Mercury is one of the most toxic elements that can cause a multitude of health problems. This study was created to determine if mercury could be causing multiple sclerosis (MS) by cross referencing 88 factors associated with MS to mercury. The results found that all but five factors could be attributed to mercury, and with the remaining five factors there was not enough evidence one way or another to possibly be associated with mercury. The hallmark change of MS is nerve demyelination, and mercury is known to cause nerve demyelination. Similar physiological and pathological changes occur in MS and mercury toxicity including those changes involved with the basal ganglia, Bell’s palsy, brain atrophy and shrinkage, brain scarring, dysmetria, myelin basic protein, myelin oliodendrocytes, glycoprotein, oligoclonal bands, oligodendrocytes, ciliary neutrophil factor, white matter, axon and myelin damage, electro encephlography, and brainstem auditory evoked potentials. Similar changes also occur in the immune system including autoimmunity, cytokine changes, gamma globulins, Epstein Barr virus, T cells, herpes virus, and urinary infections.Likewise similar changes are also found in hormones and biochemistry including myelin basic protein, myelin oliodendrocytes, glycoprotein, estriol, free radicals, glial cells, glucosteroids, female hormones, and inrerferon. The study identified. 32 physical symptoms of MS and all could all be explained by mercury toxicity as well as all 7 mental health symptoms, and all 11 ocular symptoms. MS is more prevalent in the northern latitudes. The paper hypothesized that people living in southern latitudes are exposed to the sun much more and perhaps the higher levels of vitamin D, which is anti inflamatory counteracts inflammation caused by mercury. Studies have found a correlation between MS and dental caries and dental amalgams. The greatest source of mercury comes from dental amalgams according to the WHO. Previous studies have shown MS symptoms and physiology changes improve following dental amalgam removal. The study concluded that mercury is possibly an etiological factor in multiple sclerosis.

Aim: The purpose of this paper is to summarize the research regarding the toxic health effects caused by mercury dental amalgams. Method: The study involved summarizing scientific articles in journals regarding health effects of dental amalgam mercury. Results: The science strongly suggests dental amalgam mercury may be an etiological factor in numerous health disorders. Mental health seems to be affected the most including such conditions as depression, anger, and irritability. Studies have also associated it with schizophrenia and bipolar disorders. The cardiovascular system also is affected including high blood pressure, heart rate, hemoglobin, hematocrit, and red blood cells. Subjects with amalgams have a decreased T lymphocyte percentage compared to a control, and the immunoglobins IgG, IgA, and IgE correlated with the number of amalgams. Myopia is reduced in amalgam bearing subjects but amalgam mercury is constricting the visual field. When comparing total health disorders of subjects with amalgams compared to those without, they suffered 45% more health disorders. Urine and hair mercury levels were significantly higher in subjects with amalgams compared to those without. The scientific evidence strongly suggests that amalgam mercury is associated with Alzheimer’s disease, multiple sclerosis, and amytrophic lateral sclerosis. Research has shown when amalgams are removed many health conditions improve. Conclusion: The evidence is overwhelming that mercury from dental amalgam is an etiological factor in many health disorders.

Randomised controlled trials (RCTs) are subject to bias if they lack methodological quality. Moreover, optimal and transparent reporting of RCT findings aids their critical appraisal and interpretation.The aim of this study was to ascertain whether the methodological and reporting quality of RCTs in vascular and endovascular surgery is improving.The most recent 75 and oldest 75 RCTs published in leading journals over a 10-year period (2003–2012) were identified. The reporting quality and methodological quality data of the old and new RCTs were extracted and compared. The former was analysed using the Consolidated Standards of Reporting Trials (CONSORT) statement, the latter with the Scottish Intercollegiate Guidelines Network (SIGN) checklist.Reporting quality measured by CONSORT was better in the new studies than in the old studies (0.68 [95% CI, 0.66–0.7] vs. 0.60 [95% CI, 0.58–0.62], p < .001); however, both new and old studies had similar methodological quality measured by SIGN (0.9 [IQR 0.1] vs. .09 [IQR: 0.2], p = .787). Unlike clinical items, the methodological items of the CONSORT statement were not well reported in old and new RCTs. More trials in the new group were endovascular related (33.33% vs. 17.33%, p = .038) and industry sponsored (28% vs. 6.67%, p = .001).Despite some progress, there remains room for improvement in the reporting quality of RCTs in vascular and endovascular surgery. The methodological quality of recent RCTs is similar to that of trials performed >10 years ago.

ZusammenfassungZahlreiche wissenschaftliche Arbeiten belegen einen Zusammenhang zwischen Schwermetallbelastungen und neurodegenerativen Erkrankungen wie ALS. Immer wieder in der Diskussion sind Zahnfüllungen aus Amalgam, die in Deutschland trotz vielzähliger gegenteiliger Belege noch immer als unschädlich eingestuft werden. Die WHO hat diese bereits 1991 als Hauptquelle für Quecksilberbelastungen eingestuft.Für ALS gibt es bislang keine kurative Therapie, die Prognose ist in den meisten Fällen sehr ungünstig. Eine Ausleitungstherapie mit Chelatbildnern hat sich als nicht schädlich, sondern vielmehr lebensrettend und ursächlich gezeigt, was internationale wissenschaftliche Arbeiten bestätigen.

Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine if mercury could be causing Alzheimer's disease (AD) by cross referencing the effects of mercury with 70 factors associated with AD. The results found that all these factors could be attributed to mercury. The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss-all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer's disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer's disease include BACE 1, gamma secretase, cyclooxygenase-2, cytochrome-c-oxidase, protein kinases, monoamine oxidase, nitric oxide synthetase, acetyl choline transferase, and caspases, all which can be explained by mercury toxicity. Immune and inflammatory responses seen in patients with Alzheimer's disease also occur when cells are exposed to mercury, including complement activation, cytokine expression, production of glial fibrillary acid protein antibodies and interleukin-1, transforming growth factor, beta 2 microglobulins, and phosphodiesterase 4 stimulation. Genetic factors in patients with Alzheimer's disease are also associated with mercury. Apolipoprotein E 4 allele increases the toxicity of mercury. Mercury can inhibit DNA synthesis in the hippocampus, and has been associated with genetic mutations of presenilin 1 and 2, found in AD. The abnormalities of minerals and vitamins, specifically aluminum, calcium, copper, iron, magnesium, selenium, zinc, and vitamins B1, B12, E, and C, that occur in patients with Alzheimer's disease, also occur in mercury toxicity. Aluminum has been found to increase mercury's toxicity. Likewise, similar biochemical factors in AD are affected by mercury, including changes in blood levels of homocysteine, arachidonic acid, DHEA sulfate, glutathione, hydrogen peroxide, glycosamine glycans, acetyl-L carnitine, melatonin, and HDL. Other factors seen in Alzheimer's disease, such as increased platelet activation, poor odor identification, hypertension, depression, increased incidences of herpes virus and chlamydia infections, also occur in mercury exposure. In addition, patients diagnosed with Alzheimer's disease exhibit higher levels of brain mercury, blood mercury, and tissue mercury in some studies. The greatest exogenous sources of brain mercury come from dental amalgams. Conclusion: This review of the literature strongly suggests that mercury can be a cause of Alzheimer's Disease.

SummaryDie abnehmende Spermienqualität der letzten Jahrzehnte hat dazu geführt, dass die Normwerte für das Spermiogramm herabgesetzt wurden. Die inzwischen recht umfangreiche Forschung legt den Schluss nahe, dass diverse Umweltfaktoren zur abnehmenden Spermienqualität zumindest beitragen. Dazu zählen u. a. Schwermetall- und Arsenbelastungen, der Einsatz von Glyphosat und Pestiziden in der Landwirtschaft, die Verwendung von Bisphenyl A in Verpackungen. Aber auch elektromagnetische Felder niederer Intensität, denen praktisch jeder ausgesetzt ist, z. B. durch Mobilfunk, Laptop- und WLAN-Nutzung werden diskutiert.Im Beitrag wird die aktuelle Datenlage zu den aufgrund der weiten Verbreitung wichtigsten umweltmedizinischen Faktoren für Spermienschäden zusammengefasst.

Mercury in dental amalgams : A great concern for clinical toxicology in developing countries?

Genetic background accounts for only 5 to 10% of the reported cases of Parkinson's disease (PD), while the remaining cases are of unknown etiology. It is believed that environmental factors may be involved in the causality of a large proportion of PD cases. Several PD genes are activated by xenobiotic exposure, and a link between pesticide exposure and PD has been demonstrated. Many epidemiological studies have shown an association between PD and exposure to metals such as mercury, lead, manganese, copper, iron, aluminum, bismuth, thallium, and zinc. This review explores the biological effects, the pathogenetic processes, genetic susceptibilities to metals as well as examining future strategies for PD treatment, such as chelation therapy.

ZusammenfassungIn den meisten Fällen ist die Ursache einer Morbus-Parkinson-Erkrankung unklar. Die konventionellen Behandlungsoptionen sind nicht immer ausreichend oder werden aufgrund unerwünschter Wirkungen von den Patienten abgelehnt.Verschiedene Studien legen den Einfluss von Umweltfaktoren auf die Entstehung neurodegenerativer Erkrankungen wie Morbus Parkinson nahe. Insbesondere Schwermetallbelastungen durch Zahnmaterialien scheinen eine Rolle zu spielen.Mit einer integrativen Therapie, die u. a. die Ernährung, den Mikronährstoffstatus, Schwermetallbelastungen und mögliche neurotrope Infektionen berücksichtigt, kann der Behandlungserfolg erheblich verbessert bzw. die Krankheitsprogression gestoppt werden.

Background: Amyotrophic lateral sclerosis (ALS) is a devastating disease leading to death within 3-5 years in most cases. New approaches to treating this disease are needed. Here, we report a successful therapy. Case Report: In a 49-year-old male patient suffering from muscle weakness and fasciculations, progressive muscular atrophy, a variant of ALS, was diagnosed after extensive examinations ruling out other diseases. Due to supposed mercury exposure from residual amalgam, the patient's teeth were restored. Then, the patient received sodium 2,3-dimercaptopropanesulfate (DMPS; overall 86 × 250 mg in 3 years) in combination with α-lipoic acid and followed by selenium. In addition, he took vitamins and micronutrients and kept a vegetarian diet. The excretion of metals was monitored in the urine. The success of the therapy was followed by scoring muscle weakness and fasciculations and finally by electromyography (EMG) of the affected muscles. First improvements occurred after the dental restorations. Two months after starting therapy with DMPS, the mercury level in the urine was increased (248.4 µg/g creatinine). After 1.5 years, EMG confirmed the absence of typical signs of ALS. In the course of 3 years, the patient recovered completely. Conclusions: The therapy described here is a promising approach to treating some kinds of motor neuron disease and merits further evaluation in rigorous trials.

This article reviews the clinical use of the metal chelators sodium 2,3-dimercapto-1-propanesulfonate (DMPS), meso-2,3-dimercaptosuccinic acid (DMSA), and calcium disodium edetate (CaEDTA, calcium EDTA) in overexposure and poisonings with salts of lead (Pb), mercury (Hg), and arsenic (As). DMSA has considerably lower toxicity than the classic heavy metal antagonist BAL (2,3-dimercaptopropanol) and is also less toxic than DMPS. Because of its adverse effects, CaEDTA should be replaced by DMSA as the antidote of choice in treating moderate Pb poisoning. Combination therapy with BAL and CaEDTA was previously recommended in cases of severe acute Pb poisoning with encephalopathy. We suggest that BAL in such cases acted as a shuttling Pb transporter from the intra- to the extracellular space. The present paper discusses if a combination of the extracellularly distributed DMSA with the ionophore, Monensin may provide a less toxic combination for Pb mobilization by increasing both the efflux of intracellularly deposited Pb and the urinary Pb excretion. Anyhow, oral therapy with DMSA should be continued with several intermittent courses. DMPS and DMSA are also promising antidotes in Hg poisoning, whereas DMPS seems to be a more efficient agent against As poisoning. However, new insight indicates that a combination of low-dosed BAL plus DMPS could be a preferred antidotal therapy to obtain mobilization of the intracerebral deposits into the circulation for subsequent rapid urinary excretion.

Mercury (Hg) is a persistent bio-accumulative toxic metal with unique physicochemical properties of public health concern since their natural and anthropogenic diffusions still induce high risk to human and environmental health. The goal of this review was to analyze scientific literature evaluating the role of global concerns over Hg exposure due to human exposure to ingestion of contaminated seafood (methyl-Hg) as well as elemental Hg levels of dental amalgam fillings (metallic Hg), vaccines (ethyl-Hg) and contaminated water and air (Hg chloride). Mercury has been recognized as a neurotoxicant as well as immunotoxic and designated by the World Health Organization as one of the ten most dangerous chemicals to public health. It has been shown that the half-life of inorganic Hg in human brains is several years to several decades. Mercury occurs in the environment under different chemical forms as elemental Hg (metallic), inorganic and organic Hg. Despite the raising understanding of the Hg toxicokinetics, there is still fully justified to further explore the emerging theories about its bioavailability and adverse effects in humans. In this review, we describe current research and emerging trends in Hg toxicity with the purpose of providing up-to-date information for a better understanding of the kinetics of this metal, presenting comprehensive knowledge on published data analyzing its metabolism, interaction with other metals, distribution, internal doses and targets, and reservoir organs.

SummaryNatürliche und auch künstliche Chemikalien können den Organismus schwächen und krank machen. Für viele Menschen, besonders bei bestehenden Krankheiten oder Beschwerden, kann eine regelmäßige Entgiftung sinnvoll sein. Gegen Metalle, Halbmetalle und manche radioaktive Isotope sind spezifische Gegenmittel (Antidote) verfügbar. Bei anderen Giftstoffen gibt es, außer bei einigen in der Akuttoxikologie (wie z. B. Antiseren gegenüber Schlangengiften, Atropin gegen Cholinesterasehemmstoffen) keine spezifischen Gegenmittel.Der Autor gibt einen Überblick über die wichtigsten Entgiftungsstrategien bei chronischen Beschwerden sowie praktische Hinweise.

Mercury has been introduced into the human environment in large quantities through industrial and medical processes, starting in the early nineteenth century. It is one of the most toxic substances known. Circumstantial evidence suggests that the pathology of Alzheimer’s disease (AD) might be in part caused or exacerbated by inorganic mercury (IM). We therefore present here the results of a systematic review, covering 106 studies, most of them case control and cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to IM, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro and animal models showed that IM reproduces all pathological changes seen in AD. Its high affinity for selenium and selenoproteins suggests that IM may promote neurodegenerative disorders via disruption of redox regulation. IM may therefore play a role as a co-factor in the multi-factorial development of AD. It may also increase the pathological influence of other metals already known to play a potential role in AD, such as aluminum, copper, or iron. The mechanistic model provided here explains the considerable delay until clinical symptoms can be seen. Mercury should be eliminated from biological cycles as quickly as possible.

It was claimed by the Scientific Committee on Emerging and Newly Identified Health Risks (SCENIHR)) in a report to the EU-Commission that "....no risks of adverse systemic effects exist and the current use of dental amalgam does not pose a risk of systemic disease..." [1, available from: http://ec.europa.eu/health/ph_risk/committees/04_scenihr/docs/scenihr_o_016.pdf ]. SCENIHR disregarded the toxicology of mercury and did not include most important scientific studies in their review. But the real scientific data show that: (a) Dental amalgam is by far the main source of human total mercury body burden. This is proven by autopsy studies which found 2-12 times more mercury in body tissues of individuals with dental amalgam. Autopsy studies are the most valuable and most important studies for examining the amalgam-caused mercury body burden. (b) These autopsy studies have shown consistently that many individuals with amalgam have toxic levels of mercury in their brains or kidneys. (c) There is no correlation between mercury levels in blood or urine, and the levels in body tissues or the severity of clinical symptoms. SCENIHR only relied on levels in urine or blood. (d) The half-life of mercury in the brain can last from several years to decades, thus mercury accumulates over time of amalgam exposure in body tissues to toxic levels. However, SCENIHR state that the half-life of mercury in the body is only "20-90 days". (e) Mercury vapor is about ten times more toxic than lead on human neurons and with synergistic toxicity to other metals. (f) Most studies cited by SCENIHR which conclude that amalgam fillings are safe have severe methodical flaws.

It was claimed by the Scientific Committee on Emerging and Newly Identified Health Risks (SCENIHR)) in a report to the EU-Commission that “....no risks of adverse systemic effects exist and the current use of dental amalgam does not pose a risk of systemic disease...” [1, available from: http://ec.europa.eu/health/ph_risk/committees/ 04_scenihr/docs/scenihr_o_016.pdf]. SCENIHR disregarded the toxicology of mercury and did not include most important scientific studies in their review. But the real scientific data show that: (a) Dental amalgam is by far the main source of human total mercury body burden. This is proven by autopsy studies which found 2-12 times more mercury in body tissues of individuals with dental amalgam. Autopsy studies are the most valuable and most important studies for examining the amalgam-caused mercury body burden. (b) These autopsy studies have shown consistently that many individuals with amalgam have toxic levels of mercury in their brains or kidneys. (c) There is no correlation between mercury levels in blood or urine, and the levels in body tissues or the severity of clinical symptoms. SCENIHR only relied on levels in urine or blood. (d) The half-life of mercury in the brain can last from several years to decades, thus mercury accumulates over time of amalgam exposure in body tissues to toxic levels. However, SCENIHR state that the half-life of mercury in the body is only “20-90 days”. (e) Mercury vapor is about ten times more toxic than lead on human neurons and with synergistic toxicity to other metals. (f) Most studies cited by SCENIHR which conclude that amalgam fillings are safe have severe methodical flaws. Dental amalgam is the main source of mercury in human tissues SCENIHR (Scientific Committee on Emerging and Newly Identified Health Risks) from the European Commission claim [1]: “Exposure to mercury is difficult to measure. The indications for mercury exposure are therefore normally obtained by measuring mercury levels in urine and blood of individuals.” SCENIHR did not cite any autopsy studies, which are the most reliable studies for assessing mercury levels in tissues. An approx. 2-5-fold increase of mercury levels in blood and urine in living individuals with dental amalgam as well as a 2-12 fold increase in several body tissues was observed in deceased individuals with dental amalgam [2-21]. Additionally, studies with animals have confirmed the fact that dental amalgam leads to significantly increased levels in the tissues [22-28]. According to these studies, dental amalgam is responsible for at least 60-95% of mercury deposits in human tissues. This was not acknowledged by SCENIHR. No organic mercury compounds through dental amalgam? SCENIHR [1] state that “there is no evidence that biotransformation of amalgam derived mercury takes place intra-orally in association with bacterial activity.” Correspondence: jm@zahnklinik.de Department of Environmental and integrative medicine Lohnerhofstraße 2, 78467 Constance/Germany Mutter Journal of Occupational Medicine and Toxicology 2011, 6:2 http://www.occup-med.com/content/6/1/2 © 2011 Mutter; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In contrast to this claim studies have shown that mercury (Hg) from dental amalgam is transformed into organic mercury compounds by microorganisms in the human gastrointestinal tract [29-31]. Leistevuo et al. (2001) found a three-fold increase of methylmercury levels in saliva of individuals with dental amalgam compared to individuals without amalgam, although frequency and kind of fish consumption were identical in both groups. Mercury levels in saliva exceed mercury limits for sewage in 20% of individuals with amalgam [30]. The form of methylmercury derived from dental amalgam may be much more toxic (up to 20 times) than the form of methylmercury found in fish (see section “toxicity of mercury”). Toxic mercury levels in vitro and in vivo Inorganic mercury levels of 0.02 ng Hg/g (2 μl of 0.1 μMolar Hg in 2 ml substrate) led to the total destruction of intracellular mircrotubuli and to the degeneration of axons [32]. In other experiments inorganic mercury levels of 36 ng Hg/g (0.18 μMol Hg) led to increased oxidative stress as a prerequisite for further cell damage [33,34]. Mercury vapor inhalation in doses which also occur in humans with many amalgam fillings and chewing led to pathological changes in the brains of animals after 14

Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol. Two reviewers extracted relevant data independent of each other. One thousand and forty one references were scrutinized, and 106 studies fulfilled the inclusion criteria. Most studies were case control or comparative cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible.

A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.