are no more of these solutions on the market but if you use contact lens solutions, check the label.
US Congressman Dan Burton Requests Immediate Vaccine Recall
In an October 25, 2000 letter to Department of Health and Human Services (HHS) Secretary Donna Shalala, Congressman Dan Burton (R-IN), Chairman of the House Committee on Government Reform, requested a recall of all vaccines containing Thimerosal. The mercury-based product Thimerosal is added to vaccines as a preservative.
On July 18, 2000 the Committee conducted a hearing entitled, “Mercury in Medicine: Are We Taking Unnecessary Risks?” During the hearing, the FDA admitted that children are being exposed to unsafe levels of mercury through vaccines containing Thimerosal. It was also determined that symptoms of mercury poisoning mimic symptoms of autism -- a disease that has reached epidemic levels in the United States. However, the FDA has chosen to allow pharmaceutical companies to merely phase out their use of Thimerosal, leaving mercury-containing vaccines at public and private health facilities.
In his letter to Secretary Shalala, Chairman Burton stated:
Exposure to heavy metals such as cadmium and mercury is of immediate environmental concern. The present study was aimed at establishing a direct relationship between heavy metal poisoning and thyroid dysfunction. Cadmium and mercury treatment at LD50 levels resulted in severe thyrotoxicosis in the rabbit.
Within 24 h of intramuscular administration of cadmium chloride 15 mg.kg-1 body weight (bw) and mercury chloride 20 mg.kg-1 bw, thyroid peroxidase activity increased significantly over the control with a concomitant rise in the triiodothyronine (T3) titre.
On the other hand, there was a remarkable fall in the thyroxine (T4) level, and the T3/T4 ratio was high as compared with the control. Evidence indicates that acute heavy metal lethality will induce immediate hyperthyroidism. It is suggested that T3-toxicosis may be produced by a preferential synthesis of T3 and/or preferential deiodination of T4 to T3. Measurement of T3 and T4 levels may thus be utilized as a reliable indicator of heavy metal lethality.
The following study showed that the administration of
mercury in the form of mercuric chloride causes significant alterations in
copper and zinc metabolism, but does not seem to affect iron
metabolism. While the thyroid functions were not examined in this
study, the fact that mercury has such profound effects on copper and zinc
metabolism suggests that thyroidal function will be disturbed by mercury.
The present study was designed to investigate the effect of mercuric chloride administration on copper, zinc, and iron concentrations in the liver, kidney, lung, heart, spleen, and muscle of rats.
The results showed that after dose and time exposure to mercuric chloride, the concentration of mercury in the six tissues was significantly elevated. Data showed that there were no interaction between mercury and tissue iron. There was a considerable elevation of the content of copper in the kidney and liver.
The most significant changes in the copper concentration took place in the kidneys. About a twofold increase in the copper content of the kidney was noted after exposure to mercuric chloride (3 mg and 5 mg/kg). Only slight elevations in the copper content occurred in the liver especially in high dose and longer exposure time. In the remaining organs, the copper content was not changed significantly (p > 0.05).
The most significant changes in the zinc concentration took place in liver, kidney, lung and heart (5 mg/kg). Marked changes in kidney zinc concentrations were observed at any of the specified doses. Zinc concentrations were significantly increased in kidney of rats sacrificed 9-48 h after s.c. injection of HgCl2 (5 mg/kg); in liver obtained from rats at 18, 24 or 48 h after injection; and in lung after 24 or 48 h of treatment.
The heart and spleen zinc concentrations were elevated at 24 and 48 h after injection of HgCl2 (5 mg/kg), respectively. The results of this study
implicate that effects on copper and zinc concentrations of the target tissues
of mercury may play an important role in the pathogenesis of acute mercuric
The following study suggests that mercury content in
females can be judged by hair color. Gray hair contains more organic
mercury than dark hair in both sexes, but there is a sex difference in that
mercury seems to more readily turn hair gray in females than in males.
Title: Mercury concentration in gray hair
Author: Ando T; Wakisaka I; Yanagihashi T; Tomari T; Hatano H
Source: Nippon Eiseigaku Zasshi, 43(6):1063-8 1989 Feb
Scalp hair sample were collected from 20 gray-haired males and 7 gray-haired females. Two hair samples, one each of dark hair and gray hair, obtained from each individual were selectively analysed for organic and inorganic mercury concentrations.
The following finding were made:
2) For males, no significant differences between dark hair and gray hair were found for total, organic or inorganic mercury concentrations. On the other hand, gray hair had significantly higher levels of total, organic and inorganic mercury concentrations than dark hair in females.
3) When comparison was made between the sexes, total, organic and inorganic mercury concentrations were significantly higher in males than in females for dark hair. For gray hair, however, significantly higher levels of total and organic mercury concentrations, but not of inorganic mercury concentrations, were found in males.
4) The proportion of inorganic mercury to total mercury
was higher in females than in males for both dark and gray hair. It was also
higher in gray hair than in dark hair for females.
The following study explores the detoxifying effect that selenium has on mercury. Apparently one atom of selenium combines with one atom of mercury to form a biologically inactive complex.
A pilot experiment carried out on three pigs have confirmed that interaction between inorganic mercury (203HgCl2) and selenium (Na275SeO3) after single intraperitoneal injections are qualitatively uniform in mice and pigs.
The detoxifying effect of selenium on mercury toxicity seems to be due
to a formation of a biologically inactive complex containing the elements in an
equimolar ratio. The complex is unable to pass biological barriers, placenta
and choroid plexus and is stored in the liver and the spleen.
The following study explores the interaction between mercury and selenium when administered at different times. The greatest cancellation of effects occurred when both were administered simultaneously.
Interaction of mercury and selenium was examined in mice given mercuric chloride (25 mumol/kg) intravenously with sodium selenite (25 mumol/kg, iv) according to various administration schedules. Body weight of the mice given mercuric chloride or selenite alone did not increase, but the mice given both compounds simultaneously grew as well as control mice. On the other hand, only a 1-hr shift of administration of either compound canceled the mutual detoxifying effect.
The most conspicuous changes in tissue distribution of mercury
and selenium and in gel filtration patterns of both elements accumulating in
tissues of the mice were observed when both compounds were administered
simultaneously. These experimental results indicate that the interaction of
mercuric mercury with selenite in mice occurred to the greatest extent upon
simultaneous administration, supporting the hypothesis that the interaction
primarily occurs in the blood stream.
The following study analyzed mercury and selenium
concentrations in cadavers of workers in dental offices and found that there
were increased concentrations of selenium and mercury showing that selenium
accumulated together with mercury.
Br J Ind Med 1991 Nov;48(11):729-34
Nylander M, Weiner J
Department of Environmental Hygiene, Karolinska Institute, Stockholm, Sweden.
Mercury (Hg) and selenium (Se) concentrations were determined by radiochemical neutron activation analysis in samples from the pituitary glands, occipital cortices, renal cortices, abdominal muscles, and thyroid glands of cadavers. Samples were retrieved from dental staff occupationally exposed to Hg and from the general population.
Increased concentrations of both Hg and Se in samples from dental staff showed that Se accumulated together with Hg. Regression analysis of data from the pituitary glands and occipital cortices of dental staff indicated the accumulation of Se at a rough stoichiometric ratio of 1:1 with Hg.
The same stoichiometric ratio between the elements was seen in the
renal cortices from the general population. The regression analysis showed that a substantial fraction of Se was not associated with Hg; it is assumed that this
corresponds to biologically available Se. Concentrations of biologically
available Se decreased with advancing age in the pituitary gland, but not in
other organs, and varied appreciably between organs.
The results of the following study "suggest that mercury poisoning from dental amalgam may play a role in the etiology of cardiovascular disorders." "Hemoglobin, hematocrit, and red blood cells were significantly lower when correlated to increased levels of urine mercury.
amalgam subjects had a greater incidence of chest pains, tachycardia, anemia,
fatigue, tiring easily, and being tired in the morning." This
indicates that mercury toxicity can induce anemia and all the symptoms of
anemia. We have seen elsewhere that there is a high association of anemia
with thyroid disorders. Mercury toxicity from dental amalgam would seem to
be a prime contributor to anemia and thyroid disease.
Sci Total Environ 1990 Dec 1;99(1-2):23-35
The relationship between mercury from dental amalgam and the cardiovascular system.
Department of Physiology, College of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins 80523.
The findings presented here suggest that mercury poisoning from dental amalgam may play a role in the etiology of cardiovascular disorders. Comparisons between subjects with and without amalgam showed amalgam-bearing subjects had significantly higher blood pressure, lower heart rate, lower hemoglobin, and lower hematocrit. Hemoglobin, hematocrit, and red blood cells were significantly lower when correlated to increased levels of urine mercury.
The amalgam subjects had a greater incidence of chest pains, tachycardia, anemia, fatigue, tiring easily, and being tired in the morning. The data suggest that inorganic mercury poisoning from dental amalgam does affect the cardiovascular system.
PMID: 2270468, UI: 91102526
The following study shows that mercury accumulates in various structures of the eye and that the half-life of mercury in the body probably exceeds years.
Squirrel monkeys were exposed to mercury vapour at different concentrations and for different numbers of days. The calculated total mercury absorption ranged between 1.4-2.9 mg (range of daily absorption 0.02-0.04 mg). The monkeys were killed at different intervals after the end of exposure (range 1 month - 3 years) and the eyes were enucleated. Eyes from four un-exposed monkeys were used as control material.
Mapping of the mercury distribution in the eye revealed that the non-myelin-containing portion of the optic disc was densely loaded with mercury deposits, which are mostly confined to the capillary walls and the glial columns.
The white matter of the brain does not accumulate mercury at these exposure levels, which might suggest that the myelinization process inhibits the accumulation of mercury. The pigmented epithelium of the pars plicata of the ciliary body and of the retina contained a considerable amount of mercury. This finding indicates that mercury is trapped within the melanocytes, which keeps potentially dangerous material from reaching the neural retina.
In addition, the retinal capillary walls were densely loaded with mercury deposits,
even 3 years after exposure. It was also found that the inner layers of the
retina accumulated mercury during a 3-year period. It is known
that the biological half-time of mercury in the brain may exceed years. This
seems also to be the case for the ocular tissue.
The following study is a strong indictment of the use of
mercury in dental materials. Not only is it stated that mercury causes a
reduced effectiveness against bacteria such as Chlamydia, Streptococcus, and Borrelia, and Herpes
family viruses, but mercury has been found in pre-cancerous and
cancerous tissues. Of particular interest was the authors' discovery
that cilantro (Chinese parsley) is effective in removing mercury from
the body and in reversing pre-cancerous abnormalities.
Acupunct Electrother Res 1996 Apr-Jun;21(2):133-60
Significant mercury deposits in internal organs following the removal of dental amalgam, & development of pre-cancer on the gingiva and the sides of the tongue and their represented organs as a result of inadvertent exposure to strong curing light (used to solidify synthetic dental filling material) & effective treatment: a clinical case report, along with organ representation areas for each tooth.
Omura Y, Shimotsuura Y, Fukuoka A, Fukuoka H, Nomoto T
Heart Disease Research Foundation, New York, USA.
Because of the reduced effectiveness of antibiotics against bacteria (e.g. Chlamydia trachomatis, alpha-Streptococcus, Borrelia burgdorferi, etc.) and viruses (e.g. Herpes Family Viruses) in the presence of mercury, as well as the fact that the 1st author has found that mercury exists in cancer and pre-cancer cell nuclei, the presence of dental amalgam (which contains about 50% mercury) in the human mouth is considered to be a potential hazard for the individual's health. In order to solve this problem, 3 amalgam fillings were removed from the teeth of the subject of this case study.
In order to fill the newly created empty spaces in the teeth where the amalgams had formerly existed, a synthetic dental-filling substance was introduced and to solidify the synthetic substance, curing light (wavelength range reportedly between 400-520 nm) was radiated onto the substance in order to accelerate the solidifying process by photo-polymerization. In spite of considerable care not to inhale mercury vapor or swallow minute particles of dental amalgam during the process of removing it by drilling, mercury entered the body of the subject.
Precautions such as the use of a rubber dam and strong air suction, as well as frequent water suctioning and washing of the mouth were insufficient. Significant deposits of mercury, previously non-existent, were found in the lungs, kidneys, endocrine organs, liver, and heart with abnormal low-voltage ECGs (similar to those recorded 1-3 weeks after i.v. injection of radioisotope Thallium-201 for Cardiac SPECT) in all the limb leads and V1 (but almost normal ECGs in the precordial leads V2-V6) the day after the procedures were performed.
Enhanced mercury evaporation by increased temperature and microscopic amalgam particles created by drilling may have contributed to mercury entering the lungs and G.I. system and then the blood circulation, creating abnormal deposits of mercury in the organs named above. Such mercury contamination may then contribute to intractable infections or pre-cancer.
However, these mercury deposits, which commonly occur in such cases, were successfully eliminated by the oral intake of 100 mg tablet of Chinese parsley (Cilantro) 4 times a day (for average weight adults) with a number of drug-uptake enhancement methods developed by the 1st author, including different stimulation methods on the accurate organ representation areas of the hands (which have been mapped using the Bi-Digital O-Ring Test), without injections of chelating agents. Ingestion of Chinese parsley, accompanied by drug-uptake enhancement methods, was initiated before the amalgam removal procedure and continued for about 2 to 3 weeks afterwards, and ECGs became almost normal.
During the use of strong bluish curing light to create a photo-polymerization reaction to solidify the synthetic filling material, the adjacent gingiva and the side of the tongue were inadvertently exposed. This exposure to the strong bluish light was found to produce pre-cancerous conditions in the gingiva, the exposed areas of the tongue, as well as in the corresponding organs represented on those areas of the tongue, and abnormally increased enzyme levels in the liver.
These abnormalities were also
successfully reversed by the oral intake of a mixture of EPA with DHA and
Chinese parsley, augmented by one of the non-invasive drug-uptake
enhancement methods previously described by the 1st author, repeated 4 times
each day for 2 weeks.
The following study demonstrates that in genetically susceptible species (and this may include many humans), mercury leaches from dental amalgam fillings and causes a rapid activation of the immune system. Up to a 12-fold increase in IgE concentrations were found within 3 weeks.
The mercury was also found to cause large tissue increases in
silver, copper, and selenium, which are three minerals that I suspect are
important in the control of the immune response. Selenium has been
demonstrated to be an important detoxifier of mercury and I suspect that
copper and silver are also involved in the mitigation of the toxic effects of
Dental amalgam restorations are a significant source of mercury exposure in the human population, but their potential to cause systemic health effects is highly disputed. We examined effects on the immune system by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers (from 250 to 375 mg amalgam/kg body weight).
BN rats with amalgam restorations, compared with control rats given composite resinous restorations, developed a rapid activation of the immune system, with a maximum 12-fold increase of the plasma IgE concentration after 3 wks (p < 0.001; Mann-Whitney's test). LE rats receiving amalgam restorations showed no significant increase of plasma IgE (p > 0.05).
After 12 wks, BN rats with amalgam restorations showed significantly increased (p < 0.05) titers of immune-complex (IC) deposits in the renal glomeruli and in the vessel walls of internal organs. These rats also showed a significant (p < 0.05), from six- to 130-fold, increase in tissue mercury concentration in the concentration order kidney > spleen > cerebrum occipital lobe > cerebellum > liver > thymus, and the tissue silver concentration was significantly (p < 0.05) increased from three- to 11-fold.
BN rats showed a significant (p < 0.05) increase in copper concentration in
the kidney and spleen, and in kidney selenium concentration. We
conclude that dental amalgam restorations release substantial amounts of their
elements, which accumulate in the organs and which, in genetically susceptible
rats, give rise to activation of the immune system and systemic IC deposits.
The following study indicates that mercury interferes with thyroidal function in two ways: by interfering with the production of thyroidal hormones and by interfering with the conversion of T4 to T3.
Acute effects of methylmercuric chloride and mercuric chloride on thyroidal functions were examined. The organic mercurial concentration of 4 x 10(-5) M inhibited by 50% of Na+K+ATPase in the membraneous preparation from the hog thyroid, and 6 x 10(-7) M of the inorganic mercurial showed the same extent of the inhibition.
The Mg2+ ATPase activity in the preparation was neither affected by CH3HgCl up to a concentration of 2 x 10(-3) M, nor by HgCl2 up to 1 x 10(-4) M. After an intraperitoneal injection to mice of 5 micrograms of mercurial per gram body weight daily for 2 consecutive days, the 4-hour and the 24-hour uptakes of 131I by the thyroids were partially reduced by both organic and inorganic mercurials.
A significant reduction in percentages of labeled iodothyronines was demonstrated to suggest that mercurial may cause a coupling defect in the synthesis of iodothyronines. Incubation of hog thyroglobulin with 8 x 10(-3) M of methylmercuric chloride caused no observable aberration in slab disc electrophoreogram, but the protein was apparently denatured by the same concentration of mercuric chloride suggesting that thyroglobulin may carry a large binding capacity against either mercurial, but the inorganic mercurial can be more potent denaturant of the protein.
The in vitro lysosomal hydrolysis of the mercurial-pretreated rat thyroglobulin which was labeled with 125I in vivo and fortified with the carrier hog thyroglobulin was not affected, but the direct addition of either mercurial in the medium resulted in a significant inhibition of the proteolytic action. Iodotyrosine deiodinase in the thyroid was inhibited by both mercurials in in vitro and in vivo systems. A partial reduction in the serum bound 131I-iodide in both mercurial treated groups was observed at 4 hours and 24 hours after the radioiodide administration.
The blood thyroxine
levels estimated by radioimmunoassay were quite reduced in the inorganic
mercurial treated group and also moderately reduced in the methylmercurial
treated group, indicating that the hormone secretion was affected by mercurials.
In contrast to the above study this study found that mercury inhibited the production of T4 but didn't interfere with the conversion of T4 to T3. However, they didn't seem to control for selenium levels, which is probably important to do in these types of studies.
Title Subacute toxicity of methylmercuric chloride and mercuric chloride on mouse thyroid.
Intoxication effect on mouse thyroid by prolonged administration of either CH3HgCl or HgCl2 was studied. It was found by giving CH3 203HgCl and 203HgCl2 through stomach intubation at either a single or a 30 d treatment that thyroid is a moderately susceptible organ to both mercurials. Animals were given 50, 100 and 150 micrograms/d of either mercurial in drinking water for a month.
At the lowest amount of HgCl2, body weight was increased, whereas at the highest dose, there was a transient delay in growth. With lower amounts of CH3HgCl, no change in growth was observed. However, at the highest amount, a severe growth inhibition occurred.
The thyroid weight was unaffected by lower amounts, but was significantly reduced by 150 micrograms/d of either mercurial. The 24 h radioiodide uptake in the thyroid, expressed by cpm/mg organ weight, was reduced by lower levels of mercurials. CH3HgCl and HgCl2 suppressed the rate of radioiodide incorporation into the iodothyronine fraction, but not into the iodotyrosine fractions, indicating that mercurials do not interfere with organification of iodide but do inhibit the coupling process. Serum thyroxine (T4) level was affected by mercurials, but serum triiodothyronine (T3) was not.
This result suggested that even thyroidal
secretion of T4 was inhibited by mercurials, but the peripheral conversion of T4 to T3 may not be affected in the maintenance of an active hormone level.
The following study shows that mercury interferes with the conversion of T4 to T3 in humans. Bear in mind that the majority (or all) of these workers are male and the effects of mercury on females may be ten times as high because of the acceleration effect of estrogen on mercury accumulation.
OBJECTIVE--The aim was to study whether functional impairment of the pituitary, thyroid, testes, and adrenal glands of humans occupationally exposed to mercury (Hg) vapour can be shown as a result of accumulation of Hg in these glands.
METHODS--Basal concentrations of thyrotrophin (TSH), prolactin, free thyroxine (free T4), free 3,5,3'-triiodothyronine (free T3), antibodies against thyroperoxidase, and testosterone in serum, as well as cortisol in morning urine were measured in 41 chloralkali workers exposed (10 years on average) to Hg vapour, and in 41 age matched occupationally unexposed referents. The chloralkali workers had a mean urinary Hg concentration (U-Hg) of 15 nmol/mmol (27 micrograms/g) creatinine, and a mean blood Hg concentration (B-Hg) of 46 nmol/l. For the reference group U-Hg and B-Hg were 1.9 nmol/mmol (3.3 micrograms/g) creatinine and 17 nmol/l respectively.
RESULTS--The serum free T4 concentration and the ratio free T4/free T3 were slightly, but significantly, higher in the subgroups with the highest exposure, and the serum free T3 was inversely associated with cumulative Hg exposure. This indicates a possible inhibitory effect of mercury on 5'-deiodinases, which are responsible for the conversion of T4 to the active hormone T3.
Serum total testosterone, but not free testosterone, was positively correlated with cumulative Hg exposure.
Prolactin, TSH and urinary cortisol concentrations were not significantly associated to exposure.
inhibition of the deiodination of T4 to T3, the endocrine functions studied
seem not to be affected by exposure to Hg vapour at the exposure levels of the
present study. Growth hormone secretion was not studied.
The following study, while it demonstrates species-specific differences, shows that mercury causes the production of autoantibodies in rats. Some of these autoantibodies are of the IgG class, which is known to be involved in autoimmune thyroid disease.
Repeated exposure of Brown Norway (BN) rats to relatively low doses of HgCl2 induces autoantibodies to renal antigens (e.g., laminin) and a membranous glomerulonephropathy characterized by proteinuria. In contrast, Lewis (LEW) rats are "resistant" to the autoimmune effects of mercury and, when exposed to this metal, are protected against experimental autoimmune encephalomyelitis (EAE) and Heymann's nephritis. To date, there is no information on "suppressive" effects of mercury in naturally occurring (so-called "spontaneous") rat models of autoimmune disease. Therefore, we have administered HgCl2 to diabetes-prone (DP) BB rats, animals that spontaneously develop both insulin-dependent diabetes mellitus (IDDM) and thyroiditis.
We found that DP rats treated with mercury or water for a period of 40-125 days developed autoantibodies to thyroglobulin, with a higher incidence in HgCl2-injected animals (92% vs. 56% in H2O-injected controls). A novel finding of our study was the detection of autoantibodies to laminin in the same rats, again with an increased incidence after HgCl2 treatment (83% vs. 44%).
IgG2a was the most frequently detected isotype of antibodies to laminin, followed by IgG1, IgG2b and IgG2c. The IgG isotype profile suggests that treatment with HgCl2 may activate both Th1 and Th2 lymphocytes in BB rats. In spite of these stimulatory effects on autoantibody responses, we found that there was no difference in the incidence of IDDM and thyroiditis between HgCl2-treated and control animals.
We conclude that the suppressive effects of mercury previously observed in EAE and Heymann's nephritis of LEW rats do not occur in "spontaneous" autoimmune IDDM and thyroiditis of BB rats. Therefore, immune suppression caused by HgCl2 cannot be considered a common phenomenon, but may be a genetically determined characteristic of LEW rats, possibly related to a specific or unique cytokine profile of this particular rat strain.
In contrast, while mercury does not seem to recruit,
induce or rescue regulatory T cell function in DP rats, it does stimulate
autoantibody responses in these animals.
The following study demonstrates the long half-life of mercury in animals. Mercury was still detected in the thyroid gland of a dog exposed to mercury four years after the exposure ended.
An Alsatian dog which had been fed fish contaminated with methyl mercury for 7 years was examined after its death at the age of 12, 4 years after the exposure to methyl mercury had ceased. Two dogs of the same age and breed served as controls. In the exposed dog, mercury was found in all of the organs examined; the highest concentrations were found in the kidneys, and the lowest in the gastrointestinal tract and skeletal muscles.
In the central nervous system (CNS) the mercury was fairly uniformly distributed, with 93% in the inorganic state, whereas the skeletal muscles contained approximately 30% inorganic mercury. This demonstrates time-dependent demethylation and suggests a variation in the rate from one type of tissue to another. At the time of death, the mercury level in the dog was still falling.
In the control dogs, detectable amounts (0.01 mg kg-1) of mercury were only found in the kidney and liver. The distribution of mercury was determined by a histochemical method (autometallography) for locating mercury in tissue sections.
Sections from autometallography of the central nervous system showed large deposits of mercury in all areas of the cerebral hemispheres, the brainstem and the spinal cord, including nerve cells, astrocytes, microglial cells and vessel walls. The granular layer of the cerebellar hemispheres was especially loaded, while only a few granules were present in the Purkinje cells.
In the leptomeninges the vessels and the
macrophages were heavily encrusted. High
amounts of histochemically demonstrable mercury were observed in the
liver, thyroid gland and kidney. In the control dogs, all the organs
examined were practically devoid of deposits.
The following study demonstrates that not only does mercury bind to thyroidal tissues, but methylmercury has a preferential affinity for thiol groups. Thiols are an important part of antithyroidal drugs indicating that thiols are important in normal thyroidal functioning.
Peroxidase in mouse thyroid was inhibited by mercuric chloride but not by methylmercury in in vivo and in vitro systems (Nishida, et al., J. Histochem. Cytochem., 37, 723 (1989)). To identify the reason for the difference, the present study was conducted to examine whether methylmercury is indeed bound within cells or tissues.
Mice were given radioactive methylmercury by intubation for 18 d and the tissues were dissected out and vacuum-dried. With this procedure, free methylmercury was evaporated off and the bound mercury remained.
The thyroid, liver, kidney and fats examined showed no loss of
radioactivity under the vacuum, indicating that the mercury was bound to the
thyroid, as well as the other tissues. Radioactive mercuric chloride was
nonvolatile regardless of the presence or absence of the tissues. The
preferential affinity of methylmercury for SH-containing materials was
re-confirmed by this method.
The following two studies indicate that organic and inorganic forms of mercurials have different effects on the thyroid. Methyl mercury seems to interfere with the production of thyrotropin (TSH) so that the thyroid lowers production of hormone because of the lack of stimulation by thyrotropin. Inorganic mercury seems to inhibit the production of thyroid peroxidase (TPO) which causes the thyroid to increase production of thyroid hormone as a compensatory mechanism.
This study was designed to characterize the interaction of CH3HgCl or HgCl2 with thyroid peroxidase (TPO). Two types of experiments were performed. First, the thyroids from rats that were given 5.6 mg/kg/day of either CH3HgCl or HgCl2 for 2 weeks by intubation were subjected to histochemical treatment and then to electron microscopy. TPO activities in all cell compartments were inhibited by HgCl2 but not by CH3HgCl.
Morphological observation showed that taller epithelia were induced by HgCl2, whereas flattened epithelia forming large follicles were induced by CH3HgCl. The serum thyrotropin level was substantially lowered by CH3HgCl but was unchanged by HgCl2. Second, the guaiacol oxidation by TPO in isolated and ruptured pig thyroid cells was spectrophotometrically monitored in the presence of either CH3HgCl or HgCl2. The TPO was not inhibited by CH3HgCl but was inhibited by HgCl2.
These results indicated that CH3HgCl induced a
hypothyroid state without affecting TPO, whereas HgCl2 inhibited TPO and induced
a hypertropic state owing to compensation for loss of enzyme activity, and
that the lack of inhibitory activity of CH3HgCl was not due to the inability to
penetrate the cells. Therefore, there appeared to be a differential
interaction of organic and inorganic forms of mercurials with the thyroid.
Thyroid peroxidase (TPO), the major enzyme in the thyroid hormone synthesis,
multifunctionally catalyzes (1) iodide oxidation, (2) iodination of the
precursor protein, and (3) a coupling reaction of iodotyrosyl residues. The
present study was carried out to examine the mercurial effects on
the iodination, the second step of TPO. Purified porcine thyroglobulin or bovine
serum albumin as acceptor protein was iodinated with [125I]NaI and H2O2 by
purified porcine TPO. Iodinated protein was separated by acid precipitation on
membrane filter or paper chromatography. Both CH3HgCl and HgCl2 dose-dependently
inhibited the iodination, but HgCl2 was more potent to inhibit the iodination
than CH3HgCl. These mercurial effects on the second step resemble
the effects on the third step which were already reported; but are in marked
contrast to the effects on the first step, where TPO was inhibited by HgCl2 but
never by CH3HgCl.
The following study demonstrates how mercury can damage a fetus by interfering with the selenoenzymes and thyroid hormones.
Environ Res 1999 Apr;80(3):208-14
In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain.
Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H
Department of Environmental Health Sciences,
Pregnant ICR mice were subcutaneously injected with 0,5, or 3x3 mg Hg/kg of methylmercury (MeHg) on days 12,13, and 14(G12-14) of gestation and were sacrificed on G17. Activity of selenoenzymes, including glutathione peroxidase (GPx) and 5'- or 5-iodothyronine deiodinases (5'-DI, 5-DI), was determined in fetal brain and placenta.
MeHg did not affect the concentration of Se in these tissues, while it significantly inhibited the activity of GPx in the fetal brain and placenta, but not in the maternal brain. Although the levels of thyroid hormones in the maternal and fetal plasma were not affected by MeHg, 5-DI decreased and 5'-DI increased in the fetal brain, as if they had responded to hypothyroidism. Because the level of T4 in the fetal plasma was not affected by MeHg, these changes in enzymatic activities may result in a harmful excess of T3 in the fetal brain.
In addition, 5-DI activity was increased in
the placenta of MeHg-treated mice. These effects of prenatal MeHg exposure on
fetal and placental DIs differed from those of dietary-induced Se deficiency,
where the activities of DIs were decreased or not affected. Further
evaluation of the effect of MeHg on selenoenzymes, especially 5-DIs, is
warranted. Copyright 1999 Academic Press.
In the following study the author states that ingestion of milk can increase the absorption of mercury up to 10 times. Other studies have shown that cadmium uptake can be increased significantly by simultaneous administration of estrogen. It's possible that it is the estrogen in milk which accounts for the accelerated accumulation of mercury from the diet. It is also stated that mercury in a mother is transferred to an infant through breast milk.
Z Ernahrungswiss 1990 Mar;29(1):54-73
[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in
food for infants and small children].
Walther-Straub-Institut fur Pharmakologie und Toxikologie der Ludwig-Maximilians-Universitat, Munchen, FRG.
There are differences between young and adult organisms regarding toxokinetic aspects and clinical manifestations of heavy metal intoxications. Chronically, toxic Cd intake causes a microcytotic hypochromic anemia in young rats at lower exposure levels and after shorter exposure periods than in adult animals.
Cd absorption is increased by co-administration of milk and in conjunction with iron deficiency. After long exposure periods toxic Cd concentrations accumulate in the kidney cortex; this process starts very early in life. In 3-year-old children Cd concentrations in the kidney can reach up to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg encephalopathia, and frequently cause mental retardation in adults.
Correspondingly, Hg++ accumulation in the brains of suckling rats is approx. 10 times higher than in grown animals. Milk increases the bioavailability of Hg++. In suckling rats Hg is bound to a greater extent to ligands in the erythrocytes. Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma and that is a severe hazard for breastfed children of exposed mothers. Toxic Pb concentrations can lead to Pb encephalopathia. A high percentage of surviving children have seizures and show signs of mental retardation.
Anemia and reduced intelligence scores were recently observed in children after exposure to very low levels of Pb. Pb absorption is increased in children and after co-administration of milk. There are no definite proofs for carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man. Heavy metal concentrations were found in the same order of magnitude in commercial infant formulas and in breast milk. When infant formulas are reconstituted with contaminated tap water, however, Pb and Cd concentrations can be much higher.
The average heavy metal uptake from such diets exceeds the provisional tolerable weekly intake levels set by the WHO for adults, calculated on the basis of an average food intake and a downscaled body weight. These considerations do not even provide for differences in absorption and distribution or for the increased sensitivity of children to heavy metal exposure. However, dilution effects for essential heavy metals were observed in fast-growing young children; this effect might be extrapolated to toxic metals. These theoretical considerations are compared with epidemiological evidence.
A health statistic from Baltimore shows a
decline of Pb intoxications in infants. This observation correlates with a
simultaneous decline in exposure to Pb which was due, for example, to
decreased use of lead dyes in house paints and the abolition of tin cans for
Subject: Flu Shots and mercury
If an individual has had 5 consecutive flu shots between 1970 and 1980 (the years studied) his/her chances of getting Alzheimer's Disease is 10 times higher than if he/she had one, 2 or no shots.
Dr. Fudenberg said it was so and that it was due to mercury and aluminum that is in every flu shot (and most childhood shots). The gradual mercury and aluminum buildup in the brain causes cognitive dysfunction. Is that why Alzheimer's is expected to quadruple.
What is DMSA?
What is the Urine Mercury Test?
What happens if the test result indicates high levels of mercury?
What happens after the course of DMSA is concluded?
What happens if mercury amalgam fillings are not replaced?
Can DMSA be taken the day of and day after dental work involving
mercury amalgam in order to remove any "stray" amalgam (mercury)
from the body?
How is the DMSA obtained?
Is it possible to present the prescription through prescription
insurance plans or at another pharmacy? Retail pharmacies dispense the
brand name "Chemet"
form of DMSA in 1/5 the potency recommended. The compounding pharmacy
provides the DMSA in a generic form that is substantially less costly
than the Chemet. If Chemet is used, 5 times the amount needs to be
taken. Insurance coverage may be applicable to compounding pharmacies;
check with the pharmacy when you confirm the
Are there any side effects to using DMSA?
More information about mercury?
US EPA Proposes
Autism and Mercury
This article is excerpted from Dr. O'Shea's forthcoming revised edition of The Sanctity of Human Blood.
Inquiry into vaccine safety is exploding like never before, even in the popular press. Research coming from dozens of mainstream medical studies can no longer be easily suppressed, as it has been in the past, especially with the prevalence of online information exchange.
Last September (1999), some 2,000 people, mostly MDs, assembled at the Town and Country resort in San Diego to hear the latest research on autism. Following the April 2000 Congressional hearings on autism and vaccines, this epidemic can no longer be ignored.
The figure of one autistic infant for every 150 is now widely documented.
Dr. Stephanie Cave presented enlightening data on mercury toxicity, drawn largely from the brilliant work of Sallie Bernard. Dr. Cave explained how:
By age two, American children have received 237 micrograms of mercury through vaccines alone, which far exceeds current EPA "safe" levels of .1 mcg/kg. per day. That's one-tenth of a microgram, not one microgram.
Three days in particular may be singled out as spectacularly toxic for infants:
At 4 months: DTaP and HiB on same day - 50
At 6 months: Hep B, Polio - 62.5 mcg mercury
At 15 months the child receives another 50 mcg
These figures are calculated for an infant's average weight in kilograms for each age. These one-day blasts of mercury are called "bolus doses". Although they far exceed "safe" levels, there has never been any research conducted on the toxicity of such bolus doses of mercury given to infants all these years.
Sources of Mercury
In the U.S., EPA mercury toxicity studies have involved contamination from fish, air, and other environmental sources. This is inorganic mercury (methylmercury).
Methylmercury has long been associated with serious
neurological disorders, demyelinating diseases, gut disease, and visual damage.
The mercury in vaccines, however, is in the form of thimerosal, which is 50 times more toxic than plain old mercury (methylmercury).
Reasons for this (heightened toxicity) include:
There's no blood-brain barrier in infants.
Thimerosal is organic mercury.
Once in the nerve cells, mercury is changed back to the inorganic form and becomes tightly bound. Mercury can then remain for years, like a time-release capsule, causing permanent degeneration and death of brain cells. Bernard also notes that the body normally clears mercury by fixing it to bile, but before six months of age, infants don't produce bile. Result: mercury can't be excreted.
Four separate government agencies
have set safe levels
for methylmercury, but no safe levels have ever been set for
thimerosal isn't included in toxicity studies.Theoretically, that means
that the above excesses of safe levels of mercury on the single days
listed above are actually 50 times higher. Does the fact that the
mercury is accompanied by a
vaccine somehow place it above scrutiny? The Sallie Bernard study of vaccines and mercury toxicity was probably the main reason Congress began to see the obvious correlation.
Mercury And Vaccines
Here's a curious "coincidence."
A few years ago, Bernard and her associates began to notice a striking similarity between the symptoms of autism and the symptoms of mercury poisoning. The more research she did, the more it seemed that these two diseases were virtually identical. Autism and mercury poisoning damage the: brain/nerve cells; eyes; immune system; gastrointestinal system; muscle control; and the speech center. Although mercury toxicity has been studied for decades, and EPA safety levels have been set, during all that time a child's greatest exposure to mercury - thimerosal in vaccines - was never even included in the toxicity studies!
The talk has always been about methylmercury from seafood and the environment, totally ignoring the two most toxic sources of mercury for children: vaccines and dental amalgams. The EPA has no jurisdiction over drugs. That's the FDA's job. This is why vaccines and amalgams don't even figure into the equation when it comes to setting "safe" levels of mercury. But the FDA does have jurisdiction over drugs and drug companies, right? And over drug company publications, like the Merck Manual, the standard cookbook for drugs and diseases found in every doctor's office in the world.
Surely the FDA, as the government agency charged with safeguarding the nation's health, would want the section on mercury toxicity to warn doctors about the two biggest sources for children: thimerosal and dental amalgams, wouldn't you think? Yet looking at the Merck Manual (1999), in the section on mercury poisoning (p. 2636), thimerosal and dental amalgams again are not even mentioned! How can this be, when mercury is widely acknowledged as the third most deadly toxin in the world and thimerosal and amalgams dwarf the trace amounts of mercury from fish and other environmental sources of mercury?
Only one thing can blackout information
over an entire area of study for years at a time in this way - big
money. Such an omission probably wouldn't have anything to do with the
revolving door that exists between the FDA; the EPA; the NIH; "and the
sweet positions held by their members before and after those grueling
years of public service; or with the 800 waivers of the conflict of
interest rule that the FDA has granted in the past two years to
"experts," who are paid consultants to the drug companies-consultants
who are also members of the FDA advisory committees that make decisions
about whether or not to approve vaccines and drugs..." (USA Today,
Sept. 25, 2000)
Soaking up the Mercury.
Dr. Holmes reported success using alphalipoic acid as an agent to cross the blood-brain barrier to soak up mercury. Once the mercury is brought back into the bloodstream, standard chelators like DMSA can then take it out.
Dr. Holmes has used her protocol on about 300 autistics
so far, and shows consistent increases in IQ scores.
In the face of all this new awareness, it was astounding
that in July 2000 the FDA came out with the "parallel-universe"
pronouncement that "vaccines have safe levels of mercury."
Especially after their 1998 position:
As if there were any doubt as to who's really running the show, inconceivable also is the impotence of FDA's request to the vaccine manufacturers to discontinue the use of thimerosal in vaccines (LINK TO ARTICLE ON SITE) The same month that MMWR published this, the CDC made the same milquetoast request. It's a bit like saying:
"Hey guys, since all these kids are turning into vegetables and most of our researchers know it's the mercury, would you mind not putting any more thimerosal in your vaccines, please? No hurry, though. Whenever you're ready. No need to dump all those batches of vaccine just because people are finding out it's the mercury that's destroying children's brain cells."
The members of the FDA who decide which vaccines get approved make up the advisory board. In his recent House investigation on vaccines, Rep. Dan Burton found out that financial statements of advisory board members are "incomplete."
that this is the only branch of government that allows incomplete
financials, in September 2000, Burton called the advisory board's
sweetheart arrangements with the vaccine manufacturers a "violation of
the public trust." This includes 70 percent of advisory board members
owning stock in vaccines, owning patents on vaccines, and
accepting salaries and benefits as employees of the drug companies.
A Matter of Trust.
"There is a significant safety margin incorporated into
all the acceptable mercury exposure limits. There are no data or
evidence of any harm caused by the level of exposure that some children
may have encountered in following the existing immunization schedule
... Infants and children who have received thimerosal-containing
vaccines do not need to be tested for mercury exposure" (TRY TO REPLACE
THIS WITH LINK FROM SITE MMWR, vol. 45, 1999).
It is beyond the scope of this paper to really go into the politics of mercury. In researching mercury toxicity, a whole area of "dry rot" has been unearthed that deserves its own story. This is the shocking story of how the American Dental Association and the California Dental Association have been systematically hiding the truth about mercury toxicity in fillings for decades.
Silver fillings aren't just silver.
Do you think dentists put mercury into their own families' teeth?
Ask them. Anyone who is not a dentist is not constrained by the gag
order, imposed on American dentists by the ADA, against telling
patients what many perceptive researchers in the field of mercury
toxicity already know: that no children should ever get mercury amalgam
Researchers across Europe
are generally appalled at the
massive amounts of vaccines given to American children under two years
Although Europeans are not as obsessed with vaccines as we are, they do
vaccinate.But most of Europe gives very few vaccinations to children
under two years old, primarily because of the unformed gut, immune
system, and blood-brain barrier. This intellectual isolation of ours
is a testimony to the suffocating "brain control" exerted on us by the
popular press and all media. Like sheep to the slaughter, we don't know
to be appalled by our own ignorance.
Headlining the September 2000 San Diego Conference was Andrew Wakefield, the British surgeon whose shocking new discoveries show that mercury toxicity alone is not the only factor linking vaccines with the autism epidemic. Dr. Wakefield's research centers around the MMR vaccine - measles/mumps/rubella - which does not contain thimerosal.
Expanding on his presentation at the April 2000 Burton
Dr. Wakefield explained how at least three-quarters of autistics have
pathologically blocked bowels, due to the huge swelling of the tissue
lining the intestine. In virtually every autistic patient they
examined, this nodular hyperplasia
is both an immune response and an autoimmune response that Wakefield
and O'Leary have clearly linked to the presence of measles virus from
the MMR shot. No other virus was found in those cells.
Wakefield showed graphs of the U.S. and U.K. 10 years apart that were identical in tracing the skyrocketing incidence of autism just after the MMR vaccine was introduced.He also showed how the incidence of measles had dropped over 85 percent on its own before the MMR was introduced. One incredible study cited by Wakefield showed how 76 percent of children whose mothers were exposed to atypical measles became autistic after the MMR shot! He called this a "background susceptibility" or predisposition to autism. Wakefield reminds us that in neither country have there ever been comparative studies on giving multiple vaccines (polyvalent) on the same day.
This custom of ours, with both the DPT and the MMR, is not scientific by any stretch, and is primarily for the convenience of those administering the shots, and those being paid per vaccine. As a result, there is a good chance of geometric ill effects. Then Wakefield cited the original MMR study (Buynak, Journal of the American Medical Association 1969, vol. 207). Not only was the safety of multiple vaccines never mentioned, there was no follow-up to the study to see if their conclusions were correct.
In the usual manner of testing vaccines on the live
MMR was simply tacked onto the mandatory schedule, and we've never
looked back. Despite studies in 1981 on Air Force personnel showing
major synergistic adverse effects in the gut from the combination of
rubella vaccines, the mandatory schedule went unchanged.
A Glimmer of Hope.
The massive advertising campaign about the safety of vaccines in the popular media, which is certain to be stepped up in the next few months, is going to look very hollow in the light of clean, unbiased research that is not funded by parties who stand to make billions from certain predetermined results. And the internet makes this well-referenced, scientific work accessible to the public without the usual monodimensional smokescreen from the popular press.
Ultimately, the value of the San Diego "Conference on Autism"
was its signal that autism will not be allowed to slip from the public
awareness, like so many other feature stories that come and go. The
simple truth has been unveiled, and anyone who looks can see it
clearly: our prime question should not be asking how we can cure autism
once it occurs. The evidence is now overwhelming that in most cases,
this new epidemic that we call autism is a preventable disease.
The following article on mercury is from Dr. Mercola's website, mercola.com:
The following paper has been a long time in the making.
For a practical summary of the paper and exactly what one should do, please review my mercury detoxification protocol.
Dr. Klinghardt is widely recognized as one of the most
knowledgeable physicians in mercury detoxification and it was a privilege to
be able to help him with this paper. The timing is especially appropriate in light of the mercury
lawsuit that was filed last week.
Later this month on April 24 I will be involved in a press conference
that will announce massive additional lawsuits relating to the toxicity
of mercury. These lawsuits have the potential to make the tobacco issue
look like small potatoes as the liabilities could run in the trillions
This paper reviews the published evidence supporting
amalgam toxicity and describes practical and effective clinical techniques
that facilitate mercury elimination. A literature review is provided which
documents effective mercury elimination strategies to reduce mercury toxicity
syndromes. Considering the weight of evidence supporting mercury
toxicity, it would seem prudent to select alternate dental restoration
materials and consider effective mercury elimination strategies if mercury
toxicity is present.
Mercury Exposure and Toxicity is a Prevalent and Significant Public Health Threat.
In most children, the largest source of mercury is that received from
immunizations (3, 4, 5, 6) or that transferred
to them in utero from their mother. (7, 8)
Dental Amalgams Are A Major Source Of Mercury Toxicity.
A "silver" filling, or dental amalgam, is not a true alloy. Amalgams are made up of 50% mercury. The amalgam also consists of 35% silver, 9% tin, 6% copper and a trace of zinc. 6 More than 100 million mercury fillings are placed each year in the U.S. as over 90% of dentists use them for restoring posterior teeth. 14
The mercury vapor from the amalgams is lipid soluble and passes readily through cell membranes and across the blood brain barrier. (15) The vapor serves as the primary route of mercury from amalgams into the body. It is clear that amalgam mercury transfers to human tissues, accumulates with time, and presents a potential health threat. The mercury escapes continuously during the entire life of the filling primarily in the form of vapor, ions but also abraded particles. (16, 17) Chewing, brushing, and the intake of hot fluids stimulates this release. (18, 19, 20) Statements made by dental authorities which claim that the amount of mercury exposure encountered by patients from dental amalgams is too small to be harmful, are contradicted by the literature. (21)
Animal studies show that radioactively labeled mercury released from ideally placed amalgam fillings appear quickly in the kidneys (22), brain and wall of the intestines. (23) The fact that mercury amalgam fillings are banned in some European countries is strong evidence of the clinical toxicity of this material.
Any metal tooth restoration placed in the mouth will
also produce electrogalvanic effects. When dissimilar metals are placed in the oral cavity they exert a battery-like effect because of the
electroconductivity of the saliva. The electrical current causes metal ions go
into solution at a much higher rate, thereby increasing the exposure to
mercury vapor and mercury ions manyfold. Gold placed in the vicinity of an
amalgam restoration produces a 10-fold increase in the release of mercury. (24)
Mercury's Long Half-Life in the Central Nervous System
Mercury Toxicity Symptoms
Alzheimer's Disease, (34, 35)
Patients with many (or larger, or leaking) amalgam fillings will also have an increase in the prevalence of antibiotic resistant bacteria. (49) Subclinical neuropsychological and motor control effects were also observed in dentists who had documented high mercury exposure levels. (50, 51) Amalgam use may also be related to fatigue, poor memory and certain psychological disorders. (52) There has been a recent epidemic of autism in the US (53, 54) and many investigators believe that this may be partially related to the increased exposure infants have had to mercury through the preservative thimerosal that was included in nearly all vaccines until recently. (55)
The nervous system is more sensitive to mercury toxicity than any other organ in the body. Mercury has recently been documented to be associated with arrhythmias and cardiomyopathies
as hair analysis showed mercury levels to be 20,000 higher in those
with these cardiac abnormalities. (56) Mercury exposure has also been
associated with other neurological problems such as tremors, (57)
insomnia, polyneuropathy, paresthesias, emotional lability,
irritability, personality changes, headaches, weakness, blurred vision,
dysarthria, slowed mental response and unsteady gait. (1, 58, 59)
Systemic Mercury Elimination.
The most important part of systemic elimination is to remove the source
of mercury. For most this involves amalgam removal. Individuals should
seek a dentist who is specially trained in this area as improperly
removed amalgam may result in unnecessarily high exposure to mercury.
(61) The following is a summary of the most effective agents that have
been documented in the peer-reviewed literature.
DMPS (Sodium 2,3-dimercaptopropane-1-sulfonate) is an acid-molecule with two free sulfhydryl groups that forms complexes with heavy metals such as zinc, copper, arsenic, mercury, cadmium, lead, silver, and tin. DMPS was developed in the 1950s in the former Soviet Union and has been used to effectively treat metal intoxication since the 1960s there. (62) It is a water-soluble complexing agent. Because it had potential use as an antidote for the chemical warfare agent, Lewisite, it was not available outside of the Soviet Union until 1978, at which time Heyl, a small pharmaceutical company in Berlin, Germany started to produce it. It has an abundance of international research data and an excellent safety record in removing mercury from the body (63) and has been used safely in Europe as Dimaval for many years. (64, 65, 66, 67)
DMPS is registered in Germany with the BGA (their FDA)
for the treatment of mercury poisoning but is still an investigational drug in
the United States. (68) The best and only brand of DMPS that should be used is
Heyl from Germany. Great care should also be exercised in making certain the
DMPS is compounded properly from the pharmacist. If the DMPS contacts metal
during it will be oxidized, so the compounding pharmacist must use nonmetal
needles must be used in preparing the product.
DMPS Can Be Used To Eliminate Mercury Systemically.
One should use DMPS with great caution
and NEVER use it in patients with amalgam fillings. Ideally DMPS should
be administered after 25 grams of ascorbic acid administered
intravenously. This will minimize any potential toxicity from the DMPS.
Even though DMPS has a high affinity for mercury, the highest affinity appears to be for copper and zinc (77) and supplementation needs to be used to not avoid depleting these beneficial minerals. Zinc
is particularly important when undergoing mercury chelation. (78) DMPS
is administered over a five-minute period since hypotensive effects are
possible when given intravenously as a bolus. (79, 80) Other possible
side effects include allergic reactions and skin rashes.
DMSA (meso-2, 3-dimercaptosucccinic acid) is another
mercury chelating agent. It is the only chelating agent other than
and d-penicillamine 81 that penetrates
brain cells. DMSA removes mercury both via the kidneys and via the bile. 82
The sulfhydryl groups in both DMPS and DMSA bind very tightly to mercury.
DMSA has three distinct disadvantages relative to DMPS.
First, DMPS appears to remain in the body for a longer time than DMSA. (83)
Secondly, DMPS acts more quickly than DMSA, probably because its distribution is both intracellular and extracellular. (84)
Thirdly, preparations of DMPS are available for intravenous or intramuscular use, while DMSA is available only in oral form. (85)
Since succinic acid is used in the citric acid cycle inside the cell,
DMSA has been suspected for displacing mercury towards the inside of
the cell (86) after binding mercury somewhere on its way from the
intestine to the succinic acid deficient cell. We propose therefore
that DMSA be used late in the mercury elimination process, after the
connective tissue mercury load has been reduced with DMPS. The standard
dose of DMSA is 5-10 mg/kg twice a day for two weeks. The DMSA is then
stopped for two weeks and then the cycle is repeated.
Chlorella has been shown to develop resistance to cadmium contaminated waters by synthesizing metal-binding proteins. (89) A book written for the mining industry, Biosorption of Heavy Metals, (90) details how miners use these organisms to increase the yield of precious metals in old mines. The mucopolysaccharides in chlorella's cell wall absorb rather large amounts of toxic metals similar to an ion exchange resin.
Chlorella also enhances mobilization of mercury compartmentalized in non-neurologic structures such as the gut wall, (91) muscles, ligaments, connective tissue, and bone. High doses of chlorella have been found to be very effective in Germany for mercury elimination. (92) Chlorella is an important part of the systemic mercury elimination program, as approximately 90% of the mercury is eliminated through the stool. Using large doses of chlorella facilitates fecal mercury excretion. After the intestinal mercury burden is lowered, mercury will more readily migrate into the intestine from other body tissues from where chlorella will effectively remove it.
Chlorella is not tolerated by about one-third of people
due to gastrointestinal distress. Chitosan can be effectively used as an
alternative in these individuals. Chitosan makes up most of the hull of
insects shellfish and also bind metals like mercury from the lumen of the
intestines. (93, 94, 95)
The mechanism of action is unknown.
Adequate sulfur stores are necessary to facilitate mercury's binding to sulfhydryl groups. Many individual's sulfur stores are greatly depleted which impairs sulfur containing chelating or complexing agents, such as DMPS or DMSA, effectiveness as they are metabolized and utilized as a source of sulfur.
Sulfur containing natural substances, like garlic (99, 100) and MSM (methylsulfonylmethane)
may also serve as an effective agent to supply organic sulfur for
detoxification. (101) Fresh garlic is preferred as it has many other
recently documented benefits. (102, 103, 104) The garlic is consumed
just below the threshold of social unacceptability, which is typically
1-2 cloves per day.
Vitamin E doses of 400 I.U per day have been shown to have a protective effect when the brain is exposed to methyl-mercury. (68, 105)
Selenium, 200-400 mcg daily, (106, 107, 108, 109) is a particularly important trace mineral in mercury elimination and should be used for most patients. Selenium facilitates the function of glutathione, which is also important in mercury detoxification. (110, 111, 112) Some clinicians find repetitive high dose intravenous glutathione useful, especially in neurologically compromised patients.
There is a suggestion in a rat model that (alpha) lipoic acid may also be useful, (113) but some
clinicians are concerned about the potential of lipoic acid to bring mercury
into the brain early in the stages of chelation, similar to DMSA and N-acetylcysteine (NAC), which has also been used in mercury chelation. (114) Doses larger than 50-100 mg per day should be used with caution.
Vitamin C is also a
supplement for mercury elimination as it will tend to mobilize mercury
intracellular stores. (115, 116, 117, 118, 119, 120) Some clinicians
will use it intravenously in doses of 25-100 grams IV in preference to
DMPS and DMSA.
Hyaluronic acid (HA) is a major carbohydrate component of the extracellular matrix and can be found in the skin, joints, eyes and most other organs and tissues. (121) HA is utilized in many chemotherapy protocols as a potentiating agent. (122) HA is also being utilized for many novel applications in medicine. (123, 124) Personal experience has shown that the addition of 2 ml with the DMPS tends to improve the excretion of mercury by two to four fold with virtually no toxicity.
Joseph Mercola, DO.
Dietrich Klinghardt, M.D., Ph.D.
Articles on the Internet are transitory.
LINK to Source, when available and known:
This article was discovered by me in early 2004.