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• The chronic effects of cumulative, low-dose mercury exposure are under-recognized by both mainstream and alternative health authorities and consequently by the public. Mercury can cause or contribute to most chronic illnesses, including neurological disorders, cardiovascular disease, metabolic syndrome, chronic fatigue, fibromyalgia, adrenal and thyroid problems, autoimmunity, digestive disorders, allergies, chemical sensitivities, mental illness, sleep disorders and chronic infections such as Lyme and Candida. Mercury toxicity should be suspected in individuals experiencing multiple health problems.
• Diagnosis of chronic mercury toxicity is often difficult because the body’s natural defenses may mask or delay symptoms. Natural defenses are a function of genetic susceptibility, epigenetic factors, micronutrient status and allostatic load (cumulative wear and tear on the body). Furthermore, individuals who retain mercury may counterintuitively show low levels in blood, urine and hair.
• The developmental window from conception through early childhood is one of extreme vulnerability to mercury. Mercury is an epigenetic toxicant (affecting future gene expression) as well as a neurotoxicant. Damage may be permanent; therefore, prevention is key.
• For most people, mercury is the most significant toxicant in the body. By promoting oxidative stress and depleting antioxidant defenses including the glutathione system, mercury impairs the body’s response to toxicants in general—including to mercury itself.
• Mercury toxicity creates a need for extra nutrition, both to repair damage and to provide ample enzyme co-factors, which can push blocked enzymes. Carbohydrate intolerance can be a symptom of mercury toxicity, and fat can be a preferred fuel. Many people with chronic mercury toxicity have found a nutrient-dense diet to be a useful starting point for symptom relief. Individualized supplementation may also be helpful to overcome the extreme nutritional depletion and unnatural toxic state.
Mercury is an unusually insidious toxicant that can cause or contribute to most chronic illnesses. Its effects on various body systems can be mutually reinforcing, setting up a complex process of damage and dysfunction. For example, by inhibiting the glutathione system, which is key to detoxification, mercury perpetuates a vicious cycle of susceptibility and toxicity. As a result, mercury promotes nutritional depletion, oxidative stress, hormonal disruption, immune alteration and neurotransmitter disturbances. These in turn can cause poor digestion, leaky gut, food allergies, altered gut flora and autoimmunity.
Despite its pervasive ability to damage the body, mercury easily eludes detection, and many affected individuals have no idea that their unexplained health problems are due to past or ongoing mercury exposures. Adding to the confusion, symptoms may manifest differently depending on an individual’s exposures, lifestyle, genetics and micronutrient status. In one person, mercury toxicity might show up in the form of an autoimmune issue (such as Hashimoto’s thyroiditis, multiple sclerosis or systemic lupus erythematosus), while someone else might experience mood, behavior, learning or psychiatric problems. Moreover, potentially long latencies mean that onset of symptoms sometimes occurs months or years after cessation of the exposure.1,2
Many symptoms of mercury toxicity are vague, resembling premature cellular aging. On the other hand, some symptoms are more distinct, a case in point being erethism. The term erethism (or reddening), which derives from a person’s tendency to blush,3 covers a constellation of personality traits including timidity, diffidence, contentiousness, insecurity, bluntness, rigidity, excitability and hypersensitivity to criticism and to sensory stimulation.4-6 Considering mercury’s subtle but reproducible effects on emotions, it is likely that a number of problems blamed on character, personality or stress may in fact be caused or compounded by low-level mercury toxicity.
WIDESPREAD EXPOSURE AND TOXICITY
Health authorities are unlikely to provide useful guidance on mercury risks, for several reasons. First, mercury is both technically and politically difficult to study; thus, scientific conclusions about some risks remain couched in uncertainty. Second, mercury’s effects are non-specific and multifactorial. Finally, much exposure is iatrogenic—caused by health care providers or institutions—making it an unpopular topic. Thus, the public may receive mixed messages from health authorities and agencies about the risks of routine mercury exposures, depending on whether the exposure involves dentistry, seafood consumption or vaccines.
For most people, the major sources of mercury exposure (Table 1) are elemental mercury vapor from dental amalgams and methylmercury (an organic mercury compound) from dietary fish. Ethylmercury (another organic mercury compound) in certain thimerosal-containing vaccines provides smaller amounts, but these can be highly toxic during the vulnerable windows of gestation and early childhood.
All three forms of mercury are easily absorbed and readily distributed throughout the body. Being lipophilic (having an affinity for lipids), they leave the bloodstream quickly, passing through biological membranes and concentrating in cells, including brain cells.7 Mercury is especially drawn to high-sulfur organelles (specialized cell structures) such as mitochondria. Once inside a cell, mercury (chemical symbol Hg) is soon oxidized to Hg2+, which, as a hydrophilic (water-loving) and lipophobic form of mercury, cannot easily pass through biological membranes. This form of mercury thus becomes trapped inside the cells and causes ongoing damage.7 Mercury has a particular affinity for the brain, where it may be retained indefinitely.7,8 It also accumulates in epithelial tissues, organs and glands, such as the salivary glands, thyroid, liver, pancreas, testicles, prostate, sweat glands and kidneys, and the epithelium of the intestinal tract and skin.7
According to the Environmental Protection Agency (EPA), 2-7 percent of women of childbearing age in the U.S. have blood mercury levels of concern.9 There is reason to believe that regulatory levels of concern are too lax. A 2012 study showed blunted cortisol response and higher inflammatory markers at blood mercury levels well below the EPA’s established level for potential health risks (5.8 micrograms per liter).10 In addition, four neurodevelopmental disorders (attention-deficit/hyperactivity disorder, autism, seizures and stutter) affect almost 11 percent of all U.S. births, up 30 percent over the past decade.11 Subclinical decrements in brain function are even more common, affecting up to 15 percent of births.12
Mercury’s toxicity may be amplified by exposure to other toxic metals, including lead, cadmium and aluminum. Mercury and lead, in particular, are highly synergistic. In fact, in one study, a dose of mercury sufficient to kill 1 percent of lab rats (lethal dose “LD01”), when combined with a dose of lead sufficient to kill 1 percent, killed 100 percent of the rats.13 A similar test involving mercury and aluminum in cultured neurons killed 60 percent of the cells when the two low-dose toxicants (LD01) were combined.14 Even antibiotics have been shown to enhance the uptake, retention and toxicity of mercury.14 Additionally, testosterone appears to aggravate mercury toxicity during development, while estrogen protects against it.15 This may explain why more boys than girls are diagnosed with autism spectrum disorders and attention deficit disorders.
DENTAL AMALGAM FILLINGS
Dental amalgam, the material used in “silver” fillings beginning in the nineteenth century, is about 50 percent mercury. Health and dental authorities deemed amalgam safe based on studies that were designed to detect obvious harm but did not investigate subtle or long-term effects. Consequently, a loose scientific consensus has long discounted the idea of mercury toxicity from dental amalgams, pointing to population studies showing that people with high exposures and even people with a high body burden do not necessarily have toxicity symptoms. Those who blame amalgams for their illnesses have been viewed askance.
Mercury is highly volatile, however, and amalgams continuously off-gas in the mouth. Evidence indicates that exposure from amalgams is sufficient to cause harm to susceptible people.15 The authors of the mercury chapter in the most recent metals toxicology textbook estimate that roughly 1 percent of the population is incurring clinical illness from their dental amalgams.7 This calculation is likely to be a gross underestimate because it excludes other diagnoses that may have a mercury component, such as multiple sclerosis. The World Health Organization (WHO) estimates that the typical absorbed dose of mercury from amalgams is one to twenty-two micrograms per day, with most values in the range of one to five micrograms per day.16 Various factors, including gum chewing and bruxism, can increase these exposures to an upper range of about one hundred micrograms per day.7 Preliminary evidence also suggests that certain types of electromagnetic radiation, including EMR from mobile phones and from magnetic resonance imaging (MRI) may increase the release of mercury vapor from dental amalgams.17
Within the past ten years, human studies have documented over a dozen common genetic variants that convey increased susceptibility to mercury,1,18 indicating the fact that genes drive susceptibility (and resistance) to mercury toxicity.19 Hundreds more are likely to exist, because mercury attacks sulfur in proteins and the body has tens of thousands of genetically determined sulfur-containing proteins, many of which are likely to include variants that contribute to susceptibility.7 Candidate genes are involved not only in methylation and detoxification, but in vitamin and mineral (i.e., enzyme cofactor) absorption, transport and metabolism. Unfortunately, policy makers, health authorities and the dental industry have yet to consider the issue of genetic susceptibility. Indeed, for millions of children and adults covered by subsidized dental programs (including military family dental care and Native American services), amalgam is still virtually the only option for dental restorations.
In 2009, despite much scientific evidence to the contrary, the U.S. Food and Drug Administration (FDA) reiterated the safety of dental amalgam. As of 2016, public interest groups are challenging this “final amalgam rule” in federal court. Issues to be litigated include whether amalgam is deemed an implant, which would require manufacturers to provide proof of safety, and whether the toxicity warnings that are given to dentists via labeling requirements should also be given to patients. Norway, Denmark and Sweden have banned dental amalgam, and as of May 2015, a scientific committee of the European Commission recommends that non-mercury alternatives be used in fillings for pregnant women and children.20
In fact, fetal neurons are more sensitive to the toxic effects of mercury than any other cell type.7 Mercury from the mother’s body readily crosses the placenta and accumulates in the fetus, as revealed in postmortem human and animal studies.7 In tissue culture, clear effects on nerve growth arise at mercury concentrations equivalent to those found in newborns of amalgam-bearing mothers with no other known exposures.7 Furthermore, mercury levels in amniotic fluid, cord blood, placental tissue and breast milk are significantly associated in a dose-dependent manner with the number of maternal dental amalgam fillings.7,21 Human and animal studies show increased rates of miscarriage, neonatal death, low birth weight and developmental disorders associated with mercury exposure.7
As if the cumulative effects of ongoing amalgam exposure were not enough, unsafe amalgam removal also can cause acute exposures to mercury vapor. Thus, patients wishing to replace amalgam fillings with less toxic alternatives must evaluate dentists’ use of adequate protective measures. The International Academy of Oral Medicine and Toxicology (IAOMT), a professional dental organization, has developed a protocol and training program that attempts to minimize the exposure to mercury vapor to the patient, dentist and staff during amalgam removal. In women of childbearing age, removal of amalgam should be timed so as to avoid the twelve to eighteen months preceding conception as well as pregnancy and breastfeeding.
Natural releases of mercury from the Earth’s crust and the oceans account for 60 to 70 percent of the annual releases of mercury to the atmosphere. The remaining 30 to 40 percent is attributable to human activities.7 Once released into the atmosphere through either natural or human activities, mercury is deposited in soil and water, where it enters the food chain. Mercury accumulates in fish, particularly large, long-lived ocean fish.
Mercury levels in fish vary widely by species and by individual, ranging from less than 0.1 part per million (ppm) for salmon and sardines to more than 1 ppm for some samples of tilefish, shark, swordfish and king mackerel. A typical 3.5-ounce (one-hundred-gram) serving of fish could contain anywhere from a few to more than one hundred micrograms of mercury. Tuna contains moderate levels, which vary by species. The FDA sets an action level for mercury contamination in commercial fish of 1 ppm. This means that federal officials are allowed to confiscate products that exceed this threshold—but it does not mean that they actually do so.
Due to natural releases of mercury, humans have always encountered some mercury in certain fish. As long as the body’s natural defense systems are working, one can consume mercury-containing fish in moderation. In healthy individuals, intestinal metallothioneins (a class of metal-storage molecules that can be cumulatively damaged by mercury) can sequester ingested mercury and slowly allow its excretion. Selenium, discussed below, also offers some protection against mercury and is found in fish as well as other foods.
One of the most controversial aspects surrounding vaccines is their mercury content. Prior to about 2004, many childhood vaccines contained thimerosal, a preservative and adjuvant that is 50 percent ethylmercury. Childhood exposure to thimerosal rose sharply in the U.S. during the 1990s as the U.S. Centers for Disease Control and Prevention (CDC) added new vaccines to the childhood vaccine schedule. Infants strictly adhering to the CDC vaccine schedule during this time typically received up to 187.5 micrograms of mercury in the first six months of life alone.22 As shown in Table 2, this was from three doses each of the diphtheria-tetanus-acellular pertussis (DTaP), Haemophilus influenzae type b (Hib), and hepatitis B (HB) vaccines, with additional doses of DTaP and Hib given later.23
No regulatory safety standard exists for ethylmercury. However, because ethylmercury is chemically similar to methylmercury (the form of mercury present in dietary fish), we can compare the 187.5-microgram ethylmercury dose to the safe reference dose for methylmercury set by the EPA. This reference dose is 0.1 microgram per kilogram of body weight per day for chronic exposure, equivalent to about 0.3 micrograms per day for a newborn and 0.6 micrograms per day for a six-month-old baby. Averaging the 187.5-microgram exposure (actually delivered in a number of concentrated doses) over the six-month period, the resulting dose of 1.04 micrograms per day is significantly higher than the EPA’s “safe” reference dose of 0.3–0.6 micrograms total per day for methylmercury exposure in infants. Moreover, the EPA safe reference dose for methylmercury may be too lax,24,25 especially when applied to ethylmercury. Indeed, there may be no threshold that precludes adverse neuropsychological effects in children,24,26 whose brains are rapidly developing. Furthermore, unlike methylmercury ingested from fish, injected ethylmercury is not subject to the natural defense mechanisms related to ingestion, including metallothioneins and selenium.
In 1999, the U.S. Public Health Service called for the elimination of thimerosal from childhood vaccines. Due to supply and demand issues, it took several years to transition to reduced-thimerosal and then thimerosal-free alternatives.22 However, during the period in which thimerosal began to be phased out of other pediatric vaccines, the thimerosal-containing influenza vaccine became an important new source of mercury exposure for fetuses and children. This is because the CDC began recommending in 2002 that the influenza vaccine be given to children aged six months to twenty-three months, as well as pregnant women in their second and third trimesters, even though the only vaccine approved for these groups at the time was preserved with thimerosal. 22 Next, the CDC aggressively increased the dosing and expanded the target groups for the influenza vaccine, recommending a double dose for infants at both six and seven months, plus subsequent annual doses, and a dose for all pregnant women, no longer limited to the second and third trimesters.22 As of 2013, more than half of influenza vaccines were still preserved with thimerosal,22 with the availability of non-thimerosal versions subject to supply-and-demand dynamics. A thimerosal-free flu vaccine shortage during the 2015 flu season led California’s governor to sign an exception allowing thimerosal-containing vaccines to be administered to infants and children despite a previous statewide restriction.
Like the multidose influenza vaccines, some multidose meningococcal meningitis vaccines and tetanus toxoid (booster) vaccines (not recommended for children under six years of age) also contain thimerosal as a preservative, in amounts ranging from 12.5 to 25 micrograms per dose.27,28 As of 2016, some other childhood vaccine preparations, such as the multidose DTaP and the DTaP/Hib combination vaccines, still utilize thimerosal in the manufacturing process. In these vaccines, most of the thimerosal is then filtered out, leaving “trace amounts” of thimerosal, according to the CDC.29 The end result, according to thimerosal researchers, is that “the approximate maximum lifetime exposure to [mercury] from Thimerosal-preserved vaccines…is now more than double what it would have been had the pre-2000 vaccination schedule been maintained.”22
A few isolated court cases in the U.S. and elsewhere have recognized post facto that a limited number of well-documented genetic susceptibilities to vaccine injury—including some mitochondrial disorders—have caused certain children to suffer permanent neurological damage. Genetic susceptibilities occur along a continuum, but the growing movement to mandate vaccines has so far failed to recognize this complex reality.
OTHER EXPOSURES TO MERCURY
A number of other products have exposed consumers to mercury over time. Until the 1960s, teething powders for babies contained mercury in the form of calomel, and broken mercury thermometers were a common exposure risk in many countries up to the early 2000s. Contact lens solutions contained thimerosal, and the once widely used antiseptic called Mercurochrome contained the mercury-bromine compound merbromin.
In 1998, the FDA banned mercury as an active ingredient in over-the-counter products, declaring that it was not “generally recognized as safe” (GRAS). Nevertheless, the FDA continues to allow use of mercury as an inactive ingredient, provided its content is under sixty-five parts per million. In the cosmetics realm, FDA regulations regarding cosmetics do not require labeling disclosure of ingredients that make up less than 1 percent of the product. As a result, some brands of mascara still contain thimerosal as an antimicrobial and preservative.
Compact fluorescent lamps (CFLs) typically contain about four milligrams (four thousand micrograms) of mercury, some of which is released upon breakage in the form of mercury vapor. Table 3 compares the concentration of this toxic release to various regulatory safety standards. CFL proponents argue that the energy savings offered by CFLs, which include reduced mercury emissions from coal-fired power plants, make them desirable (a debate that is beyond the scope of this article).
Finally, significant sources of local exposure to mercury may include incinerators, coal-fired power plants, crematoria and other industrial processes. For over a decade, the EPA has attempted to restrict mercury emissions from U.S. coal plants by about 90 percent, but the rule is under litigation, and legal experts predict that enforcement is years away. In some countries, gold mining techniques that employ mercury remain a significant source of exposure for miners and local populations. U.S. miners used these techniques during the Gold Rush.
DEVELOPMENTAL AND EPIGENETIC TOXICITY
The developmental period from conception through early childhood is a window of vulnerability in which both epigenetic and neurological damage can occur at exposures far lower than those known to cause toxicity in adults. Epigenetics refers to the alteration of gene expression (turning genes on and off)—usually via environmental factors—without alteration of the DNA nucleotide sequence itself, in a manner that can be passed to offspring.
Mercury is a potent epigenetic toxicant of alarming scope, with both direct and indirect effects on gene expression. Mercury directly targets the cysteine that comprises the DNA-binding sites on most gene transcription factors. In addition, it targets the cysteine in DNA methyltransferase enzymes, which play a role (DNA methylation) in normal gene expression. Indirectly, mercury promotes severe oxidative stress. Early-life stressors are known to induce changes in gene expression that set the stage
for disease in later life.30 Thus, unfortunately, exposure to mercury in either parent, even prior to conception, can affect the child’s own genetic expression.
Epigenetic damage may range from mild to severe, and the resulting phenotype may include characteristics such as dental deformities, myopia, asymmetries of the face and disproportions of the body. Such characteristics are described in Weston A. Price’s pioneering Nutrition and Physical Degeneration,31 whose ideas Chris Masterjohn subsequently developed in his research on fat-soluble vitamins; in Sally Fallon Morell’s and Thomas Cowan’s Nourishing Traditions Book of Baby and Child Care;32 and in the more epigenetically focused Deep Nutrition by Catherine and Luke Shanahan.33
MERCURY AS ANTINUTRIENT
Mercury readily binds to sulfhydryl, a type of sulfur also called a thiol. The thiol is the major reactive site within the amino acid, cysteine, which is ubiquitous in biochemically active proteins such as enzymes. The human body contains tens of thousands of enzymes, which drive most fundamental biological processes.
Mercury also binds strongly to selenium, a cofactor for several dozen enzymes involved in vital tasks such as thyroid function and brain antioxidant protection. Although said to protect against mercury toxicity, selenium’s protective scope is limited by its intracellular availability. This is governed by kidney processes that limit the amount of such minerals in the bloodstream and by specialized channels within the cell membrane that control mineral transport from the bloodstream into cells. Lipophilic mercury, on the other hand, has no such limits when entering cells. Moreover, mercury can block selenoprotein P, a substance that stores and transports selenium to cells.34 Therefore, selenium offers only limited protection against mercury exposure.
The body’s most important intracellular antioxidant mechanism is the glutathione system. Glutathione detoxifies mercury by binding it (in a process called glutathione conjugation) into a less toxic form suitable for excretion through the bile. The glutathione system has been found to be crucial in the detoxification of thimerosal.35 However, because the glutathione molecule and its related enzymes employ cysteine, they also are targets for mercury. Mercury can damage the body’s glutathione system both by depleting the glutathione molecule itself and by blocking the enzymes that synthesize and recycle glutathione and facilitate its use. By depleting glutathione and disabling the glutathione-related enzymes, mercury impairs the detoxification of many toxicants, ironically including mercury itself, thereby leading to increased toxicity.
By damaging methylation enzymes, including methionine synthase, mercury dysregulates the methylation cycle, a biochemical pathway in which the sulfur-containing amino acid, methionine, is recycled, creating two important products: s-adenosyl methionine (SAMe), the body’s universal methylator; and cysteine, the precursor for the transsulfuration pathway, which in turn produces glutathione, sulfate and taurine. By impairing the methionine synthase enzyme, mercury blocks not only detoxification via the transsulfuration pathway that produces glutathione but also the production of many hormones and neurotransmitters that require methyl donors like SAMe. A lack of methyl donors also inhibits the activity of the DNA methyltransferase enzymes, which regulate gene expression.
In addition to attacking the sulfur in enzymes, mercury attacks the sulfur in the functional proteins within cell membranes. These include membrane transport channels that allow micronutrients into cells. One result is altered homeostasis of many essential minerals, which can appear abnormally high or low on testing and is an aspect of many chronic illnesses that has no other obvious explanation. Mercury also may target the disulfide bonds in collagen, the connective tissue found in blood vessels, in the gut and throughout the body. More importantly, mercury impairs the ongoing synthesis and repair of collagen, bone and cartilage, both by impairing the necessary enzymes and by depleting vitamin C, which is a required cofactor. Thus, mercury can be implicated in arthritis, osteoporosis and connective tissue disorders.
Mercury promotes oxidative stress in several mutually reinforcing ways. Within cells, mercury concentrates in mitochondria, the organelles that synthesize ATP (adenosine triphosphate) energy. There, mercury displaces iron and copper, converting them to free radicals with the potential to cause ongoing oxidative stress unless buffered by antioxidants. Mercury also blocks mitochondrial enzymes, creating an overproduction of reactive oxygen species, including free radicals. The resulting oxidative stress further damages mitochondrial enzymes, as well as harming mitochondrial membranes and mitochondrial DNA.
Mitochondrial dysfunction can result in overproduction of lactic acid, yielding metabolic acidosis, which depletes minerals and may promote certain pathogens. Mitochondrial damage further drains cellular energy by creating a disproportionate need for repair, perpetuating a vicious cycle.21 Mitochondrial dysfunction can affect immunity, digestion, cognition and any energy-intensive system within the body and is a key component of many chronic illnesses.
Oxidative stress perpetuates another vicious cycle in which free radicals cause lipid peroxidation. In this self-propagating chain reaction, the unsaturated fatty acids in cell membranes are attacked, becoming free radicals themselves and ultimately leading to excess permeability in membranes and other barriers and provoking still more damage.
As already mentioned, metallothioneins are cysteine-rich metal storage molecules that appear to play a role in storing zinc and copper. They are found in high levels in the intestines. When metallothioneins become saturated with mercury, they can no longer store zinc or copper or protect the body from mercury.
It is much more common for mercury-affected people to suffer from low zinc than from low copper, for several reasons. First, dietary sources of zinc are more limited than for copper. Second, excess copper is excreted into the bile and removed from the body via the feces, but many people have sluggish bile flow and/or constipation, causing copper to accumulate in the liver. Additionally, estrogen dominance, which may be amplified in mercury-affected individuals due to common hormonal imbalances, causes copper retention. Estrogen dominance is common, especially in women, due to exposure to plastics, soy, flax and other estrogenic foods, as well as hormonal birth control products. Finally, copper pipes, copper IUDs and copper sulfate sprayed on crops as an antifungal (even on many organic crops) add to the overall copper load. Because copper and zinc are antagonistic, the more that copper is retained by the body, the more that zinc tends to be depleted.
Mercury induces anomalies in the transport of essential minerals such as magnesium and zinc that cause an extra need for these minerals in the diet. Furthermore, many health conditions caused by mercury toxicity are aggravated by low magnesium and/or zinc, including cardiovascular disease, fibromyalgia, autism spectrum disorder (ASD), attention deficit disorders and depression. Not every person with a history of mercury exposure is deficient in all of these nutrients, however, and it is important to note that minerals have complex synergistic and antagonistic relationships. As we have just seen, low zinc is often accompanied by high copper, and low magnesium is often accompanied by high calcium in soft tissues.
Health authorities persist in citing a subset of studies that have failed to find a causal link between ASD and mercury,36 and the association remains a taboo subject in mainstream medicine and the media. Nonetheless, many other studies suggest a connection, and such a link is widely viewed as biologically plausible.7 Autism is documented to involve oxidative stress, mitochondrial dysfunction, immune or inflammatory processes, impaired sensory processing and abnormal mineral homeostasis, all of which are consistent with mercury toxicity.37 Autistic children have been found to have significantly higher exposure to mercury during fetal development and early infancy, as measured by metals in baby teeth.38 Individuals with ASD also are frequently deficient in zinc.39 Other commonly observed mineral imbalances in ASD include low calcium, iron, magnesium, manganese and selenium, as well as high copper and elevated toxic metals, although these can sometimes be difficult to detect through testing, as described later.
Attention deficit disorder (ADD) and attention-deficit/hyperactivity disorder (ADHD) are common early findings in mercury-exposed children.18 Zinc deficiency has been identified as a biomarker for ADHD,39 and the abnormal mineral profile for ADHD appears quite similar to that for autism and mood disorders, with the exception that ADHD typically includes iron overload. Additionally, copper dysregulation is a key factor in ADHD.40 Many studies likewise report a close association between zinc deficiency and clinical depression, with severity of symptoms inversely correlated with serum zinc levels. Decreased levels of zinc, calcium, iron and selenium have been reported as risk factors for postpartum depression.39
Other neurological and psychiatric disorders associated with mercury include narcolepsy, obsessive-compulsive disorder, schizophrenia, bipolar disorder, Tourette syndrome and borderline personality disorder, as well as neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and multiple sclerosis. Each has been documented to involve oxidative stress, inflammation, mitochondrial dysfunction and mineral imbalances, all of which can be attributed to mercury. These diseases are complex, such that human studies are unlikely to find a direct causal link with any one risk factor that is strong enough to satisfy skeptics, but a growing body of evidence suggests that mercury plays a major role.41
Exacerbating the mineral dysregulation associated with these many conditions are the neurotransmitter imbalances provoked by mercury. For example, mercury increases extracellular levels of the excitatory neurotransmitter glutamate, thus overactivating glutamate receptors on cell surfaces.42 The amplification of glutamate is further exacerbated by mercury’s inhibition of the calming neurotransmitter GABA.37 Mercury blocks GABA receptors, disproportionately destroys GABA-producing Purkinje neurons and impairs glutamate decarboxylase (GAD), the enzyme responsible for converting glutamate to GABA. Furthermore, mercury’s dysregulation of glutamate and GABA is associated with depression and suicide.21,43,44
ALTERED MICROBIOTA, DIGESTIVE DYSFUNCTION AND IMMUNE HEALTH
Mercury is known to alter the intestinal microbiota, yielding increased levels of undesirable mercury-resistant bacterial species, which may also develop resistance to antibiotics.37,45,46 For example, the opportunistic yeast, Candida albicans, may overgrow, causing a host of unpleasant symptoms. This dysbiosis may be exacerbated by mercury’s dysregulation of the immune system as well as its promotion of metabolic acidosis. All of this has negative implications for digestion, immunity and mental health.47-49
Mercury also inhibits several enzymes affecting digestion, including gastric hydrogen-potassium-ATPase, the enzyme that allows the synthesis of hydrochloric acid via the stomach’s proton pump. In addition, by promoting oxidative stress, mercury moves the autonomic nervous system into sympathetic (stress) mode, inhibiting digestion. Furthermore, the mitochondrial dysfunction from which many mercury-affected individuals suffer impairs digestion as well as other bodily functions. By damaging both the gut and the blood-brain barrier, mercury leads to leaky gut, which in turn leads to food allergies and brain disorders caused by maldigested proteins entering the bloodstream. As a fairly common case in point, partially digested proteins in foods containing gluten and casein may be metabolized into the opioid peptides, gluteomorphin and casomorphin.50 This is often seen in children with ASD and explains many parental reports of symptom relief on a gluten-free, casein-free diet.
Mercury’s effects on the gut can exacerbate its effects on the immune system. Mercury is known to cause allergies, reduced immunity and autoimmunity,51 and such immune dysfunction plays a role in many chronic illnesses. Reduced immunity yields susceptibility to chronic infections such as Lyme and Candida. Finally, although technically not an allergy, multiple chemical sensitivities can result from mercury overloading the body’s detoxification system and blocking metabolic enzymes in the live and other tissues, such that common but undesirable chemicals such as fragrances are metabolized incompletely, yielding toxic intermediates.
THYROID, HPA AND STRESS-RELATED DISORDERS
Mercury concentrates in glands, including the thyroid and pituitary glands, and impairs the hypothalamus-pituitary-adrenal (HPA) axis. HPA function and thyroid function are tightly interrelated, with impairment of one system often causing impairment of the other. Mercury blocks the selenium-dependent enzyme that converts the thyroid hormone thyroxine (T4) to its active form, triiodothyronine (T3). Unfortunately, despite symptoms, the resulting hypothyroidism often goes undetected by routine blood work, which typically only tests levels of thyroid-stimulating hormone (TSH), the hormone secreted by the pituitary to signal the thyroid gland to produce T4. Further suppressing thyroid function is the mercury-induced depletion of selenium and zinc, which are co-factors for thyroid enzymes.
The oxidative stress caused by mercury is a type of chronic stress that depletes the HPA axis. Thus, mercury is implicated in the cluster of symptoms referred to as adrenal fatigue. An evolving view suggests that adrenal fatigue is not a glandular problem, but rather a brain-stress problem.52 Early-life exposure to mercury also causes epigenetic damage to the HPA axis, which can dysregulate the stress response throughout life. This may involve a tendency toward either high or low baseline cortisol as well as a loss of the dynamic cortisol response to stress.53 The latter yields a disabling feeling of unwellness and stress intolerance. High baseline cortisol, on the other hand, may feel less debilitating, but this is a catabolic state that can promote degeneration of otherwise healthy tissues.
METABOLIC DISORDERS, OBESITY AND CARDIOVASCULAR DISEASE
HPA dysregulation and thyroid dysfunction have a strong impact on metabolism and weight. As an epigenetic toxicant, mercury can cause a host of metabolic issues, including blood sugar problems, insulin resistance and stress intolerance. These symptoms can persist throughout life and into future generations. In addition, mercury impairs many enzymes needed to metabolize food into energy, including pyruvate dehydrogenase, which is required for metabolism of carbohydrates but not fats or proteins. Hypoglycemic symptoms, which are common in mercury toxicity, may not reflect true low blood sugar but may indicate impaired enzymes within the brain and/or HPA axis. Other enzymes impaired by mercury include those of the citric acid cycle and the electron transport chain, leading to low ATP energy. Mercury also blocks the insulin receptor, promoting high insulin and thus fat storage. Mercury can cause weight gain or weight loss, depending on whether metabolic dysregulation or gut dysfunction predominates.
Regarding mercury’s role in cardiovascular disease, mercury oxidizes blood vessels as well as cholesterol, leading to arterial plaque. Mercury promotes thrombosis and endothelial dysfunction in blood vessels.54 Mercury can cause high or low blood pressure depending on whether artery calcification or artery deterioration and HPA dysfunction predominate. In a remarkable example of how mercury accumulates in certain tissues, a biopsy study of thirteen patients with a type of heart failure found that mercury levels in the myocardium were twenty-two thousand times higher than normal.55
The alternative health community recognizes the role of micronutrients in promoting physical and mental health as well as optimal child development. Less well recognized is the role of toxicity in depleting one’s micronutrient status and the analogous role of micronutrient status in exacerbating or alleviating toxicities.
Mercury damage creates a need for extra nutrition, both to repair damage and to prod blocked enzymes. Nutrient-dense diets are of critical importance, and targeted supplementation may help to overcome the unnatural toxic state. Because everyone’s nutrient status is uniquely affected by mercury, it is wise to take an individual approach rather than supplement all potentially depleted nutrients across the board. In addition, it is common for people with mercury toxicity to have multiple food sensitivities, particularly to gluten, casein and soy. Dietary modifications are sometimes necessary to control the inflammation and other symptoms that result from these food sensitivities. Persisting in eating foods to which we are allergic or intolerant impairs detoxification by placing undue stress on the organs of digestion and elimination, putting the HPA axis on alert and increasing the level of inflammation in the body.
High-quality fat is a preferred fuel in mercury toxicity, supplying much-needed fat soluble vitamins and helping to stabilize blood sugar levels. It is important to eat a variety of healthy fats from both animal and plant sources. Because both brain tissue and the phospholipid bilayer of the cell membrane are built in large part from saturated fat, consumption of grassfed animal fats such as lard, tallow, ghee and butter contributes to repair. Cod liver oil, liver, extra-virgin organic olive oil, red palm oil and lard are important sources of fat-soluble vitamins.
Fat metabolism requires fewer enzymes than carbohydrate metabolism and thus has less opportunity to be blocked by mercury. Impaired enzymes slow energy production and can create toxic intermediates, which can yield food intolerances to some carbohydrate foods. Carbohydrates also can raise insulin, the fat-storage hormone, which may already be high due to mercury toxicity. Finally, high-carbohydrate foods are more likely than high-fat foods to contain antinutrients such as phytates, oxalates and lectins.
Bone broth is ideal for repairing the digestive lining and connective tissue and for supplying easily assimilated amino acids and other nutrients. Daily consumption of bone broth can help repair the excessive gut permeability that often leads mercury-toxic individuals to develop food allergies and autoimmunity. Glutamine is one of the most important amino acids needed to repair the lining of the gut. Glutamine and glycine, both abundant in bone broth, are precursors to the body’s production of glutathione. Vitamin B6 and magnesium may ease the conversion of glutamate to GABA.56 In the event of sensitivity to glutamate, it is advisable to simmer the bone broth for no longer than three to four hours.
Beet kvass can improve the flow of bile and thus improve excretion of mercury and other toxicants through the bile, particularly in individuals who tend to be constipated. Other probiotic foods such as sauerkraut are also helpful as part of a healing program. It is a good idea to start with a small amount of probiotic foods and to increase gradually as tolerated.
Foods high in vitamins A, C, D and E confer important antioxidant and immune-modulating benefits. Vitamin C, for example, helps rebuild damaged collagen and can be obtained from a variety of food sources as tolerated, although one should take care not to rely entirely on the sweeter fruits, which can be problematic for people with blood sugar issues. Good sources of vitamin C include rose hips, guava, acerola cherry, lemons, limes, oranges, grapefruit, kale, broccoli, cauliflower, Brussels sprouts, papaya, mango, pineapple, kiwi and strawberries. People who suffer from thiol sensitivity, discussed below, will need to avoid or limit the vegetables included on the list (see “Sulphur foods” in Resources sidebar below). Bearing in mind that the liver has two detoxification pathways—phase I (breaking down substances) and phase II (building new substances)—it may be wise to consume grapefruit only occasionally. This is because grapefruit can stimulate phase II and slow down phase I. (The exception is if phase I is already known to be overly active with respect to phase II.)
Mineral dysregulation is significantly more pronounced in people with chronic mercury toxicity than in the general population,57 as are other nutritional deficiencies and food intolerances. Each mercury-toxic person has a unique combination of mineral imbalances that affect how mercury toxicity is expressed and point to the particular nutrient combination that is likely to provide relief. In general, the two minerals most commonly depleted by mercury are magnesium and zinc. Organ meats are nutrient-dense and can help supply these depleted minerals as well as important vitamins. For example, liver is high in vitamins A and B12 as well as zinc, magnesium and selenium. Leafy green vegetables, nettles, properly soaked lentils (if tolerated) and properly prepared almonds also are good sources of magnesium. Nettles are a great source of numerous other vitamins and minerals and can be added to soups or enjoyed as a tea. Zinc-rich foods are critical, but unfortunately oysters, the richest source of zinc, also tend to be high in cadmium and other heavy metals. Thus, red meat and poultry, along with properly soaked sesame and pumpkin seeds and pine nuts, may more suitable sources of zinc for mercury-affected people, keeping in mind that we absorb zinc much more efficiently from animal foods than from plant sources.
Brazil nuts are a good source of selenium, and unlike fish, which is also high in selenium, do not contain potentially problematic levels of mercury. However, the selenium content of Brazil nuts varies according to the soil where the nuts are grown (as is the case for all foods). Brazil nuts are high in unsaturated fat and may not keep well if soaked extensively, but overnight soaking works well in temperate climates. Regarding the selenium in fish, evidence suggests that once the body’s natural defenses have been overrun by mercury, the selenium in seafood is less effective in buffering the mercury. Thus, people who know or suspect a mercury problem must consider both the benefits and risks in determining their fish consumption level. Those who choose to limit their seafood intake should consider taking cod liver oil and perhaps fish oil to derive some of the nutritional benefits of fish while keeping mercury exposure as low as possible.
Overall, one’s goal should be to eat the least restrictive nutrient-dense diet possible. Elimination and reintroduction of suspect foods is the best way to assess whether specific foods are problematic. Many children and adults with mercury toxicity benefit from a gluten-free, casein-free diet, while others can tolerate one or both of these foods. Additional intolerances too numerous to list may affect mercury-toxic individuals to varying degrees. Regardless of the particular diet, the body’s ability to detoxify will be reduced by intake of alcohol, sugar, refined starches, processed foods, caffeine and medications, and will cause unpleasant symptoms in many affected individuals.
The common intolerance to sulfites in wine suggests impairment of the sulfite oxidase enzyme needed to convert toxic sulfite to beneficial sulfate. This enzyme can be boosted by supplementing its cofactor, molybdenum. Because mercury blocks metabolic enzymes such as phenolsulfotransferases, some food compounds such as phenols can become partially metabolized into toxic intermediates, often resulting in reactions such as red cheeks and/or ears and hyperactivity after consuming foods high in phenols.58 Yeast overgrowth can increase sensitivity to high-thiol and high-oxalate foods.
Foods high in free thiols may be poorly tolerated by some mercury-affected individuals, particularly if the transsulfuration pathway is compromised, as can occur with molybdenum deficiency. Other sulfur-rich foods, s ch as red meat and organ meats, do not cause such problems. Of course, it is important to consume a diet that includes all the essential amino acids, including those that contain sulfur. The late Andrew Cutler, author of Amalgam Illness: Diagnosis and Treatment56 and Hair Test Interpretation: Finding Hidden Toxicities57 noted that foods high in free thiol (which include legumes, dairy, the cabbage family and eggs) can provoke symptoms in a significant subset of mercury-affected people, in part by increasing plasma cysteine, which may rise in response to mercury and its biochemical effects. Vegetarian diets are particularly deleterious to a significant subset of people suffering from mercury toxicity, because it is virtually impossible to obtain sufficient protein on a vegetarian diet that is modified to reduce free-thiol sources.
Another problematic food for many mercury-toxic individuals is cilantro leaf, which contains a chelating substance capable of redistributing mercury, thus exacerbating symptoms in sensitive individuals. Unfortunately, alternative health practitioners sometimes recommend cilantro in large amounts in both food and supplement form. Also often recommended is chlorella, which is inadvisable as a supplement due to its potential for contamination from the environment in which it is grown and to its lipopolysaccharide content, which can cause inflammatory stress.59
Unfortunately, testing for mercury toxicity is not straightforward. Mercury may accumulate in organs like the brain, even while blood, urine, fecal and hair levels are low. It is advisable to avoid urine challenge tests, which involve administering a chelator in a dosage high enough to cause significant oxidative stress due to redistribution of toxic metals to target organs such as the brain and kidneys. A porphyrin panel can reveal the footprint of toxic metals including mercury. Porphyrins are undesirable byproducts that occur when enzymes are blocked by toxicants. However, because porphyrins are easily destroyed,60 the risk of false negatives is high unless the sample is handled carefully.
A hair elements test is another option, revealing apparent dysregulation of essential mineral homeostasis—with essential hair minerals appearing abnormally high and/or low. Thus, the hair elements test may serve as an economical screening test for chronic mercury toxicity. Note that when hair essential minerals are dysregulated, a high level of an essential mineral may not indicate adequate intracellular status but may simply mean high excretion in hair.
It is beyond the scope of this nutrition-focused article to discuss mercury treatment options, but we recommend caution when considering detoxification protocols. For the highly mercury-toxic, many products may be either unsafe (such as chlorella and cilantro) or may be used in an unsafe manner (such as alpha lipoic acid). Many nutritional supplements include alpha lipoic acid without warning about its metal-chelating properties. When taken by individuals who have mercury dental amalgams or a body burden of mercury, alpha lipoic acid can pull mercury from the teeth and other tissues in an attempt to equilibrate levels throughout the body and brain. This is especially tragic when fetal exposure is involved. We suggest that anyone wishing to deepen their knowledge of mercury detoxification read the books by Andrew Cutler (see Resources sidebar).56,57 Cutler’s work is the most useful compilation of science-based explanations of mercury toxicity and its myriad effects. It should be noted that Cutler’s chelation protocol, though grounded in scientific theory, is controversial and not without risk.
Mercury’s toxicity is uniquely far-reaching, creating a biochemical train wreck in the body and having the toxic power to cause or contribute to most chronic illnesses. In addition to disrupting fundamental biochemical processes, mercury promotes oxidative stress, depletes antioxidant defenses and destroys biological barriers. It causes numerous interacting effects across multiple organ systems,21 leading to a gamut of health issues ranging from fatigue and inflammation to endocrine and immune dysregulation and mood disorders. People who have multiple health problems should consider the possibility that they are suffering from undiagnosed chronic mercury poisoning.
Mercury depletes nutrients needed for vital functions and dysregulates mineral and neurotransmitter metabolism to a greater extent than any other common toxicant. Because of mercury’s powerful antinutrient effects, a nutrient-dense diet may alleviate many symptoms of chronic mercury toxicity, but the nutritional depletion caused by mercury is so pervasive that affected individuals often also require nutritional supplementation. At the same time, it is important to note that many mercury-affected individuals are quite sensitive to a large number of foods, supplements and medications. Nonetheless, many people with a hidden mercury burden find relief by following a nutrient-dense diet, adapted as necessary to avoid gluten and/or dairy and to limit sugars and starches.
There are many reasons why chronic mercury toxicity remains under-recognized by both mainstream and alternative health authorities. These include the complicated, incomplete and easily misinterpreted scientific literature on mercury; mercury’s complex, nonlinear toxicity; the influence of genetics, epigenetics and micronutrient status in shaping mercury susceptibility; the ability of the body’s natural defenses to mask toxicity, creating long latencies between exposures and symptoms; and mercury’s varied and nonspecific symptoms, which may also be intermittent in the early stages. In addition, toxicity testing is not straightforward. Finally, because much exposure to mercury has been iatrogenic—via dental amalgams and vaccine preservatives—mercury research often is controversial. The unfortunate combination of ubiquitous exposures, iatrogenic involvement, long latencies, broad toxic effects, nonspecific symptoms and potentially irreversible damage renders chronic mercury toxicity an under-recognized epidemic.
Sara Russell, PhD, is a nutritional therapy practitioner (NTP), certified
GAPS practitioner and Weston A. Price Foundation chapter leader residing
in Italy. Sara works via phone and Skype with clients worldwide,
specializing in fertility, pregnancy and young children. To learn more
about Sara’s work, visit buildnurturerestore.com. Kristin Homme, MPP,
MPH is a retired engineer-turned-science-writer who has authored
several scientific articles in peer-reviewed journals.
This article is a slightly edited version of the original article published in the January 2017 Townsend Letter. The authors are grateful to Nori Hudson, the late Andrew Hall Cutler, Janet Kern, Marco Prina, Rebecca Rust Lee and Lana Russell for reading and providing input on various drafts of the original article.
• INTERNATIONAL ACADEMY OF ORAL MEDICINE AND TOXICOLOGY (IAOMT)
IAOMT (IAOMT.org) is a professional dental association that provides fact sheets about mercury and information about IAOMT’s safe amalgam removal protocol.
• MERCURY FREE BABY
Mercury Free Baby (mercuryfreebaby.org) is a joint project of IAOMT and the Coalition for Mercury-Free Drugs (CoMeD), which advocates for removal of mercury from all vaccines.
• DENTAL AMALGAM MERCURY SOLUTIONS (DAMS)
DAMS (amalgam.org) is a non-profit organization dedicated to educating consumers about unhealthy dental practices.
• AMALGAM ILLNESS: DIAGNOSIS AND TREATMENT
This 1999 book by Andrew Hall Cutler is still the most complete, science-based self-help book on chronic mercury toxicity. Amalgam Illness (ISBN 0967616808) is available at noamalgam.com as well as at online bookstores.
• MERCURY POISONING: THE UNDIAGNOSED EPIDEMIC
This 2013 book by David Hammond provides more context and less physiology than Cutler’s book, in a rendition that some may find more readable.
• “SULPHUR FOODS”
This resource (livingnetwork.co.za/chelationnetwork/food/high-sulfur-sulphur-food-list/) explains why some people with mercury toxicity cannot tolerate thiols and how to identify thiol intolerance.
• ENVIRONMENTAL WORKING GROUP (EWG)
The EWG offers a Skin Deep® searchable online consumer database (http://www.ewg.org/skindeep/) that provides information about body care products such as soap, shampoo, sunscreen and cosmetics.
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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2018.
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