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From the Townsend Letter
January 2017

Mercury: The Quintessential Anti-Nutrient
by Sara Russell, PhD, NTP, and Kristin G. Homme, PE(ret.), MPP, MPH
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Other Exposures
Up to the early 2000s, broken mercury thermometers were a common exposure risk in many countries. Until the 1960s, teething powders for babies contained mercury in the form of calomel. Thimerosal was used in contact lens solutions. Merbromin was once widely used as an antiseptic under the trade name Mercurochrome. In 1998, such products were banned when the FDA declared that mercury as an active ingredient in over-the-counter products was not "generally recognized as safe (GRAS)." Nevertheless, the use of mercury as an inactive ingredient is allowed by the FDA provided its content is under 65 ppm, and FDA regulations regarding cosmetics do not obligate ingredients that make up less than 1% of the product to be disclosed on the label. For instance, some brands of mascara still contain thimerosal as an antimicrobial and preservative.

Compact fluorescent lamps (CFLs) typically contain about 4 milligrams (4,000 micrograms) of mercury, some of which is released upon breakage in the form of mercury vapor. The concentration of this toxic release is compared to various regulatory safety standards in Table II. CFL proponents argue that the energy savings offered by CFLs, which includes reduced mercury emissions from coal power plants, makes them desirable; but this debate is beyond the scope of this article.

Incinerators, coal-fired power plants, crematoria, and other industrial processes may be significant sources of local exposures to mercury. For over a decade, the EPA has attempted to restrict mercury emissions from coal plants in the US by about 90%; but the rule is under litigation, and legal experts predict that enforcement is years away.
In some countries, gold mining techniques that employ mercury (which were historically employed in the US during the Gold Rush) remain a significant source of exposure for miners and local populations.

Fetal and Childhood Exposures
Fetal neurons are more sensitive to the toxic effects of mercury than any other cell type.35 Mercury from the mother's body readily crosses the placenta and accumulates in the fetus, as revealed in post-mortem human and animal studies.36 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.37 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.38,39 Human and animal studies show increased rates of miscarriage, neonatal death, low birth weight, and developmental disorders associated with mercury exposure.40

Developmental and Epigenetic Toxicity
The developmental period spanning 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, in a manner that can be passed to offspring without alteration of the DNA nucleotide sequence itself. 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 – and early-life stressors are known to induce changes in gene expression that set the stage for disease in later life.41 Thus, unfortunately, when either parent is exposed to mercury, even prior to conception, the child's own genetic expression can be affected.
ProTheraSuch 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,42 whose ideas have subsequently been developed in Chris Masterjohn's research on fat-soluble vitamins; in Sally Fallon Morell and Thomas Cowan's Nourishing Traditions Book of Baby and Child Care43; and in the more epigenetically-focused Deep Nutrition by Catherine and Luke Shanahan.44 Within the alternative health community, the role of micronutrients is well recognized to promote 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.

Genetic Susceptibilities
A loose scientific consensus has long discounted the idea of mercury toxicity from dental amalgams because population studies have shown that people with high exposures and even people with a high body burden do not necessarily have toxicity symptoms. Therefore, those who blame amalgams for their illnesses have been viewed askance. But within the past ten years, over a dozen common genetic variants that convey increased susceptibility to mercury toxicity have been documented in human studies.45,46 Moreover, hundreds more variants are likely to exist. Mercury attacks sulfur in proteins; and since the body has tens of thousands of genetically determined sulfur-containing proteins, many of these proteins are likely to include variants that contribute to susceptibility.47 Candidate genes are involved not only in methylation and detoxification but in vitamin and mineral (i.e., enzyme cofactor) absorption, transport, and metabolism. Yet genetic susceptibilities have yet to be considered by policy makers, health authorities, or the dental industry. Indeed, for millions of children and adults covered by subsidized dental programs, military family dental care, and Native American services, for example, amalgam is virtually the only option for dental restorations.
Regarding genetic susceptibilities to vaccine injury, a few isolated court cases in the US and elsewhere have recognized post facto that a limited number of well-documented genetic susceptibilities including some mitochondrial disorders have caused certain children to suffer permanent neurological damage. But genetic susceptibilities are a continuum, and the growing movement to mandate vaccines has so far failed to recognize this complex reality.

Mercury as Anti-Nutrient
Mercury's toxicity is uniquely far-reaching. It disrupts fundamental biochemical processes, promotes oxidative stress, depletes antioxidant defenses, and destroys biological barriers. It causes numerous interacting effects across multiple organ systems,48 leading to a gamut of health issues ranging from fatigue and inflammation to endocrine and immune dysregulation and mood disorders.
Mercury readily binds to sulfhydryl (-S-H), 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. Selenium is said to protect against mercury toxicity, but its 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, selenoprotein P, a substance that stores and transports selenium to cells,49 can become blocked by mercury. Therefore, selenium offers only limited protection against mercury exposure.
The body's most important intracellular antioxidant mechanism is the glutathione system. Because the glutathione molecule and its related enzymes employ cysteine, they are targets for mercury. Specifically, mercury damages 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. Glutathione detoxifies mercury by binding it (in a process called glutathione conjugation) into a less toxic form suitable for excretion through the bile. Incidentally, the glutathione system has been found to be crucial in the detoxification of thimerosal.50 By depleting glutathione and disabling the glutathione-related enzymes, mercury impairs the detoxification of many toxicants, including mercury itself, 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, for example, 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. Additionally, mercury 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 a required cofactor – vitamin C. 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 energy. There, it 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.51 Mitochondrial dysfunction affects 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, a self-propagating chain reaction in which the unsaturated fatty acids in cell membranes are attacked, becoming free radicals themselves, and ultimately leading to excess permeability in membranes and other barriers, thus provoking still more damage.
Metallothioneins are cysteine-rich metal storage molecules that appear to play a role in storing zinc and copper and 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. Dietary sources of zinc are more limited than for copper. 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. Copper pipes, copper IUDs, and copper sulfate sprayed on crops as an anti-fungal (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-induced anomalies in the transport of essential minerals such as magnesium and zinc 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 disorders, attention deficits, 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. For example, low zinc is often accompanied by high copper, and low magnesium is often accompanied by high calcium in soft tissues.
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% of the lab rats (lethal dose "LD01") when combined with a dose of lead sufficient to kill 1% of the rats resulted in killing 100% of the rats.52 A similar test involving mercury and aluminum in cultured neurons killed 60% of the cells when the two low-dose toxicants (LD01) were combined.53 Even antibiotics have been shown to enhance the uptake, retention, and toxicity of mercury.54 Additionally, testosterone appears to aggravate mercury toxicity during development while estrogen protects against it.55 In fact, more boys than girls are diagnosed with autism spectrum disorders and attention deficit.

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