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   Posted v1.0 5-18-2018, v2.0 1-6-2025 with improved charts.
This is a scientific paper from 2004 that solidly references the mercury issue.

Mercury Toxicity: A Cause for Concern In Sports & Health

"All elements are toxic at high concentrations, and some are notorious poisons even at low concentrations" - H.J.M. Bowen, Department of Chemistry, The University, Reading, England 1966

Thesis: Athletes may be in danger of metabolic disruption and mortality from unsuspected sources: Mercury containing dental amalgams and fish.

I. About Mercury

A. Mercury Defined
B. Brief Historical Timeline
C. Sources of Mercury

1. Fish
2. Dental Amalgam

II. Symptoms of Mercury Poisoning

III. Special Athletic Concerns

A. Metabolic Acidosis
B. Idiopathic Dilated Cardiomyopathy
C. Distribution of Mercury With Exercise

IV. Nutritional Factors & Mercury Detoxification

A. Selenium & Vitamin E
B. Alpha Lipoic Acid
C. Melatonin

V. Summary

VI. References


l. About Mercury

IA. Mercury Defined

"The fact that mercury can be absorbed and reach toxic levels in human tissues makes any and all exposure to that element of scientific interest" - JW Reinhardt, Department of Operative Dentistry, University of Iowa College of Dentistry, Iowa City. 1992.

Mercury is atomic number 80, has chemical symbol Hg, with an atomic mass of 200.59. It is a cumulative poison in mammals (Bowen, 118, 187) and a neurotoxin (Haley, Crinnon). Mercury can bond with itself as in the mercurous ion Hg2++, or the linear mercurous chloride Cl-Hg-Hg-Cl (Pauling, 436, 125). The mercurous ion is highly reactive and joins with the thiol class of compounds (Osterblad), and more specifically with thiol's functional sulfhydryl group (-SH) and with imino-nitrogen ligands (Smith, Haley). Every mercury compound is toxic (Emsley, 255), methylmercury compounds exceptionally so (Christian, 386, Emsley, 255). Methylmercury (CH3Hg+) is even more toxic than the mercurous ion, is present in the food chain of marine organisms (Macalady), and can be bioaccumulated partly due to its lipophilic nature (King).

lB. A Brief Historical Timeline of Mercury

30,000 BC Europe: Cave artists utilize cinnabar, mercury sulfide, in their paintings (Emsley, 258).

About 300 AD: Romans used cinnabar for cosmetics (Carpi).

1566 South America: Spanish explorers find mercury and utilize it to extract gold (Emsley, 258).

1700's - 1800's: Mercury was used in the manufacture of hats resulting in worker's cases of "Mad Hatter's disease." (Christian, 386, Fauci, 2567).

Early 1800's St. Petersburg, Russia: 60 workers die from mercury poisoning while beautifying the dome of the St. Isaac cathedral (Emsley, 260).

1810 London: 3 crew members and all bovines and fowl of the British ship Triumph die as a result of a flask of mercury rupturing at sea. The entire crew of 200 became symptomatic with mercury poisoning. (Emsley, 256).

1860: US President Abraham Lincoln ceases taking medicinal "blue pills" that contained elemental mercury due to suspected toxicity. Hirschhorn et al shows that the blue pill formula is a potential neurotoxin.

1882: E.S. Talbot publishes paper "The chemistry and physiological action of mercury as used in amalgam fillings." The dentist states: "It is one of the most objectionable articles for filling teeth that can be employed" and "Evaporation does not depend upon quality or age, but all amalgams will send off the vapor of mercury. This has been proved conclusively by its destruction of animal and vegetable life, and by chemical tests."

1895: A mercury containing dental amalgam is introduced by the dentist G.V. Black. They are commonly called "silver fillings" (Emsley, 259).

1953 -1960 Minamata Bay, Japan: Organomercury toxicity from eating contaminated fish from industrially polluted waters results in nervous system disorders and the disabling "Minamata Disease." Fish exhibited up to 50 ppm and shell fish 85 ppm methyl mercury. 134 people were ill and there were 48 deaths. Babies were born with neurological damage.

1965 Niigata, Japan: Another incident similar to the Minamata Bay disaster as the population consumes mercurified seafood (Crinnon). There were 49 people ill and 6 deaths. (Emsley, 260, Schroeder, 159, Christian, 386).

1970's Iraq: 280 die and over 5000 exhibit mercury poisoning when seed grain coated with mercury is used for food (Emsley, 259).

1975 Germany: Chronic mercury poisoning appears in users of hair bleaches. Patients exhibit 1720mg/L mercury in their nails, and 1.97mg/L mercury in urine, 400 times normal, after dimercaprol injection (Wustner).

1980's to present, Florida: Panthers in the Everglades National Park exhibit mercury toxicosis (The Florida Panther Society).

1996 Germany: A 5 year old child develops contact dermatitis following Mercurochrome (Merbromin) and later mercury contaminated PVC exposure. The child's PVC boots contained mercury chloride. Conclusion: "New hidden sources of mercury in consumer goods may represent a potential source of danger for the future, if its use is not more strictly regulated" (Koch).

1997 Dartmouth University: Dr. Karen Wetterhahn dies from a drop of methylmercury spilled on her latex glove (Carpi).

2000 Papua New Guinea: A gold miner exhibits mercurial toxicity from breathing mercury vapor while extracting gold (Reto).

2000 Phillipines: 95 inhabitants of the gold mining area Mt. Diwata show mercury toxicity and are treated with DMPS (Bose-O'Reilly).

2001 Zimbabwe: Gold miners show elevated levels of mercury in blood and urine (Matchaba-Hove).

2002 Brazilian Amazon: Fish consumption and gold mining were looked at as sources of mercury toxicity. The outcome : "The most important predictors of elevated mercury levels were high fish consumption and low income." The study also found that those reporting mercury in their ecological field had a four times greater chance of malaria infection (Crompton).

2002 Japan: A fisherman dies after suffering from Minamata Disease (methylmercury poisoning) (Eto).

2002 Vancouver BC: Dr. John Sehmer reports that a female patient diagnosed with multiple sclerosis with optic neuritis and peripheral neuropathy shows elevated blood mercury levels (63 nmol/L Hg) . The patient's boyfriend also exhibited elevated mercury levels at 59 nmol/L. Findings revealed that the couple had been eating sushi and fish four to five times weekly (Sehmer).

2002 Newport, Vermont: A female patient suffers mercury poisoning after being left with a post operative mercury weighted tube and a resultant "massive intraperitoneal load of mercury." Although she had health concerns beforehand, during the mercurial period she experienced "formication, pruritis, fatigue, irritability, insomnia, alopecia, dizziness, a gait disturbance, loss of balance and multiple falls, abdominal pain, choking, and headaches." She died soon after lung cancer appeared (Haas).

2002 Sweden: From a study of 796 dental patients amalgams were removed and antioxidant therapy provided. Blood plasma levels of mercury from dental amalgam were deemed to be "causative of ill health." "The hypothesis that metal exposure from dental amalgam can cause ill health in a susceptible part of the exposed population was supported" (Lindh).

2003 Brazil: Methylmercury exposure from fish consumption affects neuropsychological function in adults (Yokoo).

lC. Sources of Mercury

There are numerous sources of various forms of mercury: hospital waste, thermometers, fluorescent light bulbs, thermostats, dental amalgams, and fish. I will focus upon the latter two sources since they are commonly encountered in society and may represent the most often instances of occurrence.

lC-1. Fish

". . . dietary histories that encompass fish consumption should become part of a comprehensive health screening to identify those at risk for mercury accumulation" - Jane M. Hightower, California Pacific Medical Center, & Dan Moore, Geraldine Brush Research Institute, California Pacific Medical Center, San Francisco, California, USA

Fish are a chief source of methylmercury worldwide (Pickhardt). Microorganisms and bacteria in aquatic environments can process mercury ultimately yielding methylmercury compounds such as CH3Hg+ and (CH3)2Hg. When fish take in their smaller denizens and mercury, a mercurial bioamplification process begins. These fish in turn are consumed by predatory superiors. Humans, at the apex of the food chain, can be consuming fish that have concentrations of mercury 50,000 times that of their fresh water environs (Chang, 840) to 100,000 times that of ocean water in the case of tuna or swordfish (Emsley, 255). Fish consumers have a greater amount of mercury in their tissues than non-fish consumers (Schroeder, 164). Mercury contaminated fish are unsafe to consume (Hoffer, 152).

lC-2. Dental Amalgam

"It is extremely easy to demonstrate that amalgams release toxic material" - Dr. Boyd E. Haley, Professor and Chair, Department of Chemistry, University of Kentucky, Lexington, KY

An amalgam by definition contains mercury and at least one other substance. "Silver fillings" are dental amalgams containing 50% mercury (Fauci, 2566). Dental amalgams have been shown to release mercury in proportion to their number in the oral cavity (Pizzichini). The mercury in dental amalgam reacts in the oral cavity with anaerobic bacteria producing H2S (hydrogen sulfide) and CH3SH (methyl thiol) to produce supertoxins such as CH3S-Hg-S-CH3 (dimethylthiol mercury) and CH3S-Hg-Cl (methylthiol mercury chloride). An average of 43.5 micrograms of mercury per day per amalgam filling may be released without chewing, with significant increases during brushing the teeth (Haley).

Crematoriums can release 5 kilograms of mercury each year from dental fillings (Emsley 260). Significantly higher mercury levels have been found in the blood and urine of subjects with amalgams when compared to those without amalgams, and there is concern regarding nephrotoxicity (Mortada):

From the nephrotoxicity point of view, dental amalgam is an unsuitable filling material, as it may give rise to Hg toxicity. Hg levels in blood and urine are good markers of such toxicity. In these exposure conditions, renal damage is possible and may be assessed by urinary excretions of albumin, NAG, and gamma-GT.

The presence of mercury in the human system from amalgams has been shown to be pro-oxidative and to lower the Total Antioxidant Activity (TAA) (Pizzichini). Therefore, one is left with a compromised ability to neutralize free radicals, and this could lead to degenerative effects. This should be of special concern to athletes and regular exercisers that need a full TAA to neutralize free radicals with physical activity.

II. Symptoms of Mercury Poisoning

"These findings support the contention that there is peripheral nerve degeneration in Minamata patients due to toxic injury from methylmercury" - Eto, et al. National Institute for Minamata Disease, Ministry of the Environment, Minamata City, Kumamoto, Japan.

Symptoms and Signs of Mercury Poisoning May Include*:

Brain: lesions in the anterior portion of the calcarine cortex depletion of granular cells in the cerebellar cortex brain damage in the basal ganglia, cortex, and cerebellum

Oral Cavity: gingivitis amalgam "tattoo" on gum near filling loose teeth oral ulcers

Cardiovascular: arrhythmia elevated blood pressure tachycardia idiopathic dilated cardiomyopathy

Nephrotoxicity: kidney dysfunction kidney failure proteinuria

Neurotoxicity: headaches memory loss depression irritability psychosis** tremor mood swings hallucinations inability to concentrate loss of balance insomnia*** paraesthesia peripheral neuropathy peripheral nerve degeneration

Skeletal Muscle: muscle spasms muscle weakness

Metabolic: metabolic acidosis lactic acidosis

Ocular: blurred vision

Other: DNA damage ataxia fatigue death

* Fauci 2566-2567, Weinstein, Clarkson, Yokoo, Reto, Haley, Carpi, Weir, Tchounwou, Sutton.

**Symptoms of mercury poisoning are frequently mistaken for psychogenic causes (Sutton, et al). Therefore, it is imperative that clinicians and coaches alike are cognizant of the issue. A proper health inventory should be performed by competent health practitioners that are aware of the possibility of mercurialism. Symptoms may take months to appear following poisoning (Weir).

Physician Hoffer (Hoffer, 168) reports that three patients had experienced schizophrenic psychosis due to mercury poisoning. Haley shows a biochemical means for mercury to exacerbate or possibly produce Alzheimer's Disease.

*** "From the onset, insomnia is accompanied by irritability, difficulty in concentration, loss of memory, apathy and low self-esteem" - Sueli Regina G. Rossini et al regarding chronic mercury contamination.

lll. Special Athletic Concerns

Considering the aforementioned symptomatology of mercury toxicity and possible consequences, there is cause for concern in the general population. Athletes and those involved in exercise science have have specific biochemical and metabolic concerns in addition to those of the general population that may be apparent if mercury is present. These will now be addressed.

lllA. Metabolic Disruption & Acidosis

Thiols (R-SH), also known as mercaptans ("captures mercury"), are able to join with mercury to produce heavy-metal compounds (Wade, 391). Mercury can elevate membrane permeability and inhibit ATPase dependent transport (Cotran, 13). Metabolic acidosis in the form of lactacidosis may occur when mercuric ions join with lipoic acid's sulfhydryl groups (-SH) (Murray, 179). Thusly, mercury can complex the body's thiol groups, especially lipoic acid, suppressing the enzyme pyruvate dehydrogenase resulting in pyruvate to lactate conversion and thereby lactate accumulation.

Athletes suffering from lactacidosis may experience early fatigue as reported by Brancazio (190), with lactic acid elevation 10 to 15 times that of the resting state. Extreme acidosis due to metabolic disruption may allow the blood pH to drop below 7.0, thereby causing central nervous system depression. The CNS may be affected to the point where the person is "disoriented, and later comatose" (Guyton, 498). It should be noted that mercury also reduces glutathione levels (crucial for elimination of toxins), thereby potentiating toxicity from other substances.

lllB. Idiopathic Dilated Cardiomyopathy (IDCM)

"A recent report stated that the tissues of individuals who died of Idiopathic Dilated Cardiomyopathy (IDCM) had mercury levels of 178,400 ng/g tissue or 22,000 times more than their controls who died of other forms of heart disease. IDCM is a disease where young athletes drop dead during strenuous exercise" - Dr. Boyd E. Haley, Professor and Chair, Department of Chemistry, University of Kentucky, Lexington, KY

A report entitled "Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction" did indeed find such elevations of mercury in heart tissue correlated with IDCM (Frustaci). By the very nature of the term idiopathic, an unknown etiology or cause has been implied in regards to this type of cardiac disease in which the heart becomes weaker and can fail, sometimes suddenly. It is imperative that coaches and health professionals be aware of the possibility of mercurial toxicity and the potential outcome.

lllC. Distribution of Mercury With Exercise

While studying the effects of mercury exposure in exercising (swim trained) mice, Shimojo and Arai found significant distribution changes correlated with exercise. While the total mercury of the body remained the same in the experimental and control groups, the exercising experimental group revealed higher concentrations of mercury in "the heart, whole blood, red blood cells and the brain at 24 and 48 h; and in the plasma and kidneys at 24 h."

The exercising group also revealed elevated levels of the following substances in specific anatomical parts:

Red blood cells: catalase, superoxide dismutase, and glutathione peroxidase Liver: superoxide dismutase Kidneys: catalase and glutathione peroxidase

The study found that "exercise training is a factor in distribution changes of mercury after exposure to mercury vapour, though it is not a factor in the total absorption and excretion of mercury."

Evidence for the reallocation of mercury to the heart in humans has been provided by Frustaci et al. Haley provides compelling evidence for deposition of mercury in the human brain resulting in Alzheimer's like effects and neuronal damage. The distribution pattern of mercury found in mice would seem to be replicated in humans.

IV. Nutritional Factors & Mercury Detoxification

The literature mentions multiple methods for mercury elimination/amelioration once dental amalgams, contaminated fish, or other mercury sources are removed from the individual. Substances such as 2,3-dimercaptopropane-1-sulphonate (DMPS) are used in medical settings for mercury removal. Nutritional substances, occurring in foods or via supplementation, have been found according to literature as being biologically facilitative when mercury is present. Therefore, a review of nutritional substances mentioned in research literature follows:

Selenium & Vitamin E

"Selenium and vitamin E exert powerful effects in reducing acute or chronic methylmercury toxicity" - H.E. Ganther in opening statement in Modification of methylmercury toxicity and metabolism by selenium and vitamin E: possible mechanisms. 1978.

Selenium is atomic number 34, has chemical symbol Se, with an atomic mass of 78.96. The element is crucial for the formation of protective enzymes glutathione peroxidase (Christian, 340, Murray, 115) and thioredoxin reductase (McBride). Glutathione functions to eliminate toxins such as mercury (Baker, 82). Selenium works with Vitamin E in an antioxidant role (Murray, 605) thusly neutralizing free radicals (Masterton, 606).

Selenium deficiency is implicated in a reversible type of cardiomyopathy (Fauci, 1328). In China congestive heart failure known as Keshan disease, and stomach cancers, were decreased with a selenium nutritional program; selenium deficiency is also associated with low immunity and viral propagation (Emsley, 381). Selenium is listed as an antidote (Agricultural Research Service), protector (Hoffer, 165), detoxifier (Passwater, 161), or metabolic antagonist (Walford, 167), against mercury.

Food sources of selenium in excess of 100 micrograms per 100 grams include Brazil nuts, high selenium nutritive yeast, and the mushroom Albatrellus pes-caprae from Italy (with only 12.16 grams fresh weight providing the daily maximum intake of 450 micrograms**) (Emsley, 380). Keep in mind the quote from H.J.M. Bowen regarding all elements being toxic that began this paper. Selenium is no exception, with regular consumed amounts in excess of 1 mg potentiating nail and hair loss (Christian, 341).

Selenium Content of Select Foods/Herbs in ppm*:

Mercury has been described as a selenium competitor and shown to lower survival rates in mice, especially with the presence of a viral agent:

South says 90 percent of the mice given the highest dose of mercury alone—right at their limit of tolerance—survived. But the survival rate plunged to 36 percent of the mice exposed to both mercury and the innocuous coxsackievirus. About one-third of the infected mice given the highest dose of mercury had more severe heart damage, and their hearts had higher numbers of virus. (McBride).

Note that the mice had cardiac damage and viral counts were increased with significant mercury levels. One may expect that when dual exposure occurs with mercury and specific viral agents mortality rates would be higher in the general population, especially in those with low selenium intakes. A health screening including selenium intake, mercury exposure, viral infection, and heart damage factors is needed in health care/research settings to further analyze this issue.

Vitamin E has been shown to prevent neuronal damage and methylmercury toxicosis symptoms in laboratory animals. Hamsters exposed to 2.0 ppm methylmercury without Vitamin E had severe signs of mercury poisoning, while those exposed to methylmercury with the addition of 2.0 ppm Vitamin E revealed no toxic symptoms or tissue damage (Chang). Vitamin E and selenium are interdependent, and a lack of one can substitute for the other to some degree (Christian, 340). Kling found that Vitamin E was "equal or superior to all synthetic antioxidants tested in alleviating the toxicity of organic Hg poisoning" in Japanese quail. Both Kling and Ganther acknowledge protection against oxidative effects with nutrients, with Ganther (1980) emphasizing that selenium and Vitamin E display "protection afforded by low levels of the nutrients against high levels of the metal toxicants."

Vitamin E is a generic category for multiple chemical compounds with either a tocopherol or tocotrienol structure. Isoforms include alpha, beta, gamma, and delta tocopherols and tocotrienols. Alpha-tocopherol is listed as being a highly active form of Vitamin E (Christian, 286), with alpha-tocotrienol showing antioxidant, anticarcinogenic, and neuroprotective effects but with a short half life (Packer).

Alpha-Tocopherol (Vit. E) Content of Select Foods/Herbs in ppm*

Tocopherol (Vit. E) Content of Select Foods/Herbs in ppm*:

* USDA Agricultural Research Service, Dr. Duke's Phytochemical and Ethnobotanical Databases ** Emsley [calculations based on 100 g fresh weight providing 3700 mcg Se: 100g mushroom / 3700 mcg Se = x g mushroom / 450 mcg Se 3700 x = 45000 x = 12.16 g mushroom]

Alpha Lipoic Acid (ALA)

ALA, also known as thioctic acid, is an antioxidant substance with two sulfur atoms per molecule. ALA has shown ameliorative effects in rats with damage to the nervous system due to mercury poisoning (Anuradha). The functioning of ALA in the human system is of particular importance when arsenite or mercuric ions are present (Murray, 179). As mercury joins with the sulfur containing sulfhydryl groups of ALA, pyruvate dehydrogenase is prevented from functioning, with a resultant conversion of pyruvate to lactate. The symptoms are similar to a low oxygen situation in exercise or Vitamin B-1 deficiency in which high glycemic foods allow for blood glucose levels to rise resulting in lactacidosis. In severe B-1 deficiency mortality rates are high in humans with sudden blood sugar elevation.

Consider the following simplified energy pathways:

Glycogen > Glucose > Pyruvate > Acetyl-CoA > Kreb's cycle + O2 > CO2 + H2O + ATP*

Sudden blood sugar elevation can lead to pyruvate accumulation in B-1 deficiency or mercury poisoning.

Fat > Fatty Acids > AcetylCoA > Kreb's cycle + O2 > CO2 + H2O + ATP*

Fats are utilized as an energy source in this series.

The aforementioned animal study would suggest that supplemental ALA increases organismic functionality when mercury is present.

* adapted from Berger p. 51.

Melatonin

Melatonin is a naturally occurring hormone released by the pineal gland in the brain, is a powerful antioxidant, and is associated with regulation of the sleep cycle. Melatonin increases with stress (Krieger, 107), crosses the blood-brain barrier, increases glutathione peroxidase, and enhances NK (natural killer) immune cell response against viruses (Reiter, 202-203). Healthy seniors produce greater than 200% the amount of melatonin than Alzheimer's diagnosed individuals (Mishima). If mercury is a causal agent or potentiator for Alzheimer's disease, then we would expect lowered melatonin levels in ill individuals.

In a study with mice, melatonin allowed for a 100% survival rate on the 35th day of methylmercury toxicity versus 60% in the untreated group . Substances associated with oxidative damage were lowered in the melatonin group (Kim).

It should be noted that the substances mentioned as being efficacious in assisting with mercurial toxicity have a commonality: they are antioxidants. The antioxidants Vitamin E, the mineral selenium, ALA, and melatonin have been beneficial in varying capacities in animal studies regarding mercury. Note that melatonin and selenium assist in glutathione peroxidase production (Reiter, 202; Christian, 340), and ALA is "involved in the recycling of other antioxidants in the body including vitamins C and E and glutathione" (Wollin & Jones).

Summary

"The resistance to the evidence of mercury poisoning is typical of resistance to new medical knowledge and declined only when the opponents and sceptics grew old and disappeared from the scene" - A. Dally regarding "pink disease", (mercury poisoning from babies teething powders), Wellcome Institute for the History of Medicine, London. 1987.

1. Every mercury compound is toxic.
2. Fish consumers have more mercury in their systems than non-fish consumers.
3. Those with dental amalgams have more mercury than those without amalgams.
4. There are substantial health risks associated with mercury exposure.
5. Mercury depletes glutathione, thereby interfering with removal of other toxins.
6. Mercury exposed mice had higher viral counts and rates of heart damage than non-mercury exposed mice.
7. Mercury lowers the TAA (total antioxidant activity) while increasing peroxidation and oxidative stress.
8. Research has shown that raising the TAA with antioxidants has beneficial effects regarding mercury toxicity.
9. Specific concerns regarding mercury in the health and sports communities include Idiopathic Dilated Cardiomyopathy (IDCM), metabolic acidosis, and redistribution of mercury with exercise.
10. General concerns regarding mercury include heart, kidney, and brain damage, chronic fatigue from disrupted metabolic pathways, and possibly Alzheimer's disease.

Closing thought:

ΔT, delta T, represents a change in temperature and is of concern to those in the sciences. Physicist Paul Hewitt has noted that people can be unaware of ΔT if the change is gradual over time. A true example he has utilized was of a couple falling asleep, then being overheated to death in a hot tub due to a faulty thermostat. They were unaware of the slow change in ΔT, then went to sleep to never awake. He recommend always being aware of the environment, because ΔT could represent many things. In the case of mercury, our ΔT could easily be a change in bodily toxin levels. Will we wake up before it's too late?

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