Mercury has been recognized since prehistoric times as a toxic metal. Lately, interest in mercury poisoning is increasing due to;
The most threatening mercury compound is organic methylmercury, although there is risk of contamination from inorganic mercury compounds as well.
Mercury can enter the body through the lungs, through food and water, and by direct physical contact.
Commonly used silver amalgam dental fillings contain about 50 percent mercury. Older dental fillings may contain higher amounts. There is increasing evidence that mercury is leached from dental amalgam and that mercury can vaporize from fillings. Fillings which crack can also be a source of mercury toxicity.
Silver amalgam fillings also generate negative electrical potentials in the mouth which can detrimentally affect one's health status.
There are alternatives to silver amalgam fillings, including gold alloys and composite quartz-resin materials.
The concentration of mercury in fish varies directly with the size of the fish, inasmuch as mercury is more concentrated at each step upward as one goes up the food chain.
Tuna and swordfish are the most common fish contaminated with mercury. Most swordfish are kept off the market today for this reason. Albacore tuna has been found to be safer than the larger species of tuna.
While fish contain selenium, which helps to neutralize the toxic effects of mercury, we do not recommend eating tuna fish more than twice a week, due to mercury contamination.
Mercury in industrial waste is a common water contaminant. Mercury used in fungicides and slimicides easily finds its way into water supplies. Sewage sludge is commonly contaminated with mercury.
Mercury is commonly used as a treatment to prevent fungal growth on seeds.
Because of its bacteriostatic properties, mercury is a common ingredient in antiseptics (Mercurochrome, Merthiolate) and contact lens solution. Mercury is also found in the thiazide diuretics and in some hemorrhoid medications.
Methylmercury easily crosses the placenta into the growing fetus. Other mercurial compounds pass with less ease. Mercury compounds can also be transferred through breast milk to nursing babies. Levels in breast milk are about five percent of those of blood.
It is believed that fetuses are the group most susceptible to mercury toxicity. Infants excrete mercury more slowly than adults.
Mercury is widely used in industry and in a variety of products, e.g., felt, fungicides, algicides used in swimming pools, adhesives, floor waxes, fabric softeners, slimicides, and in the production of chlorine.
Both blood and hair are used to detect mercury toxicity. In the study by Marsh et al. (1974), hair levels generally correlated directly with blood levels.
Absolute levels in the hair were about 300 times higher than in the blood. (Prasad 1976). Hair can also provide a chronological account of mercury excretion by measuring mercury content of different segments of a hair sample.
Mercury is well absorbed through the lungs, the gastrointestinal tract, and the skin. Methylmercury compounds vaporize easily and if inhaled in large amounts, can destroy lung tissue.
Organic complexing produces methylmercury compounds, which are more toxic, especially to the central nervous system. Only seven percent of ingested inorganic mercury is absorbed, but at least 95% of ingested methylmercury is absorbed. Zinc, cadmium, and manganese can enhance absorption of inorganic mercury.
Absorption of mercury through the skin has resulted in fatal poisoning.
Elemental mercury is oxidized upon ingestion to ionic mercury, most likely facilitated by catalase. Catalase is an iron-containing enzyme.
Most ingested mercury is then bound to metallothionein, a binding protein, or to a metallothionein-like plasma protein, and transported by the blood plasma.
The various mercury compounds can be converted one to another by intestinal bacteria and certain liver enzymes.
The main target organ for mercury is the kidney, although deposition in the brain is common. Ingestion of alcohol reduces blood and brain levels, but increases liver concentrations of mercury.
According to G. Kazantis, Mercury and the Kidney, Trans Soc. Occup. Med. 20:54, 1970, the kidney retains more mercury than any other organ in the body. However, in postmortem samples from mercury mine workers in Yugoslavia, the highest concentration of mercury was found in the thyroid and pituitary glands, suggesting that retention may be higher in these organs than in the kidneys.
Biliary excretion is the preferred route of excretion of mercury. Biliary excretion is enhanced by the chelating agent BAL (a compound developed as an antidote to mercury and arsenic poisoning). Some mercury is clearly reabsorbed in the intestinal tract; the exact proportion depends upon the form of mercury.
Mercury is also eliminated in saliva, through the pancreas, through intestinal wall secretion, and through nails and hair.
In acute mercury poisoning, excretion occurs at a rate of about one percent per day. However, our research indicates that sequestered mercury will remain in storage for years.
Cysteine (an amino acid) and selenium delayed or prevented toxicity when administered simultaneously with mercury in animals. However, neither caused greater excretion of mercury in feces nor urine.
Mercury compounds inhibit ATPase, an enzyme that breaks down ATP, inhibiting energy release in all cells.
Degeneration of nerve fibers occurs, particularly the peripheral sensory nerve fibers. Besides sensory nerve damage, motor conduction speed was reduced in persons with high hair mercury.
The most common sensory effects of mercury toxicity are paresthesia, or a tingling sensation, pain in limbs, and visual and auditory disturbances. Motor disturbances are exhibited by changes in gait, weakness, falling, slurred speech, and tremors. Other symptoms are headaches, rashes and various emotional disturbances.
Mercury has been shown to concentrate in the thyroid and pituitary glands, interfering with their function. Impairment of adrenal gland activity also occurs.
Impairment of adrenal gland activity due to mercury toxicity can cause fatigue, low blood sugar, and allergies.
Mercury toxicity causes impairment of copper metabolism, and is a common cause hair loss.
Loss of appetite may result from mercury-induced depletion of zinc in the brain.
Refers to a failure of muscular coordination. Mercury toxicity results in uncontrolled, slow movements that are a symptom of nervous system toxicity.
Studies reveal a higher incidence of cerebral palsy, mental retardation and neurological deficits including hyper-reflexia and delayed development.
Fetuses retain more mercury than adults. The placenta provides no barrier to mercury. Infants may actually act as a sink for this metal.
Skerfring, Hanson, and Lindsten (1970) found chromosome damage in humans exposed to mercury through consumption of mercury-poisoned fish.
An interesting effect of mercury toxicity is an exaggerated tendency to blush in embarrassment.
Depression may be due to mercury accumulation in the thyroid and pituitary glands causing a slowing of the metabolic rate.
Skin problems may be caused by a mercury-induced zinc depletion.
Discouragement has been repeatedly described in individuals suffering from mercury toxicity.
Damage to cranial nerve fibers can result in dizziness or vertigo.
Fatigue may be due to the effects of mercury toxicity on the adrenal, thyroid and pituitary glands, or interference with cellular energy production.
Mercury has an affinity for the acoustic nerve, eventually resulting in hearing loss.
Elevated hair levels of mercury were found in a study of emotionally disturbed children (Marlowe et al.).
Recent research indicates that mercury can have a detrimental effect upon immune system activity.
Neurological damage due to mercury can cause insomnia in certain individuals.
Mercury can cause sodium retention and other electrolyte imbalances, which contribute to impaired kidney function.
Mood swings and emotional instability are frequently associated with mercury toxicity.
Damage to nerve fibers can affect all mental functions including memory.
These may be due to the intimate association between mercury and copper toxicity. Copper toxicity is known to contribute to the causation of migraine headaches.
Hyper-irritability is a common manifestation of mercury toxicity. In addition, copper toxicity may be involved in the causation of mood swings.
Behavior changes and emotional difficulties are commonly ascribed with mercury poisoning.
Tingling or paresthesia is one of the early signs of mercury poisoning.
Peripheral nerve damage is an early sign of mercury toxicity and can cause pain in limbs.
Skin rashes and blushing are commonly associated with mercury poisoning.
Acute mercury toxicity is a frequent cause of excessive salivation.
Copper toxicity and zinc depletion related to mercury toxicity may contribute to symptoms of schizophrenia.
Mercury accumulation in the thyroid gland, detrimentally affects thyroid activity.
Mercury toxic individuals may avoid friends and public places and become despondent.
Tremors are usually the first symptom of mercury toxicity. The tremor usually begins in the face, then progresses to the hands. Later the tongue is affected, speech becomes slow and slurred and the gait becomes ataxic. The tremor is an intention tremor, meaning that the more one tries to control it, the worse it becomes.
Vision loss occurs due to damage to the optic nerve, not retinal damage.
Motor nerves are affected by mercury toxicity. The end result is muscle weakness.
Copper Toxicity Associated with Mercury Toxicity
Individuals who show high serum copper levels, tremor of the hands, ataxia, and intermittent schizophrenic symptoms with wide mood swings should be studied as possible victims of mercury poisoning.
Mercury appears to inhibit copper absorption from the intestine. However, we find that those individuals with mercury toxicity often later display copper toxicity as well.
Zinc depletion of the brain is associated with mercury toxicity.
Mercury protects against selenium toxicity by binding with selenium.
Selenium protects against methylmercury intoxication and other forms of mercury. It appears selenium in tuna fish protects against mercury toxicity. Mercury-selenium complexes are formed.
"To summarize, heavy metal intoxication of the brain can cause hyperactivity in animals and presumably in some children. This hyperactivity in rats may be accompanied by a displacement of a sedative metal, such as zinc, from the brain. We know that zinc will antagonize mercury toxicity."
"It appears that metallothionein, induced by giving zinc, complexes with mercury." (Bremmer, 1976)
Detoxification of mercury, as with the other toxic metals, is accomplished most effectively, in our experience, by a combination of increasing overall energy levels, enhancing activity of the eliminative organs and the administration of mercury antagonists and chelating agents.
A tissue mineral analysis is of value in designing nutritional programs which balance the tissue electrolytes and enhance the energy pathways. By so doing, increased biochemical energy is made available to facilitate excretion of mercury from tissue reservoirs.
Several methods are used for congenital hemochromatosis. Phlebotomy, or bleeding, is still used. Desferroxamine-B is a chelating agent that is occasionally used to enhance urinary excretion of iron.
For acquired iron toxicity, we have devised a very effective nutritional protocol using a combination of approaches. All the following measures should be done together for optimum results:
Mercury is excreted primarily through the liver and kidneys. Herbs and nutrients which enhance liver activity may be helpful, including sulfur, inositol, choline, methionine, copper and other nutrients.
Kidney activity may be enhanced by the administration of kidney glandular substance and synergetic factors.
Vitamin C binds heavy metals such as copper, lead, cadmium, and mercury, and facilitates their excretion by the kidneys.
Selenium, if given during mercury exposure, can delay or prevent mercury toxicity symptoms. However, studies vary with species and the type of mercury compound used. Selenium tended to decrease kidney mercury, but increased mercury deposition in the liver and brain. Selenium administered after mercury exposure probably cannot increase elimination of mercury.