Chronic Fatigue Syndrome, Fibromyalgia, Scleroderma, Lupus, Rheumatoid Arthritis, MCS: The Mercury Connection

0 Flares Twitter 0 Facebook 0 Google+ 0 LinkedIn 0 0 Flares ×

Chronic fatigue syndrome (CFS) is characterized by fatigue, neurologic symptoms, including headaches, brain fog, mood disorders, and motor dysfunction. Millions of people in the U.S. suffer from CFS. An estimated three to six million patients in the US are affected by fibromyalgia (FMS). Spect scans of those with CFS have found that the majority have over 5 times more areas of regional brain damage and reduced blood flow in the cerebral cortex area of the brain than controls. The majority studied were also found to have increased Th2 inflammatory cytokine activity and a blunted DHEA response curve to I.V. ATCH indicative of hypothalamic/adrenal deficiency such as relative glucocorticoid deficiency.

CFS and fibromyalgia patients have also been found to commonly have abnormal enzymatic processes that affect the sodium-potassium ATPase energy channels, which appear to be a major factor in the condition and for which mercury is a known cause. This also has been found to result in inflammatory processes that cause muscle tissue damage and result in higher levels of urinary excretion of creatine, choline, and glycine in CFS, and higher levels of excretion of choline, taurine, citrate, and trimethyl amine oxide in FM. Supplementation of creatine has been found to result in improved muscle mitochondrial function in such patients. FM is further characterized by muscle and fibrous tissue pain, and its prevalence has been estimated at greater than 7% in women aged 60-79 years and 3.4% for all women. A Swedish study found that in one county, 11.6% of women over 35 surveyed had symptoms of fibromyalgia, while 5.5% of men reported such symptoms. A study found that for a group of patients that had both CFS and FM, all had high homocysteine levels, a marker of inflammation. Other factors in CFS and fibromyalgia include oxidative stress, metal sensitivity, adrenal fatigue, autoimmunity, organic acid imbalances, food allergies, digestive malabsorption of essential nutrients, along with overgrowth of intestinal yeasts, bacteria, or parasites. Research suggests that as many as 75% of individuals with fibromyalgia have bacterial overgrowth in the small bowel. Clinical experience has found that the pathogen overgrowths cannot be fully eliminated without detoxification of mercury and toxic metals which facilitate the pathogen overgrowths. Tests also found mercury accumulation in the limbic system and muscle tissues of a sample of fibromyalgia patients’ tests, and significant improvement after dental revision to replace amalgam fillings and deal with toxic root-canal teeth and cavitations.

Factors other than metals that can be involved in chronic fatigue include drug side effects, estrogenic chemicals, chronic stress related adrenal fatigue, hypothyroidism, and poor diet, although toxic metals and other toxics can be factors in hypothyroidism and adrenal fatigue. Drugs known to reduce thryroid and adrenal function include birth control pills, hormone replacement drugs, statins, blood pressure medications, anti-histamines, migraine medications, muscle relaxers, pain meds, evista, tamoxifen, tri-cyclic antidepressants, etc.

Birth control pills and HR drugs deplete essential vitamins and minerals, including vitamin B, vitamin C, magnesium, zinc, and tyrosine. Statins and blood pressure medications can damage the liver and deplete the essential enzyme CoQ10, causing cardiovascular problems and fatigue. Large numbers have obesity and fatigue related to insufficient exercise and poor diets with too much sweets, sodas, high glycemic starches, low fiber, etc. The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic susceptibility, which determines individuals’ immune sensitivity and ability to detoxify metals. Inherited defects in detoxification of environmental chemicals may promote toxicity and fatigue in CFS. Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals, or have an inability to detoxify metals due to deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals.

A study involving 930 fatigued patients saw more than half (62%) test positive for metal allergy. The majority of those who went on to remove the offending metal reported substantial health improvements. When metal particles enter the body (through any number of sources, including dental amalgam fillings) they bind with proteins. This happens to everyone, hypersensitive or not. With hypersensitive people, the new structure is falsely identified by the immune system as a foreign invader. The white blood cells, or lymphocytes, go into attack mode. The activated immune system will up-regulate the activity of certain brain structures (hypothalamus) and adrenal glands. The brain perceives a warning about danger and prepares for defense against the invader. This stress mode will last as long as the inflammation process is fueled by toxic metals, which have synergistic effects. This will result in fatigue while the attack is being carried out by the lymphocytes. When antibodies are produced to attack the protein, the condition becomes far more serious—possibly leading to neuropsychiatric disorders. For those with chronic conditions, fatigue regardless of the underlying disease is primarily associated with hypersensitivity to inorganic and organic mercury, nickel, and gold.

Mercury Sources and Exposure Levels

Amalgam fillings are the largest source of mercury in most people with daily exposures documented to commonly be above government health guidelines. This is due to continuous vaporization of mercury from amalgam in the mouth, along with galvanic currents from mixed metals in the mouth that deposit the mercury in the gums and oral cavity. Due to the high daily mercury exposure and excretion into home and business sewers of those with amalgam, dental amalgam is also the largest source of the high levels of mercury found in all sewers and sewer sludge and thus a significant source of mercury in rivers, lakes, bays, fish, and crops. People also get significant exposure from vaccinations, fish, and dental office vapor.

When amalgam was placed into teeth of monkeys and rats, within one year mercury was found to have accumulated in the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone glands, and lymph glands. People also commonly get exposures to mercury and other toxic metals, such as lead, arsenic, nickel, and aluminum, from food, water, and other sources. All of these are highly neurotoxic and are documented to cause neurological damage which can result in chronic neurological conditions over time. Mercury induced lipid peroxidation has been found to be a major factor in mercury’s neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide dismutase (SOD). Antioxidants have been found to protect against such mercury neurotoxicity.

Mercury (especially mercury vapor) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, hypothalamus, thyroid gland, adrenal gland, and occipital cortex in direct proportion to the number and extent of amalgam surfaces. Thus mercury has a greater effect on the functions of these areas. The range in one study was 2.4 to 28.7 parts per billion (ppb), and one study found on average that 77% of the mercury in the occipital cortex was inorganic.

Effects of Mercury (and Toxic Metal) Exposure

Some of the factors documented to be involved in inflammatory conditions like CFS, FMS, lupus, rheumatoid arthritis, etc. and in programmed cell death, apoptosis, of neurons and immune cells in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. include:

  • inducement of the inflammatory cytokine Tumor Necrosis Factor-alpha(TNFa),
  • reactive oxygen species and oxidative stress,
  • reduced glutathione levels,
  • liver enzyme effects and inhibition of protein kinase C and cytochrome P450,
  • nitric oxide and peroxynitrite toxicity,
  • excitotoxicity and lipid peroxidation,
  • excess free cysteine level
  • excess glutamate toxicity,
  • excess dopamine toxicity,
  • beta-amyloid generation,
  • increased calcium influx toxicity and DNA fragmentation,
  • mitochondrial membrane dysfunction, and
  • autoimmunity.

Mercury and toxic metals exposure causes all of these factors.

TNFa (tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death (apoptosis). This process is involved in inflammatory conditions like CFS, FM, RA, lupus, etc. and in degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids are part of the control mechanism for the TNFa inflammatory and apoptosis mechanism. Glutathione is an amino acid that is a normal cellular mechanism for controlling inflammation and apoptosis. When glutathione is depleted in the brain, reactive oxidative species increase, and CNS and cell signaling mechanisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results, and neurological damage. Mercury has been shown to induce TNFa, deplete glutathione, and increase glutamate, dopamine, and calcium related toxicity, causing inflammatory effects and cellular apoptosis in neuronal and immune cells. Mercury’s biochemical damage at the cellular level includes:

  • DNA damage,
  • inhibition of DNA and RNA synthesis,
  • alteration of protein structure,
  • alteration of the transport and signaling mechanisms of calcium,
  • inhibition of glucose transport, and of enzyme function and
  • transport/absorption of other essential nutrients,
  • induction of free radical formation,
  • depletion of cellular glutathione (necessary for detoxification processes),
  • inhibition of glutathione peroxidase enzyme,
  • inhibition of glutamate uptake,
  • induction of peroxynitrite and lipid peroxidation damage,
  • abnormal migration of neurons in the cerebral cortex,
  • immune system damage,
  • affects dopamine uptake by neuronal synaptosomes,
  • inducement of inflammatory cytokines, and
  • inducement of autoimmunity.

Mercury’s activation of inflammatory cytokines and Th2 helper immune cells suppresses the cytotoxic response of T-cells and natural killer immune cells that are the body’s main defense against viruses and such biological pathogens.

A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids appears to be a major part of the connection to allergic/immune reactive conditions, such as lupus (SLE), scleroderma, and RA as well as CFS and FMS that are also related to inflammatory cytokine processes and autoimmunity. One study found that insertion of amalgam fillings or nickel dental materials causes a suppression of the number of T-lympocytes and impairs the T-4/T-8 ratio. Low T4/T8 ratio has been found to be a factor in lupus, anemia, MS, eczema, inflammatory bowel disease, and glomerulonephritis.

Mercury-induced autoimmunity in animals and humans has been found to be associated with mercury’s expression of major histocompatibility complex (MHC) class II genes. Both mercuric and methylmercury chlorides caused dose dependent reduction in immune B-cell production. B-cell expression of IgE receptors were significantly reduced, with a rapid and sustained elevation in intracellular levels of calcium induced. Mercury and other toxic metals also form inorganic compounds with OH, NH2, CL, in addition to the SH radical and thus inhibit many cellular enzyme processes, coenzymes, hormones, and blood cells. Mercury has been found to impair conversion of thyroid T4 hormone to the active T3 form as well as to cause autoimmune thyroiditis common to such patients. In general, immune activation from toxic metals such as mercury, resulting in cytokine release and abnormalities of the hypothalamus-pituitary-adrenal axis, can cause changes in the brain, hypocortisolism, fatigue, and severe psychological symptoms, such as profound fatigue, muscoskeletal pain, sleep disturbances, gastrointestinal, and neurological problems as are seen in CFS, fibromyalgia, and autoimmune thyroiditis. Such hypersensitivity has been found most common in those with genetic predisposition to heavy metal sensitivity, such as found more frequently in patients with human lymphocyte antigens (HLA-DRA). A significant portion of the population appears to fall in this category.

Mercury exposure through dental fillings appears to be a major factor in chronic fatigue syndrome (CFS) and fibromyalgia through its effects on ATP and immune system (lymphocyte reactivity, neutrophil activity, effects on T-cells and B-cells) as well as its promotion of growth of candida albicans in the body and the methylation of inorganic mercury by candida and intestional bacteria to the extremely toxic methyl mercury form, which like mercury vapor crosses the blood-brain barrier, and also damages and weakens the immune system. Mercury vapor or inorganic mercury has been shown in animal studies to induce autoimmune reactions and disease through effects on immune system T-cells. Chronic immune activation is common in CFS, with increase in activated CD8+ cytotoxic T-cells and decreased NK cells. Numbers of suppressor-inducer T cells and NK cells have been found to be inversely correlated with urine mercury levels. CFS and FMS patients usually improve and immune reactivity is reduced when amalgam fillings are replaced.

Heavy metal toxicity has been found to be a common co-factor in FMS, as well as root canaled teeth and jawbone cavitations. Nickel has been often found to be a factor in chronic autoimmune conditions like CFS and Lupus. Chronic neurological conditions appear to be primarily caused by chronic or acute brain inflammation. The brain is very sensitive to inflammation. Disturbances in metabolic networks (e.g., immuno-inflammatory processes, insulin-glucose homeostasis, adipokine synthesis and secretion, intra-cellular signaling cascades, and mitochondrial respiration) have been shown to be major factors in chronic neurological conditions. Inflammatory chemicals such as mercury, aluminum, and other toxic metals as well as other excitotoxins, including MSG and aspartame, cause high levels of free radicals, lipid peroxidation, inflammatory cytokines, and oxidative stress in the brain and cardiovascular systems. Exposures to heavy metal toxins can impair energy production and burden the detoxification system. Oxidative stress caused by unstable free radical molecules can damage the energy-producing mechanisms inside the body’s cells. Fatigue and/or muscle pain can develop from toxic stress when the body is unable to detoxify harmful waste products or toxins from the environment.

Mercury and other toxic metals inhibit astrocyte function in the brain and CNS, causing increased glutamate and calcium related neurotoxicity. Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage. Nitric oxide related toxicity caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD) has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS.

These inflammatory processes damage cell structures including DNA, mitochondria, and cell membranes. They also activate microglia cells in the brain, which control brain inflammation and immunity. Once activated, the microglia secrete large amounts of neurotoxic substances such as glutamate, an excitotoxin, which adds to inflammation and stimulates the area of the brain associated with anxiety. Inflammation also disrupts brain neurotransmitters resulting in reduced levels of serotonin, dopamine, and norepinephrine, which can lead to depression. Some of the main causes of such disturbances that have been documented include vaccines, mercury, aluminum, other toxic metals, MSG, aspartame, etc.

Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions. Mercury and cadmium inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes.

Fatigue is a hallmark symptom of thyroid or adrenal hormone imbalances. Mercury lymphocyte reactivity, effects on glutamate in the CNS, and mercury-induced hypothyroidism induce CFS-type symptoms, including profound tiredness, musculoskeletal pain, sleep disturbances, gastrointestinal and neurological problems along with other CFS symptoms and fibromyalgia. Mercury has been found to be a common cause of fibromyalgia. Glutamate is the most abundant amino acid in the body and in the CNS acts as excitory neurotransmitter, which also causes inflow of calcium. Astrocytes, a type of cell in the brain, and CNS, with the task of keeping clean the area around nerve cells and facilitating neurotransmission, have a function of neutralizing excess glutamate by transforming it to glutamic acid. If astrocytes are not able to rapidly neutralize excess glutamate, then a buildup of glutamate and calcium occurs, causing swelling and neurotoxic effects. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS, causing increased glutamate and calcium related neurotoxicity which are responsible for much of the fibromyalgia symptoms. This is also a factor in conditions such as CFS, Parkinson’s, and ALS. Animal studies have confirmed that increased levels of glutamate (or aspartate, another amino acid excitory neurotransmitter) cause increased sensitivity to pain, as well as higher body temperature—both found in CFS/Fibromyalgia. Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage. Medical studies and doctors treating fibromyalgia have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on fibromyalgia. Some that have been found to be effective include vitamin B6, methyl cobalamine (B12), L-carnitine, choline, ginseng, Ginkgo biloba, vitamins C and E, nicotine, and omega 3 fatty acids (fish and flaxseed oil-GLA, EPA, DHA). Other supplements that also have been found to help are magnesium and malic acid. Avoidance of exictotoxins like MSG and aspartame has been found to eliminate symptoms in some with fibromyalgia.

Clinical tests of patients with chronic neurological conditions, lupus (SLE), and rheumatoid arthritis have found that the patients generally have elevated plasma cysteine to sulfate ratios, with the average being 500% higher than controls, and in general being poor sulfur oxidizers. This means that these patients have insufficient sulfates available to carry out necessary bodily processes. Mercury has been shown to diminish and block sulfur oxidation and thus reduce glutathione levels, which is the part of this process involved in detoxifying and excretion of toxics like mercury. Glutathione is produced through the sulfur oxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects, while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe. Mercury has also been found to play a part in inducing intolerance and neuronal problems through blockage of the P-450 liver enzymatic process.

Mercury from amalgam interferes with production of cytokines that activate macrophage and neutrophils, disabling early control of viruses and leading to enhanced infection. Mercury’s activation of inflammatory cytokines and Th2 helper immune cells suppresses the cytotoxic response of T-cells and natural killer immune cells that are the body’s main defense against viruses and such biological pathogens. Animal studies have confirmed that mercury increases effects of the herpes simplex virus type 2 for example. Mercury damages the immune system and in those with chronic conditions has been found to commonly facilitate infestation by pathogens such as viruses, harmful bacteria, candida, mycoplasma, and parasites. The majority of those tested who have CFS or FMS have been found to have infections of mycoplasma, human herpes Virus-6, XMRV, cytomeglivirus, or bacterial infections such as intracellular chlamydia. Clinics treating these conditions commonly find such pathogens to be a factor in the condition. Mercury detoxification and treatment of these pathogens results in significant improvement in the majority of those treated. Studies have also found bilberry extract, curcumin, carotenoids, and chlorophyll supplements to be effective in suppressing effects of viruses such as Epstein-Barr or XMRV. Supplementation with chlorella has been found to result in beneficial effects when used in patients’ chronic conditions such as ulcerative colitis, hypertension, or fibromyalgia. Doctors such as D. Klinghardt have suggested that the mechanism by which chlorella improves treatment of such conditions is metal detoxification, which is the main mechanism of action of chlorella and has been found to greatly improve intestinal function.

Mercury exposure causes high levels of oxidative stress/reactive oxygen species (ROS), which has been found to be a major factor in apoptosis and neurological disease, including dopamine or glutamate related apoptosis. Mercury and quinones form conjugates with thiol compounds such as glutathione and cysteine and cause depletion of glutathione, which is necessary to mitigate reactive damage. Such congugates are found to be highest in the brain substantia nigra with similar congugates formed with L-Dopa and dopamine in Parkinson’s disease. Mercury depletion of GSH and damage to cellular mitochondria and the increased lipid peroxidation in protein and DNA oxidation in the brain appear to be a major factor in Parkinson’s disease.

Multiple Chemical Sensitivity

Many cases of Multiple Chemical Sensitivity (MCS) develop following exposures to heavy metal toxins, such as mercury. Mercury exposure results in oxidative stress, reduced glutathione, increased peroxynitrite, all of which are found in virtually all with MCS or CFS or FM, which have overlapping symptoms and factors. Oxidative stress from reactive free radicals or deficient glutathione, and the resulting increased peroxynitrite can inactivate important mitochondrial enzymes and interfere with energy production in MCS or CFS. Inherited impairments in detoxification function can also interact with environmental factors to promote MCS. Defects in the body’s ability to neutralize environmental chemicals lead directly to the accumulation of toxins. The body’s ability to neutralize and excrete environmental toxins depends on the availability of key nutrients. Some cases of MCS may be secondary to “leaky gut” and the passage of toxins or food particles into the system. Mal-digestion of critical nutrients, as well as intestinal infection (bacteria, yeast, or parasites), may aggravate MCS. Intestinal overgrowth of yeast, the passage of Candida toxins into the system, or parasites may further chemical sensitivities in MCS or CFS.

Treatment of CFS, Fibromyalgia, Multiple Chemical Sensitivity, etc.

It has been well documented by hundreds of medical studies including thousands of tested subjects and by scientific panels that “amalgam fillings” are the largest source of mercury in people and that those with several amalgam fillings often have daily exposures exceeding the Government Health Standards for mercury. Thus among those most susceptible, significant neurological and immune effects related to amalgam fillings are common. Symptoms of those with CFS, fibromyalgia, or thyroid-related conditions usually improve significantly after proper amalgam replacement. In thousands of cases who underwent amalgam replacement, the majority recovered or had significant improvement in symptoms for muscular/joint pain/fibromyalgia, Chronic Fatigue Syndrome (CFS), lupus, autoimmune thyroiditis, multiple chemical sensitivities, as well as many other conditions. Of one group of 86 patients with CFS symptoms, 78% reported significant health improvements after replacement of amalgam fillings within a relatively short period, and the MELISA immune reactivity test found significant reduction in lymphocyte reactivity compared to pre removal tests. The improvement in symptoms and lymphocyte reactivity imply that most of the Hg-induced lymphocyte reactivity is allergenic in nature. Although patch tests for mercury allergy are often given for unresolved oral symptoms, this is not generally recommended as a high percentage of such problems are resolved irrespective of the outcome of a patch test.

Exposure to compounds such as DDT/DDE and hexachlorobenzene has also been found to be highly correlated with chronic fatigue. Sick building syndrome (SBS) related to toxic exposures is usually characterized by upper respiratory complaints, headache, and mild fatigue, but the more serious CFS is often also associated with SBS.

Other Treatments for CFS and FM

Nutrition and nutritional support have been found to play significant roles in CFS/FM alleviation. Adrenal fatigue related to long term stress and hypothyroidism is a common factor in chronic fatigue. Adequate supply of vitamins and essential minerals as well as antioxidants have been found to benefit such conditions to counteract free radicals and oxidative stress caused by the conditions. Avoidance of too many sweets, sodas, high glycemic starches, etc. and more exercise such as walking, yoga, Pilates, etc. can make major improvement in chronic fatigue. Adding more raw, steamed, and sautéed greens, seafood, fruit, and other vegetables can also make a large difference. Glyconutrients such as Mannatech Ambrotose and Immunostart have also been found to be effective in reducing the effects of CFS and FM. Immunostart has been documented to be effective in detoxing toxic metals.

Adrenal and/or thyroid fatigue can be reversed over time through such means along with adaptagenic herbs such as Cordyceps senensis, Rhodiola rosea, Aswagandha, Panax giseng, licorice root and supplementing Pantethine (B5), magnesium, vit C, DHEA, R-lipoic acis, and EFAs. Hormone testing such as Genova and ZRT lab tests along with morning temperature monitoring can help in assessing needs. Minerals often deficient related to thyroid fatigue include iodine, sea salt, selenium, magnesium, and zinc, along with the amino acid tyrosine and B vitamins.

Some of the conditions found in people with CFS or FM or MCS include:

  • immune effects,
  • energy metabolism problems,
  • inflammation,
  • adrenal fatigue,
  • homocystein metabolism,
  • fatigue,
  • stress,
  • brain neurotransmitter imbalances, and
  • leaky gut.

In addition to metals detox, supplementation has been found clinically effective to deal with these conditions:

  • Immune (ginseng echineacea, EFAs, curcumin)
  • Energy metabolism (CoQ10, NADH, L-carnatine, magnesium)
  • Adrenal fatigue (DHEA, licorice, sodium)
  • Stress (glutamine, Adapton)
  • Neurotransmitters (tyrosine)
  • Homocysteine (B6, B12, folic acid, SAMe)
  • Inflammation (antioxidants: N-acetyl-cysteine, alpha lipoic acid)
  • Fatigue (ginseng, Mate)
  • Digestive support (digestive enzymes, probiotics).

Tests are readily available to check for hormone levels often out of imbalance in these conditions such as DHEA, cortisol, thyroid, and testosterone in older men.

B. E. Vickery’s testing showed all fibromyalgia patients to have five common conditions, regardless of their symptoms: 1) protein deficiency 2) degenerating spinal disks 3) sulfur deficiency 4) heavy metal toxicity, and 5) viral infection.

References

1. Hussain S, et al. Mercuric chloride-induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain. J Environ Sci Health B. 1997; 32(3): 395-409.

2. Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998; 71: S37-9.

3. Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.

4. Jay D. Glutathione inhibits SOD activity of Hg. Arch Inst Cardiol Mex. 1998; 68(6): 457-61.

5. El-Demerdash FM. Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. J Environ Sci Health B. 2001; 36(4): 489-99.

6. Tan S, et al. Oxidative stress induces programmed cell death in neuronal cells. J Neurochem. 1998; 71(1): 95-105.

7. Matsuda T, Takuma K, Lee E, et al. Apoptosis of astroglial cells. Nippon Yakurigaku Zasshi. 1998; 112 (1): 24P.

8. Lee YW, Ha MS, Kim YK. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001; 26(11): 1187-93.

9. Shruti PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: Glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002; 705: 694-702.

10. Galic N, Ferencic Z, et al. Dental amalgam mercury exposure in rats. Biometals. 1999; 12(3): 227-31.

11. Arvidson B, Arvidsson J, Johansson K. Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994; 7 (3): 261-3.

12. Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol. 1990; 52(3): 291-9.

13. Hahn L, et al. Distribution of mercury released from amalgam fillings into monkey tissues. FASEB J. 1990; 4: 5536.

14. Zamm AF. Removal of dental mercury: Often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990; 5(53): 138-142.

15. Markovich, et al. Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol App Pharmacol. 1999; 154(2): 181-7.

16. McFadden SA. Xenobiotic metabolism and adverse environmental response: Sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3): 43-65.

17. Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry. 1999; 46(3): 420-4.

18. Henriksson J, Tjalve H. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998; 77(2): 130 40.

19. Huggins HA, Levy TE. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc.; 1999.

20. Rodgers JS, Hocker JR, et al. Mercuric ion inhibition of eukaryotic transcription factor binding to DNA. Biochem Pharmacol. 2001; 61(12): 1543-50.

21. Hansen K, et al. A survey of metal induced mutagenicity in vitro and in vivo. J Amer Coll Toxicol. 1984; 3: 381-430.

22. Knapp LT, Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem. 2000.

23. Jenner P. Oxidative mechanisms in PD. Mov Disord. 1998; 13(1): 24-34.

24. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

25. Badou A, et al. HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels. J Biol Chem. 1997; 272(51): 32411-8.

26. Veprintsev DB. Pb2+ and Hg2+ binding to alpha-lactalbumin. Biochem Mol Biol Int. 1996 ; 39(6): 1255-65.

27. Buzard GS, Kasprzak KS. Possible roles of nitric oxide and redox cell signaling in metal-induced toxicity and carcinogenesis: A review. Environ Pathol Toxicol Oncol. 2000; 19(3):179-99.

28. Kingman A, Albertini T, Brown LJ. Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population. J Dent Res. 1998; 77(3): 461-71.

29. Lund ME, et al. Treatment of acute MeHg poisoning by NAC. J Toxicol Clin Toxicol. 1984; 22(1): 31-49.

30. Livardjani F, Ledig M, Kopp P, Dahlet M, Leroy M, Jaeger A. Lung and blood superoxide dismutase activity in mercury vapor exposed rats: Effect of N-acetylcysteine treatment. Toxicology. 1991; 66(3): 289-95.

31. Nicole A, et al. Direct evidence for glutathione as mediator of apoptosis in neuronal cells. Biomed Pharmacother. 1998; 52(9): 349-55.

32. Spencer JP, et al. Cysteine & GSH in PD: Mechanisms involving ROS. J Neurochem. 1998; 71(5): 2112-22.

33. Bains JS, et al. Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death. Brain Res Rev. 1997; 25(3): 335-58.

34. Medina S, Martinez M, Hernanz A, Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42. Free Radic Res. 2002; 36(11): 1179-84.

35. Pocernich CB, et al. Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: Relevance to brain lipid peroxidation in neurodegenerative disease. Neurochem Int. 2001; 39(2): 141-9.

36. Offen D, et al. Use of thiols in treatment of PD. Exp Neurol. 1996; 141(1): 32-9.

37. Pearce RK, Owen A, Daniel S, Jenner P, Marsden CD. Alterations in the distribution of glutathione in the substantia nigra in Parkinson’s disease. J Neural Transm. 1997.

38. Shen XM, et al. Neurobehavioral effects of NAC conjugates of dopamine: Possible relevance for Parkinson’s disease. Chem Res Toxicol. 1996; 9(7): 1117-26.

39. Li H, Shen XM, Dryhurst G. Brain mitochondria catalyze the oxidation of 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxylic acid (DHBT-1) to intermediates that irreversibly inhibit complex I and scavenge glutathione: potential relevance to the pathogenesis of Parkinson’s disease. J Neurochem. 1998; 71(5): 2049-62.

40. Araragi S, Sato M, et al. Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003; 184(1): 1-9.

41. Bjorkman L, et al. Mercury in saliva and feces after removal of amalgam fillings. Toxicol App Pharmacol. 1997; 144(1): 156-62.

42. Veltman JC, et al. Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland. Arch Biochem Biophys. 1986; 248(2): 467-78.

43. Riedl AG, et al. P450 and hemeoxygenase enzymes in the basal ganglia and their roles in Parkinson’s disease. Adv Neurol. 1999; 80: 271-86.

44. Zamm AV. Dental mercury: A factor that aggravates and induces xenobiotic intolerance. J. Orthmol. Med. 1991; 6(2): 67-77.

45. Ostman PO, et al. Clinical & histologic changes after removal of amalgam. Oral Surgery, Oral Medicine, and Endodontics. 1996; 81(4): 459-465.

46. Ibbotson SH, et al. The relevance of amalgam replacement on oral lichenoid reactions. British Journal of Dermatology. 1996; 134(3): 420-3.

47. Bratel J, et al. Effect of replacement of dental amalgam on OLR. Journal of Dentistry. 1996; 24(1-2): 41-45.

48. Koch P, et al. Oral lesions and symptoms related to metals. Dermatol. 1999; 41(3): 422-430.

49. Berglund F. Case Reports Spanning 150 years on the Adverse Effects of Dental Amalgam. Orlando, FL: Bio-Probe; 1995.

50. Tuthill JY. Mercurial neurosis resulting from amalgam fillings. The Brooklyn Medical Journal. 1898; 12(12): 725-742.

51. Lichtenberg HJ. Elimination of symptoms by removal of dental amalgam from mercury poisoned patients. J Orthomol Med. 1993; 8:145-148, 1993.

52. Lichtenberg HJ. Symptoms before and after proper amalgam removal in relation to serum globulin reaction to metals. J Orthomol Med. 1996; 11(4): 195-9.

53. Goldberg AF, et al. Effect of amalgam restorations on whole body potassium and bone mineral content in older men. Gen Dent. 1996; 44(3): 246-8.

54. Schirrmacher K. Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells. Calcif Tissue Int. 1998; 63(2):134-9.

55. Quig D. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.

56. de Ceaurriz J, et al. Role of gamma-glutamyltraspeptidase(GGC) and extracellular glutathione in dissipation of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.

57. Berndt WO, et al. Renal glutathione and mercury uptake. Fundam Appl Toxicol. 1985; 5(5):832-9.

58. Zalups RK, Barfuss DW. Accumulation and handling of inorganic mercury in the kidney after co-administration with glutathione. J Toxicol Environ Health. 1995; 44(4): 385-99.

59. Clarkson TW, et al. Billiary secretion of glutathione-metal complexes. Fundam Appl Toxicol. 1985; 5(5): 816-31.

60. Glavinskiaia TA, et al. Complexons in the treatment of lupus erghematousus. Dermatol Venerol. 1980; 12: 24-28.

61. Aschner M, et al. Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury. Brain Res. 1997; 778(1): 222-32.

62. Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system. Biol Signals. 1994; 3: 181-7.

63. O’Halloran TV. Transition metals in control of gene expression. Science. 1993; 261(5122): 715-25.

64. Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem. 1991; 266(19):12695-702.

65. Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct. 1995; 20(3): 233-8.

66. Tibbling L, Stejskal VDM, et al. Immunolocial and brain MRI changes in patients with suspected metal intoxication. Int J Occup Med Toxicol. 1995; 4(2): 285-294.

67. Ronnback L, et al. Chronic encephalopaties induced by low doses of mercury or lead. Br J Ind Med. 1992; 49: 233-240.

68. Langauer-Lewowicka H. Changes in the nervous system due to occupational metallic mercury poisoning. Neurol Neurochir Pol. 1997; 31(5): 905-13.

69. Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes. Yonsei Med J. 1995; 36(3): 299-305.

70. Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology. 1992; 76(3): 245-56.

71. Albrecht J, Matyja E. Glutamate: A potential mediator of inorganic mercury toxicity. Metab Brain Dis. 1996; 11: 175-84.

72. Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive: Implications to pro-inflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998; 273(32): 20354-62.

73. Pahan K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J Biol Chem. 1999; 274: 7528-7536.

74. Xu J, Yeh CH, et al. Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998; 273(26): 16521-6.

75. Dbaibo GS, El-Assaad W, et al. Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001; 503(1): 7-12.

76. Liu B, Hannun YA, et al. Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death. J Biol Chem. 1998; 273(18): 11313-20.

77. Noda M, Wataha JC, et al. Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003; 19(2):101-5.

78. Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: Differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002; 7(1): 67-74.

79. Dastych J, Metcalfe DD, et al. Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999; 103(6): 1108-14.

80. Tortarolo M, Veglianese P, et al. Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression. Mol Cell Neurosci. 2003; 23(2): 180-92.

81. Ariza ME, Bijur GN, Williams MV. Lead and mercury mutagenesis: Role of H2O2, superoxide dismutase, and xanthine oxidase. Environ Mol Mutagen. 1998; 31(4): 352-61.

82. Ariza ME, et al. Mercury mutagenisis. Biochem Mol Toxicol. 1999; 13(2):107-12.

83. Ariza ME, et al. Mutagenic effect of mercury. In Vivo. 1994; 8(4): 559-63.

84. Langworth, et al. Effects of low exposure to inorganic mercury on the human immune system. Scand J Work Environ Health. 1993; 19(6): 405-413.

85. Walum E, et al. Use of primary cultures to study astrocytic regulatory functions. Clin Exp Pharmoacol Physiol. 1995; 22: 284-7.

86. Kerkhoff H, Troost D, Louwerse ES. Inflammatory cells in the peripheral nervous system in motor neuron disease. Acta Neuropathol. 1993; 85: 560-5.

87. Appel Sh, Smith RG. Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv Neurol. 1995; 68: 47-57.

88. Mathieson PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995; 102(2): 229-30.

89. Heo Y, Parsons PJ, Lawrence DA. Lead differentially modifies cytokine production in vitro and in vivo. Toxicol App Pharmacol. 1996; 138:149-57.

90. Murdoch RD, Pepys J. Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol. 1986; 80: 405-11.

91. Lu SC. Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J. 1999; 13(10): 1169-83.

92. Zalups RK, et al. Nephrotoxicity of inorganic mercury co-administered with L-cysteine. Toxicology. 1996; 109(1): 15-29.

93. Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003; 62(1): 55-65.

94. Bapu C, Purohit RC, Sood PP. Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994; 13(12): 815-23.

95. Danielsson BRG, et al. Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus. Biol Res Preg Perinatal. 1984(3): 102-109.

96. Ziff MF. Documented clinical side effects to dental amalgams. Adv Dent Res. 1992; 1(6): 131-134.

97. Yannai S, et al. Transformations of inorganic mercury by candida albicans and saccharomyces cerevisiae. Applied Envir Microbiology. 1991; 7: 245-247.

98. Zorn NE, et al. A relationship between Vit B-12, mercury uptake, and methylation. Life Sci. 1990; 47(2):167-73.

99. Yamada, Tonomura. Formation of methylmercury compounds from inorganic mercury by chlostridium cochlearium. J Ferment Technol. 1972; 50: 1590-1660.

100. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cell viability. Immunopharmacologicol Immunotoxical. 1992; 14(3): 555-77.

101. Miller MA, et al. Mercuric chloride induces apoptosis in human T lymphocytes. Toxicol App Pharmacol. 1998; 153(2): 250-7.

102. Rossi AD, Viviani B, Vahter M. Inorganic mercury modifies Ca2+ signals, triggers apoptosis, and potentiates NMDA toxicity in cerebral granule neurons. Cell Death and Differentiation. 1997; 4(4): 317-24.

103. Goering PL, Thomas D, Rojko JL, Lucas AD. Mercuric chloride-induced apoptosis is dependent on protein synthesis. Toxicol Lett. 1999; 105(3): 183-95.

104. Rogers S. The E.I. Syndrome: An Rx for Environmental Illness. Keats Publishing; 1986.

105. Berglund F, et al. Improved health after removal of dental amalgam fillings. Swedish Assoc. of Dental Mercury Patients. 1998.

106. Bigazzi PE. Autoimmunity and heavy metals. Lupus. 1994; 3: 449-453.

107. Pollard KM, Pearson Dl, Hultman P. Lupus-prone mice as model to study
xenobiotic-induced autoimmunity. Environ Health Perspect. 1999; 107(5): 729-735.

108. Nielsen JB; Hultman P. Experimental studies on genetically determined susceptibility to mercury-induced autoimmune response. Ren Fail. 1999; 21(3-4): 343-8.

109. Feighery L, Collins C, Anti-transglutaminase antibodies and the serological diagnosis of coeliac disease. Br J Biomed Sci. 2003; 60(1):14-8.

110. Mayes M. Epidemiologic studies of environmental agents and systemic autoimmune diseases. Environ Health Perspect. 1999; 107(5): 743-8.

111. Bigazzi PE. Metals and kidney autoimmunity. Environ Health Perspect. 1999; 107 (5): 753-65.

112. Hamre HJ. Mercury from dental amalgam and chronic fatigue syndrome. The CFIDS Chronicle. 1994: 44-47.

113. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphoctes and monocytes: Alterations in cellular glutathione content. Immunopharmacol Immunotoxicol. 1993; 15(2-3): 273-90.

114. Al-Saleh I, Shinwari N. Urinary mercury levels in females: Influence of dental amalgam fillings. Biometals. 1997; 10(4): 315.

115. Zabinski Z, Dabrowski Z, Moszczynski P, Rutowski J. The activity of erythrocyte enzymes and basic indices of peripheral blood from workers chronically exposed to mercury vapors. Toxico Ind Health. 2000; 16(2): 58-64.

116. Woods JS, et al. Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity. Physiol Pharmocol. 1996; 74(2): 210-15.

117. Strubelt O, Kremer J, et al. Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver. J Toxicol Environ Health. 1996; 47(3): 267-83.

118. Kaliman PA, Nikitchenko IV, Sokol OA, Strel’chenko EV. Regulation of heme oxygenase activity in rat liver during oxidative stress induced by cobalt chloride and mercury chloride. Biochemistry (Mosc). 2001; 66(1): 77-82.

119. Kumar SV, Maitra S, Bhattacharya S. In vitro binding of inorganic mercury to the plasma membrane of rat platelet affects Na+-K+-Atpase activity and platelet aggregation. Biometals. 2002; 15(1): 51-7.

120. Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: A common pathway in central nervous system disorders. J Assoc Physicians India. 2002; 50: 400-6.

121. Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance and myalgic encephalomyelitis. Int J Neurosci. 2003;113(5): 683-701.

122. Kurup RK, Kurup PA, Hypothalamic digoxin and hemispheric chemical dominance–relation to the pathogenesis of senile osteoporosis, degenerative osteoarthritis, and spondylosis. Int J Neurosci. 2003; 113(3): 341-59.

123. Danielsson BR, et al. Behavioral effects of prenatal metallic mercury inhalation exposure in rats. Neurotoxicol Teratol. 1993; 15(6): 391-6.

124. Fredriksson, et al. Prenatal exposure to metallic mercury vapour and methylmercury produce interactive behavioral changes in adult rats. Neurotoxicol Teratol. 1996; 18(2): 129-34.

125. Lohmann K, et al. Multiple chemical sensitivity disorder in patients with neuroltoxic illnesses. Gesundheitswesen. 1996;58(6): 322-31.

126. Duuet P, et al. Glomerulonephritis induced by heavy metals. Arch Toxicol. 1982. 50:187-194.

127. Robinson CJG, et al. Mercuric chloride induced antinuclear antibodies in mice. Toxicol Appl Pharmacol. 1986; 86:159-169.

128. Andres P. IgA-IgG disease in the intestines of rats ingesting HgCl. Clin Immun Immunopath. 1984; 30: 488-494.

129. Cossi, et al. Benefiecial effect of human therapeutic IV-Ig in mercury induced autoimmune disease. Clin Exp Immunol. 1991.

130. El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral assessment of neurotoxicity and autoimmune mechanisms. Contact Dermatitis. 1999; 41(1): 60-1.

131. Eggleston DW. Effect of dental amalgam and nickel alloys on T-lympocytes. J Prosthet Dent. 1984; 51(5): 617-623.

132. Park SH, et al. Effects of occupational metallic mercury vapor exposure on suppressor-inducer(CD4+CD45RA+) T lymphocytes and CD57+CD16+ natural killer cells. Int Arch Occup Environ Health. 2000; 73(8): 537-42.

133. BJ Shenker. Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction. Environ Res. 1998, 77(2):149-159.

134. Insug O, et al. Mercuric compounds inhibit human monocyte function by inducing apoptosis: Evidence for formation of reactive oxygen species(ROS), development of mitochondrial membrane permeability, and loss of reductive reserve. Toxicology; 1997; 124(3): 211-24.

135. Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance, and pathogenesis of pulmonary diseases. Int J Neurosci. 2003; 113(2): 235-58.

136. Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992; 262(5. 2): F830-6.

137. Walczak-Drzewiecka A, Wyczolkowska J, Dastych J. Environmentally relevant metal and transition metal ions enhance Fc epsilon RI-mediated mast cell activation. Environ Health Perspect. 2003; 111(5): 708-13.

138. Hunter I, Cobban HJ, Vandenabeele P, MacEwan DJ, Nixon GF. Tumor necrosis factor-alpha-induced activation of RhoA in airway smooth muscle cells: Role in the Ca2+ sensitization of myosin light chain20 phosphorylation. Mol Pharmacol. 2003; 63(3): 714-21.

139. Hisatome I, Kurata Y, et al. Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region. Biophys J. 2000; 79(3): 1336-45.

140. Bhattacharya S, Sen S, et al. Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997; 10(3):157-62.

141. Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992; 262(5.2): F830-6.

142. Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.

143. Wagner CA, el al. Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes. Am J Physiol. 1996; 271(4.2): F926-30.

144. Lewis RN, Bowler K. Rat brain (Na+-K)ATPase: Modulation of its ouabain-sensitive K+-PNPPase activity by thimerosal. Int J Biochem. 1983; 15(1): 5-7.

145. Hobson M, Harris L, Ware L, Chetty CS. Effects of cadmium and mercury on Na(+)-K(+) ATPase and uptake of 3H-dopamine in rat brain synaptosomes. Arch Int Physiol Biochem. 1990; 98(5): 291-6.

146. Hobson M, Rajanna B. Influence of mercury on uptake of dopamine and norepinephrine. Toxicol Letters. 1985; 27(2-3): 7-14.

147. McKay SJ, Reynolds JN, Racz WJ. Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatial slices. Can J Physiol Pharmacol. 1986; 64(12): 1507-14.

148. Scheuhammer AM, Cherian MG. Effects of heavy metal cations, sulfhydryl reagents and other chemical agents on striatal D2 dopamine receptors. Biochem Pharmacol. 1985; 34(19): 3405-13.

149. Hoyt KR, et al. Mechanisms of dopamine-induced cell death and differences from glutamate induced cell death. Exp Neurol. 1997; 143(2): 269-81.

150. Offen D, et al. Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels. Neurology. 1998; 51(4):1100-3.

151. Huggins HA, Levy TE. Cerebrospinal fluid protein changes in MS after dental amalgam removal. Alternative Med Rev. 1998; 3(4): 295-300.

152. Huggins Applied Healing. www.hugginsappliedhealing.com/

153. Bucio L, et al. Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res. 1999; 423(1-2): 65-72.

154. Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002; 70(5): 694-702.

155. Snyder RD, Lachmann PJ. Thiol involvement in the inhibition of DNA repair by metals in mammalian cells. Source Mol Toxicol. 1989; 2(2): 117-28.

156. Verschaeve L, et al. Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes. Mutat Res. 1985; 157(2-3): 221-6.

157. Verschaeve L. Genetic damage induced by low level mercury exposure. Envir Res. 1976; 12: 306-10.

158. Merchant RE, Andre CA. Dietary supplementation with chlorella pyrenoidosa produces positive results in patients with cancer or suffering from certain common chronic illnesses. Townsend Letter for Doctors & Patients. 2001.

159. Soderstrom S, Fredriksson A, Dencker L, Ebendal T, The effect of mercury vapor on cholinergic neurons in the fetal brain. Brain Research & Developmental Brain Res. 1995; 85: 96-108.

160. Abdulla EM, et al. Comparison of neurite outgrowth with neurofilament protein levels in neuroblastoma cells following mercuric oxide exposure. Clin Exp Pharmocol Physiol. 1995; 22(5): 362-3.

161. Leong CC, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport. 2001; 12(4): 733-7.

162. Stejskal VDM, et al. Mercury-specific Lymphocytes: an indication of mercury allergy in man. J. of Clinical Immunology. 1996; 16(1): 31-40.

163. Warfyinge K, et al. Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice. Toxicol App Pharmacol. 1995; 132(2): 299-309.

164. Bagenstose LM, et al. Mercury induced autoimmunity in humans. Immunol Res. 1999; 20(1): 67-78.

165. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability. Immunopharmacol Immunotoxicol. 1993; 15(1): 87-112.

166. Daum JR. Immunotoxicology of mercury and cadmium on B-lymphocytes. Int J Immunopharmacol. 1993; 15(3): 383-94.

167. Johansson U, et al. The genotype determines the B cell response in mercury-treated mice. Int Arch Allergy Immunol. 1998; 116(4): 295-305.

168. Zinecker S. Amalgam: Quecksilberdamfe bis ins gehirn. der Kassenarzt. 1992; 32(4): 23.

169. Siblerud RL. Relationship between dental amalgam and health. Toxic Substances Journal. 1990; 10: 425-444.

170. Wilkinson LJ, Waring RH. Cysteine dioxygenase: Modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002; 16(4): 481-3.

171. Heafield MT, et al. Plasma cysteine and sulphate levels in patients with motor neuron disease, Parkinson’s disease, and Alzheimer’s disease. Neurosci Lett. 1990; 110(1-2): 216-20.

172. Pean A, et al. Pathways of cysteine metabolism in MND/ALS. J Neurol Sci. 1994; 124: 59-61.

173. Steventon GB, et al. Xenobiotic metabolism in motor neuron disease. Lancet. 1988: 644-47.

174. Gordon C, et al. Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE). Lancet. 1992; 339: 8784-6.

175. Emory P, et al. Poor sulphoxidation in patients with rheumatoid arthritis. Ann Rheum Dis. 1992; 51(3): 318-20.

176. Bradley H, et al. Sulfate metabolism is abnormal in patients with rheumatoid arthritis: Confirmation by in vivo biochemical findings. J Rheumatol. 1994; 21(7): 1192-6.

177. Perry TL, et al. Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase deficiency. Ann Neural. 1985; 18(4): 482-489.

178. Freitas AJ, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Res. 1996; 738(2): 257-64.

179. Yallapragoda PR, et al. Inhibition of calcium transport by Hg salts in rat cerebellum and cerebral cortex. J Appl Toxicol. 1996; 164(4): 325-30.

180. Chavez E, et al. Mitochondrial calcium release by Hg+2. J Biol Chem. 1988; 263(8): 3582.

181. Szucs, et al. Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol Neurobiol. 1997; 17(3): 273-8.

182. Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.

183. Rossi AD, et al, Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J. 1993; 7: 1507-14.

184. Boadi WY, et al. In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res. 1992; 57(1): 96-106.

185. Boadi WY. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity. Pharmacol. 1992; 116(1): 17-23.

186. Urbach J, et al. Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Reprod Toxicol. 1992; 6(1): 69-75.

187. Karp W, Gale TF, et al. Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters. Environ Res. 1985; 36: 351-358.

188. Karp WB, et al. Correlation of human placental enzymatic activity with tracemetal concentration in placenta. Environ Res. 1977; 13: 470- 477.

189. Boot JH. Effects of SH-blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct. 1995; 20(3): 233-8.

190. Iioka H, et al. The effect of inorganic mercury on placental amino acid transport. Nippon Sanka Fujinka Gakkai Zasshi. 1987; 39(2): 202-6.

191. Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A, et al. Metal-specific memory lymphoctes: Biomarkers of sensitivity in man. Neuroendocrinology Letters. 1999; 20: 289-298.

192. Sterzl I, Prochazkova J, Stejaskal VDM et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.

193. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuroendocrinology Letters. 2004; 25(3): 211-8. http://www.nel.edu/pdf_/25_3/NEL250304A07_Prochazkova_.pdf

194. Clauw DJ. The pathogenesis of chronic pain and fatigue syndromes: Fibromyalgia. Med Hypothesis. 1995; 44: 369-78.

195. Hanson S, Fibromyalgia, glutamate, and mercury. Heavy Metal Bulletin. 1999; 4: 3-6.

196. Kistner A. Quecksilbervergiftung durch amalgam: Diagnose und therapie. ZWR. 1995; 104(5): 412-417.

197. Villegas J, Martinez R, Andres A, Crespo D. Accumulation of mercury in neurosecretory neurons of mice after long-term exposure to oral mercuric chloride. Neurosci Lett. 1999; 271: 93-96.

198. Kozik MB, Gramza G. Histochemical changes in the neurosecretory hypothalic nuclei as a result of an intoxication with mercury compounds. Acta Histochem Suppl. 1980; 22: 367-80.

199. MacDonald EM, Mann AH, Thomas HC. Interferons as mediatorors of psychiatric morbidity. Lancet. 1978: 1175-78.

200. Hickie I, Lloyd A. Are cytokines associated with neuropsychiatric syndrome in humans? Int J Immunopharm. 1995; 4: 285-294.

201. Komaroff AL, Buchwald DS. Chronic fatigue syndrome: An update. Ann Rev Med. 1998; 49: 1-13.

202. Buchwald DS, Wener MH, Kith P. Markers of inflammation and immune activation in CFS. J Rheumatol. 1997; 24: 372-76.

203. Demitrack MA, Dale JK. Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin endocrinol Metabol. 1991; 73:1224-1234.

204. Turnbull AV, Rivier C. Regulation of the HPA axis by cytokines. Brain Behav Immun. 1995; 20: 253-75.

205. Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with Polyglanular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.

206. Sterzl I, Hrda P, Prochazkova J, Bartova J, Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek. 1999; 45(9): 527-31.

207. Saito K. Analysis of a genetic factor of metal allergy-polymorphism of HLA-DR-DO gene. Kokubyo Gakkai Zasschi. 1996; 63: 53-69.

208. Prochazkova J, Ivaskova E, Bartova J, Stejskal VDM. Immunogentic findings in patients with altered tolerance to heavy metals. Eur J Human Genet. 1998; 6: 175.

209. Schwermetallbelastung G. Bei atopischer dermatitis und psoriasis. Biol Med. 1996; 2: 65-68.

210. Godfrey ME. Candida, dysbiosis, and amalgam. J. Adv. Med. 1996; 9(2).

211. Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology. Neuroendocrinology Letters. 1999; 20: 345-358.

212. Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptyl peptidase IV from human placenta. Eur J Biochem. 1982; 126(2): 359-65.

213. Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta. 1978; 82(1-2): 185-92.

214. Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996; 10(6): 435-40.

215. Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993; 44(1): 13-8.

216. Plaitakis A, Constantakakis E. Altered metabolism of excitatory amino acids, N-acetyl-aspartate and N-acetyl-aspartyl-glutamate in amyotrophic lateral sclerosis. Brain Res. 1993; 30(3-4): 381-6.

217. Rothstein JD, Martin LJ, Kuncl RW. Decreased glutamate transport by the brain and spinal cord in ALS. New Engl J Med. 1992; 326: 1464-8.

218. Leigh PN. Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne DB, ed. Neurodegenerative Diseases. WB Saunder Co; 1997: 473-88.

219. Froissard P, et al. Role of glutathione metabolism in the glutamate-induced programmed cell death of neuronal cells. Eur J Pharmacol. 1997; 236(1): 93-99.

220. Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes. Yonsei Med J. 1995; 36(3): 299-305.

221. Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology. 1992; 76(3): 245-56.

222. Albrecht J, Matyja E. Glutamate: A potential mediator of inorganic mercury toxicity. Metab Brain Dis. 1996; 11:175-84.

223. Tirosh O, Sen CK, Roy S, Packer L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death. Neuroscience. 2000; 97(3): 531-41.

224. Folkers K, et al. Biochemical evidence for a deficiency of vitamin B6 in subjects reacting to MSL-Glutamate. Biochem Biophys Res Comm. 1981; 100: 972.

225. Felipo V, et al. L-carnatine increases the affinity of glutamate for quisqualate receptors and prevents glutamate neurotoxicity. Neurochemical Research. 1994; 19(3): 373-377.

226. Akaike A, et al. Protective effects of a vitamin-B12 analog (methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. European J of Pharmacology. 1993; 241(1):1-6.

227. Sutton KG, McRory JE, Guthrie H, Snutch TP. P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A. Nature. 1999; 401(6755): 800-4.

228. Kidd RF. Results of dental amalgam removal and mercury detoxification. Altern Ther Health Med. 2000; 6(4): 49-55.

229. Olanow CW, Arendash GW. Metals and free radicals in neurodegeneration. Curr Opin Neurol. 1994; 7(6): 548-58.

230. Panasiuk J. Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. Przegl Dermatol. 1980; 67(6): 823-9.

231. Barnett JH. Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis. 1990; 46(5): 430-2.

232. Regland B, Zachrisson O, Stejskal V, Gottfries C. Nickel allergy is found in a majority of women with chronic fatigue syndrome and muscle pain–and may be triggered by cigarette smoke and dietary nickel intake. Journal of Chronic Fatigue Syndrome. 2001; 8(1). http://www.melisa.org/pdf/cfs_nickel.pdf

233. Olivieri G, Brack C, Muller-Spahn F, et al. Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000; 74(1): 231-6.

234. Tabner BJ, Turnbull S, El-Agnaf OM, Allsop D. Formation of hydrogen peroxide and hydroxyl radicals from A(beta) and alpha-synuclein as a possible mechanism of cell death in Alzheimer’s disease and Parkinson’s disease. Free Radic Biol Med. 2002; 32(11): 1076-83.

235. Ho PI, Collins SC, et al. Homocysteine potentiates beta-amyloid neurotoxicity: Role of oxidative stress. J Neurochem. 2001; 78(2): 249-53.

236. Overzet K, Gensler TJ, Kim SJ, et al. Small nucleolar RNP scleroderma autoantigens associate with phosphorylated serine/arginine splicing factors during apoptosis. Arthritis Rheum. 2000; 43(6): 1327-36.

237. van Benschoten MM. Acupoint energetics of mercury toxicity and amalgam removal with case studies. American Journal of Acupuncture. 1994; 22(3): 251-262.

238. Schwartz RB, Garada BM, Komaroff AL, Gleit M, Holman BL. Detection of intracranial abnormalities in patients with chronic fatigue syndrome: Comparison of MRI and SPECT. Am J Roentgenol. 1994; 162(4): 935-41.

239. Ichiso M, Salit IE, Abbey SE. Assessment of regional cerebral perfusion by SPECT in CFS. Nucl Med Commun. 1992; 13: 767-72.

240. Patarca-Monero R, Klimas NG, Fletcher MA. Immunotherapy of chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome. 2001; 8(1): 3-37.

241. DeBecker P, De Meirleir K, Joos E, Velkeniers B. DHEA response to I.V. ACTH in patients with CFS. Horm Metab Res. 1999; 31(1): 18-21.

242. De Meirleir K, Bisbal C, Campine I, De Becker, et al. A 37 kDa 1-5A binding protein as a potential biochemical marker for CFS. Am J Med. 2000; 108(2): 99-10.

243. Suhadolnik RJ, Peterson DL, Obrien K, et al. Biochemical evidence for a novel low molecular weight 2-5A-dependent Rnase L in CFS. J Interferon Cytokine Res. 1997; 17(7): 377-85.

244. Chaudhuri A, Watson WS, Pearn J, Behan PO. The symptoms of chronic fatigue syndrome are related to abnormal ion channel function. Med Hypotheses. 2000; 54(1): 59-63.

245. Straus SE, et al. CFS and allergy. J Allergy Clin Immunol. 1988; 81(5): 791-95.

246. Straus SE, et al. Evidence of Epstein-Barr virus infection in CFS. Annals of Internal Med. 1985, 102(1): 7-16.

247. Jones JF, et al. Annals of Internal Med, Evidence for active Epstein-Barr Virus in patients with chronic unexplained illness. Annals of Internal Med. 1985; 102(1): 1-6.

248. Tyler AN. Influenza A virus: Factor in fibromyalgia? Alt Med Rev. 1997, 2(2): 82-86.

249. Teitelbaum J, Bird B. Effective treatment of CFS, report on 64 patients. J Musculoskeletal Pain. 1995; 3(4): 91-100.

250. Behan PO, et al. Effect of high doses of essential fatty acids on postviral fatigue syndrome. Acta Neurol Scand. 1990; 82: 209-216.

251. Abraham GE, Flechas JD. Rationale for the use of magnesium and malic acid in fibromyalgis treatment. Journal of Nutritional Medicine. 1992; 3:40-52.

252. Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001; 35(6): 702-6.

253. Shibata N, Nagai R, Kobayashi M. Morphological evidence for lipid peroxidation and protein glycoxidation in spinal cords from sporadic amyotrophic lateral sclerosis patients. Brain Res. 2001; 917(1): 97-104.

254. Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol. 1999; 9(1):165-86.

255. Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res. 2000; 32(2):115-24.

256. Bridi R, Crossetti FP, Steffen VM, Henriques AT. The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761). Phytother Res. 2001; 15(5): 449-51.

257. Li Y, Liu L, Barger SW, Mrak RE, Griffin WS. Vitamin E suppression of microglial activation is neuroprotective. J Neurosci Res. 2001; 66 (2): 163-70.

258. Doble A. The role of excitotoxicity in neurodegenerative disease: Implications for therapy. Pharmacol Ther. 1999; 81(3):163-221.

259. Urushitani M, Shimohama S. N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+)overload in acute excitotoxic motor neuron death: A mechanism distinct from chronic neurotoxicity after Ca(2+) influx. J Neurosci Res. 2001; 63(5): 377-87.

260. Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol. 1999; 9(1):165-86.

261. Vielhaber S, Kaufmann J, Kunz WS. Effect of Creatine Supplementation on metabolite levels in ALS motor cortices. Exp Neurol. 2001; 172(2): 377-82.

262. Landay AL, Jessop C, Lenette ET. Chronic fatigue syndrome: clinical condition associated with immune activation. Lancet. 1991; 338: 707-12.

263. Caliguri M, Murray C, Buchwald D. Phenotypic and functional deficiency of natural killer cells in patients with CFS. J Immunol. 1987; 139: 3306-13.

264. Barker E, Fujirmura SF, Fadern MB. Immunologic abnormalities associated with CFS. Clin Infect Dis. 1994; 18: 136-41.

265. Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol. 2001; 60(4): 838-46.

266. Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury. J Environ Sci Health B. 2001; 36(5): 687-97.

267. Miyamoto K, Nakanishi H, et al. Involvement of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity. Brain Res. 2001; 901(1-2): 252-8.

268. Anuradha B, Varalakshmi P. Protective role of DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation. Pharmacol Res. 1999; 39(1): 67-80.

269. Urushitani M, Shimohama S. The role of nitric oxide in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2001; 2(2): 71-81.

270. Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: The role of peroxynitrite. Brain Res Brain Res Rev. 1999; 30(2): 153-63.

271. Aoyama K, Matsubara K, Kobayashi S. Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases. Ann Neurol. 2000; 47(4): 524-7.

272. Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol. 2001; 60(4): 838-46.

273. Goldenberg DL. Fibromyalgia, chronic fatigue syndrome, and myofascial pain. Curr Opin Rheumatol. 1996; 8: 113-123.

274. Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med. 1997; 22(1-2): 359-78.

275. McCarty MF. Versatile cytoprotective activity of lipoic acid may reflect its ability to activate signaling intermediates that trigger the heat-shock and phase II responses. Med Hypotheses. 2001; 57(3): 313-7.

276. Whiteman M, Tritschler H, Halliwell B. Protection against peroxynitrite-dependent tyrosine nitration and alpha 1-antiproteinase inactivation by oxidized and reduced lipoic acid. FEBS Lett. 1996; 379(1): 74-6.

277. Patrick L. Mercury toxicity and antioxidants: Part 1: Role of glutathione and alpha-lipoic acid in the treatment of mercury toxicity. Altern Med Rev. 2002; 7(6): 456-71.

278. Klinghardt D, Mercola J. Mercury toxicity and systemic elimination agents. J of Nutritional and Environmental Medicine. 2001; 11: 53-62.

279. Kidd RF. Results of dental amalgam removal and mercury detoxification. Alternative Therapies. 2000; 6(4): 49-55.

280. Chester AC, Levine PH. The natural history of concurrent sick building syndrome and chronic fatigue syndrome. J Psychiatr Res. 1997; 31(1): 51-7.

281. McIntyre R, et al. Should depressive syndromes be reclassified as metabolic syndrome type II? Ann Clin Psychiatry. 2007; 19(4): 257-64. www.naturalstresscare.org/Media/McIntyre_2007.pdf

282. McIntyre RS, Soczynska JK, Kennedy SH, et al. Inflammation, depression and dementia: Are they connected? Neurochem Res. 2007; 32(10): 1749-56.

283. Blaylock R. Are you the victim of hidden allergies? Blaylock Wellness Report. 2007; 4(11).

284. Blaylock R. Food additives: What you eat can kill you. Blaylock Wellness Report. 4(10).

285. Rayssiguier Y, Gueux E, et al. High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006; 19(4): 237-43.

286. Bo S, Durazzo M, Pagano G. et al. Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006; 84(5):1062-9.

287. Guerrero-Romero F, Rodríguez-Morán. Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev. 2006; 22(6): 471-6.

288. Dandona P. Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008; 83(3): 333-42.

289. Vasdev S, Gill V, Singal P. Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007; 49(1): 48-63.

290. Barnes DM. Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005; 19(2): 207-14.

291. Barnes DM, Kircher EA. Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003; 75(2): 368-77.

292. Barnes DM, Hanlon PR, Kircher EA. Heavy metal-induced inhibition of active transport in the rat small intestine in vitro: Interaction with other ions. Comp Biochem Physiol C. 1986; 84(2): 363-8.

293. Iturri SJ, Peña A. Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980; 598(1): 100-14.

Print Friendly, PDF & Email