Depression and Other Neurotransmitter Related Conditions: The Mercury Connection

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Introduction

There are several types of depression and mood disorders, including neurotic depression, manic-depression, postpartum depression, anxious depression, agitated depression/panic attacks, obsessive-compulsive disorder, attention deficit disorder, etc. This review covers all of these disorders to some degree. Prescription and over-the-counter drugs that commonly are a factor in depressive disorders include Accutane, acid blockers, Alprazolam, Ambien, Anabolic steroids, Beta-blockers, birth control pills, butalbital, chemotherapy, digoxin, hormone replacement drugs, pednisone, Quinalone antibiotics, Valium, etc. Thould be taken into account.

According to Dr. Gerald Klerman, based on National Institute of Health studies, there has been a huge increase (over 500 %) in the rate of depression and chronic neurological problems over the last 3 decades. A random sample of Oregon high school students found that over 16% had been diagnosed with depression. According to ECA samples, otherwise healthy people born in recent decades face a 10 fold increase in incidence of major depressive episodes compared to those sampled who were born in earlier decades. Over 6 million Americans over 65 suffer from major depression while another 5 million suffer from depressive symptoms. Every year, at least 230 million prescriptions for antidepressants are filled, making them one of the most prescribed drugs in the United States. The psychiatric industry itself is a $330 billion industry.

Several factors appear to be contributing to this:

  • neurological birth defects and developmental conditions due to increased levels of vaccinations, fetal exposure to alcohol, tobacco smoke, drugs, toxic metals such as lead, mercury, cadmium, etc., other neurotoxic chemicals such as pesticides, nitrates, etc., and other endocrine system/hormonal system disrupting chemicals such as dioxins, phthalates, etc. Studies by the National Academy of Sciences indicate that these affect close to 40% of all children in the U.S., more in some populations than others;
  • changes in dietary habits, resulting in nutrient, vitamin, and mineral deficiencies or imbalances and blood sugar imbalances, and increased consumption of inflammatory excitotoxins, such as aspartame, MSG, and high fructose corn syrup; and
  • stress in family and workplace environments.

Groups of primary care patients aged 18-65 years from 333 randomly chosen public or private clinics throughout the whole country of Poland, totaling 7289, coming for a regular visit were asked to participate in a study of the prevalence of depressive disorders. 71% of the participants were female. All patients filled in the Beck Depression Inventory (BDI). The prevalence of depressive disorders in the whole sample was 23.3%.

The number of people with anxiety disorders is close to the number with mood disorders. The primary types of anxiety disorders are phobias, panic attacks, generalized anxiety disorder (GAD), and obsessive-compulsive disorder (OCD). At least 20 million people are affected at some time by these conditions. Similar large numbers are affected by attention disorders, including attention deficit hyperactive disorder (ADHD), dyslexia, and schizophrenia. The Centers for Disease Control’s new survey shows 5.4 million schoolchildren have been diagnosed with attention-deficit/hyperactivity disorder (AD/HD). That’s 10%. In fact from the years 2003 to 2007, the number of kids between four and 17 with AD/HD jumped by one million, a 22% increase. However, large surveys of elementary level student records found much higher levels—with over 20% of elementary school boys in some areas being treated for ADD. Similar levels of children have been found to have mood or anxiety disorders. At least 4% of adults have also been found to have ADHD symptoms. Studies have found that long-term use of stimulant drugs commonly is not effective in the long run and causes significant adverse neurological and health effects. There are more effective options available to deal with such conditions without such adverse effects, including dealing with the underlying causes and diet, exercise, and supplement options that deal with underlying deficiencies.

Twenty-plus years of research on antidepressants, from the old tricyclics to the newer selective serotonin reuptake inhibitors (SSRIs) show that their benefit is hardly more than what patients get when they take a placebo. Also that they don’t deal with some of the main causes of depression. Long-term increased stress hormones such as cortisol appear to often be a larger factor in depressive conditions than reduced serotonin. In Britain, the agency that assesses which treatments are effective enough for the government to pay for stopped recommending antidepressants as a first-line treatment, especially for mild or moderate depression. A spokesperson for Pfizer, which makes Zoloft, added that the fact that antidepressants “commonly fail to separate from placebo” is “a fact well known by the FDA, academia, and industry.” Antidepressants are significantly more effective than a placebo in patients suffering only from the most severe depression. The serotonin-deficit theory of depression is built on a hypothesis that has little support. Tianeptine, a new drug sold in France and some other countries (but not the U.S.), is as effective as Prozac-like antidepressants that keep the synapses well supplied with serotonin even though the mechanism of the new drug is to lower brain levels of serotonin. “If depression can be equally affected by drugs that increase serotonin and by drugs that decrease it,” says Kirsch, “it’s hard to imagine how the benefits can be due to their chemical activity.” SSRIs often provide temporary improvement in some depressive conditions, but there effects usually don’t last over time and the often cause loss of sex drive and other adverse effects. Exercises, diet modification, including reduction of sweets, and supplementing deficient vitamins and minerals have been found more effective treatments in the long term. Supplements found to often help adrenal fatigue include, licorice extract, Panax ginseng, DHEA, Rhodiola, pantehine, and Eleuthero. Exercise routines found to be helpful include walking, yoga, and pilates. Since 1996, scientific researchers and doctors in clinical practice have been studying the effects of EMPowerplus mineral supplementation program on mental and mood disorders such as bipolar disorder. Results have been very encouraging and significant. Low cellular levels of the omega-3 oil DHA have also been found to be associated with bipolar disorder.

II. Causes of Depression and Anxiety

There appears to be both a psychological/mind basis as well as physical/chemical basis for depression and anxiety. Nutritional deficiencies, environmental factors, methylation deficiencies, hormonal imbalances, and stress clearly can lead to depression and anxiety, but they also facilitate psychological factors. Based on clinical experience, anxiety and hyperventilation and panic attacks appear to often be related to a person burying their feelings about their circumstances. Depression often occurs where a person has suppressed anger, anger turned inward. Chronic anger has been found to be linked to increased risk of recurrent heart attacks and cardiac death. The brain amygdala controls fear and anger and inflammatory conditions such as excess glutamate or stress have been found to reduce its control and to increase anger or fear. Other heart risks have also been linked to depression, anxiety, repressed anger and isolation or infrequent social interactions. These factors, which lead to increased risks of heart disease, have been correlated with elevated cholesterol, blood pressure, variable heart rate plus increased arterial thickness and plaque accumulation. Studies estimate that 20 to 40 percent of all sudden cardiac deaths will be triggered by some type of acute emotional stressor. Dealing with nutritional deficiencies and environmental factors, along with being honest with yourself, acknowledging anger or feelings rather than assigning blame, and doing what makes you feel good usually leads to reduced depression or anxiety.

The levels of brain neurotransmitters such as dopamine, norepinephrine, and serotonin, appear to be major factors in controlling moods, and appear to be affected by lifestyle, diet, philosophy, and environmental factors. Some are more susceptible to depression than others, and thus more affected by diet and environmental factors.

Chronic or acute brain inflammation appears to be a primary factor in depression. 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 depressive disorders and other 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. Overexposure to heavy metals like lead, mercury, copper, and zinc has been shown to induce anxiety or depression. Accumulation of mercury in the brain limbic system with resulting oxidative stress and inflammation has been found to commonly be a factor in depression.

Studies have found that oxidative stress from reactive oxygen species (such as caused by mercury and toxic metals) causes increased insulin resistance, whereas reducing reactive oxygen species lowers insulin resistance. Insulin resistance has been found to be a significant factor in metabolic syndrome, cognitive decline, cardiovascular disease, depression, cancer, etc. Mercury and cadmium inhibit magnesium and zinc levels as well as inhibiting glucose transfer. Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions. These are additional mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance and conditions such as diabetes, depression, etc. As documented later, for those who have several amalgam fillings, replacement of the amalgam greatly lowers mercury and toxic metal exposure, lowers reactive oxygen species and related damage, and brings significant improvement in the health of people with conditions caused by oxidative damage and insulin resistance. It has also been documented that supplementation with antioxidants such as green tea extract, bilberries, curcumin, N-acetyl-cysteine, etc. and supplements such as DHEA, Goat’s Rue, cinnamon, quercetin, and vanadyl sulfate reduces inflammatory cytokine effects and lowers insulin resistance.

Many studies have found toxic metal exposure, such as mercury, lead, cadmium, and manganese, commonly causes depression and other mood and neurological disorders. Young adults with higher blood lead levels are more likely to have major depressive disorder (MDD) or panic disorder, even if they have exposure to lead levels generally considered safe. The brain has elaborate protective mechanisms for regulating neurotransmitters such as glutamate, which is the most abundant of all neurotransmitters. When these protective regulatory mechanisms are damaged or affected, chronic neurological conditions such as Parkinson’s can result. 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 toxicty 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. Excess extracellular glutamate has been found to be strongly related to neurological conditions such as Alzheimer’s, Parkinson’s, ALS, OCD, depression, etc. Psychotropic drugs that were thought to alleviate depression by raising monoamine levels have now been found to work by inhibiting glutamate receptors, thus reducing inflammation. Hypericin, the active ingredient in St John’s Wort used to treat depression also, has been found to inhibit the release of glutamate into the brain and protect against excitotoxicity.

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. Microglia are the main immune cells in the brain. 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. This has been called immunoexcitotoxicity, which has been demonstrated to be a significant factor in many chronic psychiatric disorders including schizophrenia, PTSD, autism, suicides. Inflammation also disrupts brain neurotransmitters resulting in reduced levels of serotonin, dopamine, and norepinephrine. Some of the main causes of such disturbances that have been documented include vaccines, mercury, aluminum, other toxic metals, MSG, aspartame, other food additives, etc.

Studies have shown that an increase in the inflammatory biomarker CRP(C-reactive protein) predicts the onset of depression in elderly people who had no prior history of depression, and that depression is also linked with high levels of other inflammatory biomarkers—such as IL-6. Inflammation also causes reduced levels and/or reduced effectiveness of the main brain-calming neurotransmitter. It is the balance between brain excitatory neurotransmitters like Glutamate and the calming neurotransmitters like GABA that allows normal functioning, and imbalances lead to psychiatric disorders.

Excitotoxic exposures and food additives are extremely common and affect most children, and can have major impacts on the brain over time, resulting in faulty brain-wiring, magnified aggressiveness, rage reactions, obsessions, panic attacks, and other neurological and mood disorders. Studies have found that food-based excitotoxins can raise brain glutamate levels by as much as a factor of 50, causing inflammation and resulting in damage to the brain and brain regulatory mechanisms over time. This is especially true of the prefrontal cortex which controls judgment, regulates risk-taking, and suppresses socially inappropriate behavior. A study found that those with bipolar disorder have much lower levels than normal of the omega-3 DHA in the orbitofrontal cortex area of the brain which regulates behavior. Those most susceptible to such excitotoxic effects are babies and the elderly and is especially damaging for those who suffer from reactive hypoglycemia. Studies have found that eliminating such food-based excitotoxins in school diets resulted in greatly reduced behavioral problems and inattention problems. The majority of the body’s immune system is found in the digestive system, and inflammatory bowel diseases and food intolerances, which induce inflammation in the intestines, have also been found to be factors in brain inflammation and related psychiatric disorders.

It had been thought that low serotonin levels in the brain were a major factor in depression because inflammatory disorders (or infections) cause measured serotonin levels in the blood to fall significantly. However, further studies have found that inflammation activates microglia, which metabolize the serotonin precursor tryptophan into the highly brain-toxic excitoxin quinolinic acid, while also reducing the number of astrocytes, which metabolize tryptophan into a brain protective chemical kynurenine. This imbalance has been found to be associated with psychiatric conditions such as depression and anxiety. It has also been found that those with depression or anxiety disorders have low levels of the brain-protective substance/brain growth stimulator. This is supplied by the astrocytes, which have been seen to be decreased in inflammatory conditions such as depression. Seratonin, which is also decreased, stimulates the release of BDGF. The mineral zinc has also been found to increase BDGF as well as the protective substance BDNF, and to reduce excitotoxicity, though it’s also possible to get too much zinc. Zinc deficiency can cause conditions such as depression, and zinc supplementation can improve depression in such circumstances. A zinc status can be determined through hair test or red blood cell test.

Hormone imbalance has been found to be a common factor in depression and learning disabilities and thyroid imbalances have also been found to cause depression and ADHD. Mercury and other endocrine disrupting chemicals such as phthalates have been found to commonly cause hypothyroidism. Imbalances in DHEA and cortisol may underlie depression, particularly when stress and obesity are present. Estrogen imbalances in post-menapausal women, low testosterone levels in some men, low DHEA levels, and hypothyroid conditions have been found to be common factors in depression. Subclinical hypothyroidism and/or the presence of thyroid peroxidase antibodies (TPOAb) has been found to be associated with subfertility, infertility, spontaneous abortion, placental abruption, preterm delivery, gestational hypertension, preeclampsia, postpartum thyroid dysfunction, depression (including postpartum depression), and impaired cognitive and psychomotor child development. It is recommended to suspect thyroid pathology if such conditions are present.

Most studies support a relationship between thyroid state and cognition, particularly slowed information processing speed, reduced efficiency in executive functions, and poor learning. Furthermore, hypo-thyroidism is associated with an increased susceptibility to depression and reductions in health-related quality of life. Controlled studies suggest that cognitive and mood symptoms improve with thyroid treatment, though the data are limited by diverse treatment methodologies. Functional neuroimaging data provide support for the mood and cognitive findings and treatment reversibility for both overt and subclincial hypothoidism. 94 patients with subclinical hypothyroidism and a control group were evaluated to determine the prevalence of psychiatric disorders. The prevalence of depressive symptoms based on Beck’s Scale among subclinical hypothyroidism patients was about 2.3 times higher than among controls (45.6% vs 20.9%, p =0.006). Anxiety symptoms were also more frequent in the hypothyroid group.

Postpartum thyroiditis (PPT) is the occurrence, in the postpartum period, of transient hyperthyroidism and/or transient hypothyroidism, with most women returning to the euthyroid state by 1 year postpartum. However PPT frequently reoccurs in subsequent pregnancies and approximately 25% of women with a history of PPT will develop permanent hypothyroidism in the ensuing 10 years. The mean prevalence of PPT in 2 studies was 7.5%. Postpartum thyroiditis is an autoimmune disorder, and thyroid antibody-positive women in the first trimester have a 33% to 50% chance of developing thyroiditis in the postpartum period. There was a 70% chance of developing recurrent PPT after a first attack, and a 25% risk even in women who were only anti-TPO positive without thyroid dysfunction during the first postpartum period. For this group of women with PPT, 46% had postpartum depression in one or more pregnancies.

In a study of effects of hypothyroid or thyroiditis during pregnancy, infants of women with hypothyroxinemia at 12 weeks gestation had significantly lower scores on the Neonatal Behavioral Assessment Scale orientation index compared with normal subjects. Regression analysis showed that first-trimester maternal free thyroid hormone was a significant predictor of orientation scores. This study confirmed that maternal hypothyroxinemia constitutes a serious risk factor for neurodevelopmental difficulties that can be identified in neonates as young as 3 weeks of age. Because of such evidence, in November 2002, the American Association of Clinical Endocrinologists (AACE) recommended screening all women considering conception and/or all pregnant women in the first trimester for thyroid dysfunction. For a group of women with PPT, 46% had postpartum depression in one or more pregnancies.

As will be shown, there is considerable evidence that depression/neurological problems can be caused by many physiological problems related to past toxic exposures or combinations of these. Where physiological problems are contributing factors, determination of the underlying cause from assessing the persons past medical history, diet, blood tests, hair tests, etc. can be useful to identifying and correcting any nutritional deficiencies or imbalances or identifying other problems to be dealt with. There is considerable evidence mercury exposure is among the most common significant exposures that commonly cause such effects, although many are also exposed to lead, arsenic, and pesticides that have similar effects and effects are synergistic or cumulative.

III. Mercury Exposure Levels from Amalgam and Other Sources

Amalgam fillings have been documented to leak significant levels of mercury continuously due to high vapor pressure of mercury and galvanic action between mixed metals in the mouth. The average person with several fillings gets significant exposure of mercury daily, much more than from any other source and more than that prescribed by U.S. Government health guidelines. Mercury in pregnant women is also documented to cross the placenta and accumulate in the fetus to levels higher than in the mother. Since mercury from amalgam fillings of a mother is also transmitted to nursing infants in significant amounts, mercury from their mom’s dental fillings has been found to be the largest source of mercury to the fetus and a significant source of mercury in infants, which has produced developmental problems that affect children later in life. Young children have been receiving significant levels of mercury (thimerasol which is used as a preservative in vaccines) and large numbers have been found to be significantly adversely affected because of receiving larger numbers of vaccinations, especially at very early ages before the blood-brain barrier matures. People also get significant prenatal and postnatal exposures to other toxic metals such as lead, arsenic, cadmium, aluminum, etc. which have also been found to commonly cause significant neurological effects. The top 3 toxic substances affecting large numbers of people in the U.S. adversely according to EPA/ATSDR are mercury, lead, and arsenic. A 2009 study found that inorganic mercury levels in people have been increasing in recent years. It used data from the U.S. Centers for Disease Control.

Prevention’s National Health Nutrition Examination Survey (NHANES) found that, while inorganic mercury was detected in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006. Surveys in all states using hair tests have found dangerous levels of mercury in an average of 22 % of the population, with over 30% in some states like Florida and New York. A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings (more mercury exposure) have significantly higher levels of chronic health conditions. The conditions where the number of dental amalgam surfaces were most highly correlated with disease incidence were MS, epilepsy, migraines, mental disorders, diseases of the nervous system, disorders of the thyroid gland, cancer, and infectious diseases.

IV. Toxic and Immune Reactive Effects of Mercury.

Mercury is neurotoxic (kills or damages brain and nerve cells); generates high levels of reactive oxygen species (ROS) and oxidative stress, depletes gluatathione and thiols—causing increased neurotoxicity from interactions of ROS, glutamate, and dopamine; kills or inhibits production of brain tubulin cells; inhibits production of neurotransmitters by inhibiting calcium-dependent neurotransmitter release, dihydroteridine reductase, nitric oxide synthase; blocks neurotransmitter amino acids; and effects phenylalanine, tyrosine and tryptophan transport to neurons. Toxic metals as well as genetic factors commonly cause systemic methylation deficiencies, which are documented to commonly be a factor in chronic conditions, such as depression, autism, etc.

Numerous studies have found long-term chronic low doses of mercury cause neurological, memory, behavior, sleep, and mood problems. Neurological problems are among the most common and serious effects of mercury, and include memory loss, moodiness, depression, anger and sudden bursts of anger/rage, self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or resist obsessions or compulsions, etc. Many studies of patients with major neurological diseases have found evidence amalgam fillings may play a major role in development of conditions such as depression, schizophrenia, memory problems, and other more serious neurological diseases such as MS, ALS, Parkinson’s, and Alzheimer’s.

Some factors that have been documented in depression are low serotonin levels, abnormal glucose tolerance (hypoglycemia), and low folate levels, which mercury has also been found to cause. Occupational exposure to mercury has been documented to cause depression and anxiety. Acute exposure to mercury vapor has been found to cause chronic depression, anxiety, and obsessive-compulsive. One mechanism by which mercury has been found to be a factor in aggressiveness and violence is its documented inhibition of the brain transmitter acetylcholinesterase. Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior.

Mercury (and other toxic metals) has been found to accumulate in the pineal gland and reduce melatonin levels, which is thought to be a significant factor in mercury’s toxic effects. Melatonin has found to have a significant protective action against methyl mercury toxicity, likely from antioxidative effect of melatonin on the MMC induced neurotoxicity. Disrupted sleep from low melatonin, or Seasonal Affective Disorder with excessive melatonin production, can result in depression. Elatonin is important in regulating mood and improving sleep and increasing quality of life by regulating your body’s circadian rhythms—while scientific evidence indicates that it has helpful anti-inflammatory and antioxidant properties that can support your heart, too.

There is also evidence that mercury affects neurotransmitter levels which have effects on conditions such as depression, mood disorders, ADHD, etc. There is evidence that mercury can block the dopamine-hydroxylase(DBH) enzyme. This enzyme synthesizes noradrenaline, and low noradrenaline can cause fatigue and depression. Mercury molecules can block all copper-catalysed dithiolane oxidases, such as coproporphyrin oxidase and DBH. Mercury and other toxic metals have been found to accumulate in the pineal gland and reduce melatonin levels, which is thought to be a significant factor in mercury’s toxic effects. There is evidence that mercury can block the dopamine-beta-hydroxylase (DBH) enzyme. DBH is used to make the noradrenaline neurotransmitter and low noradrenaline can cause fatigue and depression. Mercury molecules can block all copper catalyzed dithiolane oxidases, such as coproporphyrin oxidase and DBH.

Workers occupationally exposed to mercury at levels within guidelines have been found to have impairment of lytic activity of neutrophils and reduced ability of neutraphils to kill invaders, such as candida. The balance of yeasts found in the intestine can be a factor in neurological conditions such as depression. Evidence suggests Candida albicans may activate depressive symptoms and fatigue by promoting ethanol production, a known central nervous system depressant. Behavior changes are also associated with Candida’s inherent toxin—canditoxin and/or by its tendency to compete with the host organism for essential dietary nutrients. Immune Th1 cells inhibit candida by cytokine related activation of macrophages and neutrophils. Development of Th2 type immune responses deactivates such defenses. Mercury inhibits macrophage and neutraphil defense against candida by its effects on Th1 and Th2 cytokine effects. Candida overgrowth results in production of the highly toxic canditoxin and ethanol, which are known to cause fatigue, toxicity, and depressive symptoms.

Mercury causes decreased lithium levels, which is a factor in neurological diseases such as depression and Alzheimer’s. Lithium protects brain cells against excess glutamate and calcium, and low levels cause abnormal brain cell balance and neurological disturbances. Medical texts on neurology point out that chronic mercurialism is often not recognized by diagnosticians and misdiagnosed as dementia or neurosis or functional psychosis or just “nerves.” Early manifestations are likely to be subtle and diagnosis difficult: insomnia, nervousness, mild tremor, impaired judgment and coordination, decreased mental efficiency, emotional lability, headache, fatigue, loss of sexual drive, depression, etc. are often mistakenly ascribed to psychogenic causes. Very high levels of mercury are found in brain memory areas such as the cerebral cortex and hippocampus of patients with diseases with memory related symptoms.

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 neurological conditions, such as autism, schizophrenia, manic-depressive, ADD, and depression. For example mercury has been found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein. Studies involving a large sample schizophrenic or autistic patients found that over 90 % of those tested had high levels of the milk protein beta-casomorphin-7 in their blood and urine and defective enzymatic processes for digesting milk protein. Similar findings have been confirmed for ADD and mania patients. Elimination of milk products from the diet has been found to improve these conditions in large numbers of patients. Such populations have also been found to have high levels of mercury and to recover after mercury detoxification. As mercury levels are reduced the protein binding is reduced in the enzymatic process occurs. Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes and neurotransmitter amino acids, enzymatic processes involving vitamins B6 and B12, effects on the cytochrome-C energy processes, along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, chromium, and lithium.

When a pathological state exists, the body’s finely balanced symbiosis may be damaged and cease to function normally. Beneficial essential bacteria may be damaged, causing the malabsorption of critical vitamins and minerals. If the damage is extensive and/or long lasting, pathogens including pathogenic yeast and gram negative bacilli will begin to fill the vacuum left by the healthy bacteria. The metabolism of these pathogens is different and foods are no longer broken down in the same way. Proteins that previously would be broken down to their constituent amino acids are only partially digested, leaving long chains of amino acids called peptides. Our entire body is built from proteins, which are themselves built from chains of peptides. Certain peptides are extremely bioactive (ie., they interact strongly with other proteins in the body). Mercury and toxic metals cause dysbiosis and inhibit the function of the enzymes needed to digest gluten and casein, resulting in peptides in the blood which have significant neurological effects including depression, anxiety, and schizophrenia. A side effect of dysbiosis (incorrect gut microorganisms) is that the gut becomes leaky (ie., it passes larger molecules than would normally be the case). Thus peptides, which should normally be broken down to amino acids, leave the gut and enter the blood stream intact, where they are delivered to other organs. Casein and Gluten proteins and mixture of proteins common in many foods break down to form very potent opio-peptides when acted on by certain pathogenic bacteria. These peptides have a narcotic action and act on opiate receptors in the brain, triggering major changes in brain function including depression, anxiety, schizophrenia, etc. Certain pathogens, more plentiful during dysbiosis, have been found to methylate mercury to its organic form, which is more readily taken up by the blood and redistributed. Taking antibiotics is another cause of such dysbiosis.

Studies have shown a significant association between hypothyrodism and mood disorders, such as depression. Mercury from dental amalgam has been documented to cause hypothyroidism. The majority of patients tested with hypothyroidism or thyroiditis and treated with dental amalgam replacement significantly improved after replacement.

Numerous studies have found long term chronic low doses of mercury cause neurological, memory, behavior, sleep, and mood problems. Neurological effects have been documented at very low levels of exposure (urine Hg< 4 ug/L), levels commonly received by those with amalgam fillings. One of the studies at a German University assessed 20,000 people. There is also evidence that fetal or infant exposure causes delayed neurotoxicity evidenced in serious effect at middle age. Studies of groups of patients with amalgam fillings found significantly more neurological, memory, mood, and behavioral problems than the control groups. Increased mercury levels from amalgam are documented to cause increased neurological problems related to lowered levels of neurotransmitters dopamine, serotonin, norepinephrine, and acetylcholinesterase. The reduced neurotransmitter levels in those with amalgam appear to be a factor encouraging smoking since nicotine increases these neurotransmitter levels, and a much higher percentage of those with amalgam smoke than in those without amalgam had reduced levels.

Based on thousands of clinically-followed cases by doctors, replacement of amalgam fillings resulted in the cure or significant improvement in the majority of cases for: depression, schizophrenia, insomnia, anger, anxiety & mental confusion, and memory disorders. For example, in a study of amalgam replacement for 56 persons who suffered from chronic depression, 16 had the condition eliminated and 34 had significant improvement after a year or 4 years.

One of the most common causes of depression and mood disorders has been documented to be past toxic exposures such as mercury or pesticides, and the majority treated for these at clinics that deal with such conditions have either recovered or shown significant improvement. Amalgam dental fillings have been found the most common source of such toxic exposures, with mercury thimerosal from vaccinations also affecting millions of children. Many doctors treating depression and mood disorder conditions related to toxic exposures also usually recommend supplementing the deficient essential minerals that mercury affects by affecting cell membrane permeability and blocking cellular enzymatic processes, often obtaining a hair element test to determine imbalances and needs. The body requires adequate, but not excessive, amounts of trace minerals and nutrients for proper functioning. Under certain conditions, excesses or deficiencies of many of these elements can set off symptoms of depression. Subnormal levels of zinc, for example, are associated with treatment resistant depression. And deficiencies of magnesium can provoke a wide range of psychiatric symptoms related to depression, ranging from apathy to psychosis. Research on manic patients, on the other hand, has revealed elevated vanadium in the hair, significantly higher levels than those measured in both a control group and a group of recovered manic patients.

V. The Danger of Vaccinations

Chronic over activation of the immune system has been found to be a major factor in neurological and cardiovascular conditions. Immune adjuvants in vaccines including aluminum, mercury, special lipids, and even MSG in some cause activation of the immune system which can last for months. This causes inflammation of the brain that is magnified by each additional vaccination with more immune adjuvants. The high number of vaccinations in a short period of time has been found to be a major cause of autism spectrum and other inflammatory conditions in children and also to be major factors in inflammatory conditions of older adults, such as depression, Alzheimer’s, Parkinson’s, etc. Flu vaccinations in those over 55 years of age have been found to increase the risk of Alzheimer’s by over 500%, along with increased risk of major depression.

VI. Treatment of Depression

Anyone with depression should be examined and tested for toxic metal exposure or exposures to other toxics. Detoxification should be carried out as appropriate. Those with several amalgam fillings or metal crowns over amalgams are getting high exposures of extremely toxic substances that are highly inflammatory so should have the problematic dental work replaced. Everyone should also be checked for problematic root-canal teeth and jawbone cavitations, which likewise are highly inflammatory and can have major impacts on the immune system and health. Reducing glutamate levels and blocking glutamate receptors can significantly improve depression.

Diet and lifestyle are important factors in preventing or controlling depression. One should avoid alcohol, sugar, caffeine, and inflammatory substances, such as MSG, aspartame, high-fructose corn syrup, fluoride, pesticides, aluminum in foods, mercury fillings, most vaccinations (esp. flu vac.), etc. Stress causes increased stress hormones and inflammation, which can be major factors in depression and anxiety disorders. Reduce stress and get regular exercise. Yoga and meditation have been found to be helpful for many. Studies have found that dietary choices play a major role in psychological wellbeing, so proper diet is important. Behavioral problems and criminal behavior are correlated to toxic or excitotoxic exposures and diet choices. Properly formulated nutritional supplements and diet modification have been found to be effective in treating ADHD, depression, and anxiety disorders.

Studies and clinical experience have found that diet plays a role in depression and diet measures commonly avoid, cure, or significantly improve depression. B Vitamins and magnesium deficiencies have been found to be factors in depression and anxiety. Supplementation to assure proper levels is beneficial in treatment. Many people, particularly women over 65, have B-12 deficiencies and respond dramatically to injections of the vitamin. All B vitamins can boost mood; they work by facilitating neurotransmitter function. B vitamins are critical for preventing other maladies, including heart disease, cancer, and Alzheimer’s.

Suggested Dosage:
Take at least 800 micrograms of folate, 1,000 mcg of B-12, and 25 to 50 milligrams of B-6. A B-complex vitamin should do the trick, says Hyman, and if you’re depressed, take more. Take them in combination because otherwise one can mask another B vitamin deficiency

The supplement 5-HTP has been shown by many studies and clinical experience to often be effective in treating or controlling depression. Double blind studies have found 5-HTP to be as effective as SSRIs and other types of antidepressants at treating depression. Tryptophan likewise has been found beneficial in some with depression. However, studies have also cast doubt on serotonin levels as the main cause in depression and found both 5-HTP and SSRIs have limited effect on many with depression. SSRIs appear to be attempting to suppress symptoms related to one type of imbalance found in many with depression rather than the underlying causes.

SAMe (400-1600 mg) and Inositol have been found to be effective in treating depression and anxiety with effectiveness at least as much as pharmaceutical antidepressants and much less adverse effects. SAMe is an amino acid combination produced by humans, animals, and plants. Supplements come from a synthetic version produced in a lab that has shown a lot of promise in European studies. It may affect the synthesis of neurotransmitters, but it has fewer side effects than 5-HTP and fewer drug interactions than Saint-John’s Wort. Dosage can range from 400 to 1,200 mg a day, although high doses can cause jitteriness and insomnia. Risks: People with bipolar disorder shouldn’t use it without supervision because it can trigger mania.

Inositol has been found to be effective for treating OCD, panic disorders, and bipolar depression, with effectiveness at least as much as SSRIs and less adverse effects. St. John’s Wort (300 mg x 3) also has been found effective for many and is one of the best-known remedies. It is best for mild to moderate depression. Suggested Dosage: Start on a dose of 300 mg (standardized to 0.3 percent hypericin extract) two to three times a day, depending on severity of depression; it can take three weeks for benefits to show. Risks: It may interfere with up to half of all drugs, prescription and over-the-counter.

Amino acids are the building blocks of neurotransmitters; 5-HTP is the most popular. Taking it can elevate mood in cases of depression, anxiety, and panic attacks, and relieve insomnia. 5-HTP increases production of the neurotransmitter serotonin. Suggested Dosage: Start with a low dose, 50 mg two to three times a day; after two weeks, increase the dose to 100 mg three times a day. Risks: Mild nausea or diarrhea. Before starting, get off antidepressants (under a doctor’s supervision); the combination can produce an overload of serotonin. Tyrosine is another amino acid found to often be useful in overcoming depression.

Lower levels of fish oil (EPA) have been found to be significantly related to depression. Elderly people have been found to be of special risk regarding depression. Studies have found higher levels of EPA to be associated with lower likelihood of depression or dementia in the elderly. Theoflavins from black or green tea and curcumin (turmeric) have also been found to be significantly effective against inflammation, which is a major factor in depression. Poor digestion results in poor mineral and nutrient absorption and is a factor in many chronic conditions. Digestive problems often increase with aging, due to reductions in digestive enzyme production and availability as well as increased proliferation of pathogenic organisms. Supplementation with digestive enzymes and probiotics often significantly improves digestion and improves digestive related conditions. Adrenal fatigue and long-term increased stress hormones, such as cortisol, have been found to be common factors in depressive disorders. Prescription hydrocortisone can help in the short term, but supplements found to often help adrenal fatigue include: licorice extract, Panax ginseng, DHEA, Rhodiola, pantehine, and Eleuthero. Exercise routines found to be helpful with depressive disorders include walking, yoga, and Pilates. Deep breathing exercises and meditation have also been found to be beneficial in alleviation of depressive disorders.

Hypothyroidism is also often a factor in depressive conditions, and treatments such as mercury detoxification and supplements such as iodine, zinc, copper, selenium, tyrosine, vitamins C, E, B12, and Ashwagandha extract are often helpful when this is a factor.

Birth control pills and artificial hormone replacement drugs can deplete nutrients such as vitamin B6 and create estrogen/progestin imbalances, which can be a factor in depression. Supplementing with Vitamin C, multivitamin B complex, magnesium, iodine, and tyrosine have been found to be helpful in this situation.

Essential fatty acids (EPA/DHA) benefits are among the best documented. The reason they’re so effective is EFAs are part of every cell membrane, and if those membranes aren’t functioning well, then neither is your brain. Suggested Dosage: For depression, take at least 2,000 to 4,000 mg of fish oil a day (should be purified or distilled so it’s free of heavy metals). Risks: Very safe, albeit unstable. Since it can oxidize in your body, take it along with other antioxidants, like natural vitamin E (400 IUs a day).

DHEA is a hormone marketed in Europe specifically for postmenopausal depression, though it may be helpful for other forms as well. It has been used in conjunction with estrogen to treat hot flashes. Suggested Dosage:10 to 200 mg a day. Risks: Any hormonal supplement not properly monitored has the potential to increase cancer risk.

Rhodiola rosea is considered an adaptogen, which means it can increase your resistance to a variety of stressors. It may be good for mild to moderately depressed patients. Suggested Dosage: Take 100 to 200 mg three times a day, standardized to 3 percent rosavin. Risks: More than 1,500 mg a day can cause irritability or insomnia.

Other nutrients found to cause depression when low or to usually be low in depression patients or to be effective additions in treating depression include: ginkgo biloba, DHEA, natural progesterone, pregnenolone, DMAE, L-Carnitine, NADH, Phenylalanine, Folic Acid, Vit B12 (cobalamine), B6, other B vitamins, choline, vit D, vit C, potassium, and testosterone in men over 40. A product that contains several of these nutrients is Happiness 1-2-3 (vit B complex, magnesium, St.John’s Wort, L-Theanine, 5-HTP, magnolia). Other companies referenced here have similar combinations. Anxiety disorders include panic disorder, OCD, PTSD, phobias, and general anxiety disorder. As previously noted, anxiety or panic disorders may be related to burying feelings. Panic disorder is characterized by repeated episodes of intense fear and affects 3 to 6 million. Obsessive-Compulsive Disorder (OCD) is characterized by anxious thoughts and uncontrollable ritualistic behavior. Some studies have suggested OCD patients usually have high glutamate levels, which overexcites areas of the brain. Post-Traumatic Stress Disorder is a debilitating illness resulting from a traumatic event or events. It affects a large number of people. Phobias are irrational fears of things or situations and affect over 10% of the population.

Generalized Anxiety Disorder (GAD) is chronic, daily worrying about health, finances, work, family, etc. Stress is a psychological and physical response to the demands of daily life that exceed the person’s ability to cope successfully. Stress can have physical effects; prolonged stress can have debilitating effects. Two conventional non-pharmaceutical treatments for anxiety are behavioral therapy (breathing techniques, exposure therapy, etc.) and cognitive therapy (modification of thinking patterns).

As previously note, environmental toxins can be a factor in causing nutritional deficiencies, imbalances, and inflammation related to anxiety disorders and reductions in exposures have been found to be beneficial. Hypoglycemia may be a factor in some anxiety disorders—eat more frequent small quantities including protein, nuts, etc. Many are adversely affected by stimulants, such as caffeine. Irregular or insufficient sleep patterns can be a significant factor. Regular exercise is generally beneficial in anxiety disorders. Massage therapy, including aromatherapy is often helpful, along with meditation and deep breathing exercises. Music, yoga, muscle relaxation techniques, biofeedback, etc. are also often helpful.

Deficiency of B vitamins and magnesium has been found to be common factors in anxiety disorders. Taking fish oil is a commonly used, helpful treatment for anxiety in Europe and is very successful for fighting fatigue, etc. Theanine (green tea extract) is calming and lowers blood pressure.

Ginseng has been found effective for many post-menapausal women’s anxiety, fatigue, and depression. Reishi has helped some. A product with several of these nutrients is Calming Balance (vit B complex, magnesium, L-Theanine, Magnolia extract).

Mercury impairs alfa-adrenergic receptors, astrocytic dopamine uptake, and serotonergic 5-HT2 receptor. The last one is stimulated by cocaine and LSD, so at least those drugs may be abused more due to mercury. We can remember that PhD Alfred Stock, leading early century mercury/chelator chemist stated that only cocaine was able to reverse his mental impairments form mercury, which as a chemist was easily available, and it was also legal at the time yet, in the early century.

Many of my patients reported the lifting of depression, anxiety, moodiness within a very short time of the total mercury decontamination of their mouths. I do not know the mechanism for that, and I am reporting this point so that those able to study the link between psychiatric illness and mercury would tell me one day what the mechanism is. The question here is that mercury, though out of the mouth, is not out of the brain in such a short time (two weeks) so, could these psychiatric illnesses be caused by the galvanic currents alone? I do not know. Virtually 100% of the dozens of patients I’ve had suffering depression improve within two weeks. One patient, who was depressed before amalgam removal, told me today that she now has a positive attitude to life that she did not have before, and that she feels like a child!

Kindest regards.

Hesham El-Essawy

(This was mostly snipped from a much larger paper with over 3000 medical study references regarding common toxic exposures to mercury that are affecting large numbers of people with neurological effects.)

References

  1. Mossner R, Mikova O, Koutsilieri E, et al. Consensus paper of the WFSBP Task Force on Biological Markers. World Journal of Biological Psychiatry. 2007; 8(3): 141-174.
  2. Wojnar M, Nawacka-Pawlaczyk D, Urbaski R, Cwikliska-Jurkowska M, Rybakowski J. The study of the prevalence of depressive disorders in primary care patients in Poland. Wiad Lek. 2007; 60(3-4):109-13.
  3. Zárate A, Basurto L, Hernández M. Thyroid malfunction in women. Ginecol Obstet Mex. 2001 May; 69: 200-5.
  4. Wier FA, Farley CL. Clinical controversies in screening women for thyroid disorders during pregnancy. J Midwifery Women’s Health. 2006 May-Jun; 51(3):152-8.
  5. Stagnaro-Green. A postpartum thyroiditis. Best Pract Res Clin Endocrinol Metab. 2004 Jun; 182: 303-16.
  6. Stagnaro-Green A. Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab Clin North Am. 2000 Jun; 29(2): 417-30.
  7. Harris B. Postpartum depression and thyroid antibody status. Thyroid. 1999 Jul; 9(7): 699-703.
  8. Kooistra L, Crawford S, van Baar AL, Brouwers EP, Pop VJ. Neonatal effects of maternal hypothyroxinemia during early pregnancy. Pediatrics. 2006 Jan; 117(1):161-7.
  9. Davis JD, Tremont G. Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrine. 2007 Mar; 32(1): 49-65.
  10. Almeida C, Brasil MA, Costa AJ et al. Subclinical hypothyroidism: Psychiatric disorders and symptoms. Rev Bras Psiquiatr. 2007 Jun; 29(2):157-9.
  11. Engel SM, Miodovnik A, Canfield RL, et al. Prenatal phthalate exposure is associated with childhood behavior and executive functioning. Environmental Health Perspective. 2010 Apr; 118(4): 565-71.
  12. S.Hussain 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 May; 32(3): 395-409.
  13. Tan S, et al. Oxidative stress induces programmed cell death in neuronal cells. J Neurochem. 1998, 71(1): 95-105.
  14. Bains, JS et al. Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death. Brain Res Rev. 1999; 25(3): 335-58.
  15. Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998 Sept; 71: S37-9.
  16. Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.
  17. Pocernich CB, Cardin AL, Racine CL, Lauderback CM, Allan Butterfield D. 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 Aug; 39(2):141-9.
  18. Insulin resistance: The surprising cause behind this highly destructive process. Vitamin Research News. 2008; 22(6).
  19. Houstis N, Rosen ED, Lander ES. Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature. 2006, Apr 13; 440(7086): 944-8.
  20. Meigs JB, Larson MG, et al. Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: The Framingham Offspring Study. 2007, Oct; 30(10): 2539-35.
  21. Cohen S. The 24 Hour Pharmacist. Rodale Books, 2007.
  22. Horrocks LA, Yeo YK. Health benefits of docosahexaenoic acid (DHA). Pharmacol Res. 1999; 40(3):211-25.
  23. McNamara RK, et al. DHA levels in people with bipolar disorder. Psychiatry Res. 2008; 160: 285-299.
  24. Hibbeln JR, et al. Do plasma polyunsaturates predict hostility and violence? World Rev Nutr Diet. 1996; 82:175-86.
  25. Kirby A, et al. Improved behavior and attention associated with higher levels of cellular omega-3 levels. Res Dev Disabl. 2010; 31: 731-742.
  26. Coklin SM, et al. Excess omega-6 oils correlated to depressive disorders. Psychosom Med. 2007; 69: 932-934.
  27. Kirsch I, Sapirstein G. 1998 Listening to Prozac but hearing placebo. Prevention & Treatment. 2002.
  28. Emperor’s new drugs: Exploding the anti-depressant myth. JAMA. 2010; 303(1): 47-53.
  29. Störtebecker P. Mercury Poisoning from Dental Amalgam: A Hazard to the Human Brain. Bio-Probe, Inc., 1986.
  30. Huggins HA, Levy, TE. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc., 1999.
  31. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.
  32. 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. J Biol Chem. 1997 Dec 19; 272(51): 32411-8.
  33. Sin YM, Teh WF, Wong MK, Reddy PK. Effect of mercury on glutathione and thyroid hormones. Bulletin of Environmental Contamination and Toxicology. 1990; 44(4): 616-622.
  34. Kawada J, et al. Effects of inorganic and methyl mercury on thyroidal function. J Pharmacobiodyn. 1980; 3(3):149-59.
  35. Ghosh N. Thyrotoxicity of cadmium and mercury. Biomed Environ Sci. 1992; 5(3): 236-40.
  36. Goldman, Blackburn, The effect of mercuric chloride on thyroid function of the Rat. Toxic App Pharm. 1979; 48: 49-55.
  37. Kabuto M. Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress. Arch Toxicol. 1991; 65(2):164-7.
  38. Lutz E, et al. Concentrations of mercury in brain and kidney of fetuses and infants. Journal of Trace Elements in Medicine and Biology. 1996; 10: 61-67.
  39. Drasch G, et al. Mercury burden of human fetal and infant tissues. Eur J Pediatr. 1994; 153: 607-610.
  40. Smith, DL. Mental effects of mercury poisoning. South Med J. 1978; 71: 904-5.
  41. Bittner AC, et al. Behavior effects of low level mercury exposure among dental professionals. Neurotoxicology & Teratology. 1998; 20(4): 429-39.
  42. Waly M, Olteanu H, Deth RC, et al. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: A target for neurodevelopmental toxins and thimerosal span. Mol Psychiatry. 2004 Apr; 9(4): 358-70.
  43. Lindqvist B, et al. Effects of removing amalgam fillings from patients with diseases affecting the immune system. Med Sci Res. 1996; 24(5): 355-356.
  44. Berglund F. Case Reports Spanning 150 Years on the Adverse Effects of Dental Amalgam. Bio-Probe, 1995.
  45. Lichtenberg HJ. Elimination of symptoms by removal of dental amalgam from mercury poisoned patients. J Orthomol Med. 1993; 8:145-148.
  46. Lichtenberg H. Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals. J Orthomol Med. 1996, 11(4):195-203.
  47. Siblerud RL, et al. Psychometric evidence that mercury from dental fillings may be a factor in depression, anger, and anxiety. Psychol Rep. 1994; 74(1).
  48. Henningsson M, et al. Defensive characteristics in individuals with amalgam illness. Acta Odont Scand. 1996; 54(3): 176-181.
  49. Liang YX, et al. Psychological effects of low exposure to mercury vapor. Environmental Med Research. 1993; 60(2): 320-327.
  50. Kampe T, et al. Personality traits of adolescents with intact and repaired dentitions. Acta Odont Scand. 1986; 44: 95.
  51. Kishi R, et al. Residual neurobehavioral effects of chronic exposure to mercury vapor. Occupat Envir Med. 1994; 1: 35-41.
  52. Aschner M, et al. Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury. Brain Res. 1997; 778(1): 222-32.
  53. O’Halloran TV. Transition metals in control of gene expression. Science. 1993; 261(5122): 715-25.
  54. 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.
  55. Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct. 1995; 20(3): 233-8.
  56. Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system. Biol Signals. 1994; 3:181-7.
  57. Hall G. V-TOX, Mercury levels excreted after Vit C IV as chelator—by number of fillings. Int Symposium & Status Quo and Perspectives of Amalgam and Other Dental Materials; European Academy, Ostzenhausen/Germany. April 29-May 1, 1994.
  58. Ronnback L, et al. Chronic encephalopaties induced by low doses of mercury or lead. Br J Ind Med. 1992; 49: 233-240.
  59. Langauer-Lewowicka H. Changes in the nervous system due to occupational metallic mercury poisoning. Neurol Neurochir Pol. 1997 Sep-Oct; 31(5): 905-13.
  60. Langauer-Lewowicka H. Chronic toxic encephalopathies. Med Pr. 1982; 33(1-3):113-7.
  61. Tirado V, Garcia MA et al. Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia). Rev Neurol. 2000 Oct 16-31; 31(8): 712-6.
  62. Haut MW, Morrow LA, et al. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999; 6(4): 193-200.
  63. Kobal GD, Kobal AB, et al. Personality traits in miners with past occupational elemental mercury exposure. Environmental Health Perspectives. 2006 Feb; 114(2): 290-6.
  64. Ono B, et al. Reduced tyrosine uptake in strains sensitive to inorganic mercury. Genet. 1987; 11(5): 399.
  65. Siblerud RL. Health effects after dental amalgam removal. J Orthomol Med. 1990; 5(2): 95-106.
  66. Siblerud RL, et al. Evidence that mercury from dental fillings may be an etiological factor in smoking. Toxicol Lett. 1993; 68(3): 307.
  67. Ariza ME, Bijur GN, Williams MV. Lead and mercury mutagenesis: Role of H2O2, superoxide dismustase, and xanthine oxidase. Environ Mol Mutagen. 1998; 31(4): 352-61.
  68. LeFever, GB. The extent of drug therapy for attention deficit-hyperactivity disorder among children in public schools. American Journal of Public Health. 1999; 89(9): 1359-64.
  69. Brownstein, D. Iodine: Why You Need It, Why You Can’t Live Without It. 4th ed. Medical Alternatives Press, 2008.
  70. Soderstrom S, Fredriksson A, Dencker L, Ebendal T. The effect of mercury vapor on cholinergic neurons in the fetal brain. Brain Res. 1995; 85: 96-108.
  71. Niederhofer H. Ginkgo biloba treating patients with attention-deficit disorder. Phytother Res. 2009; 21(4): 26-7.
  72. Kidd PM. Autism, an extreme challenge to integrative medicine. Part 2: medical Management. Altern Med Rev. 2002 Dec; 7(6): 472-99.
  73. Mathieson, PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995; 102(2): 229-30.
  74. Wolfe P. Fillings, mercury, you. Mothering Magazine. 1987.
  75. 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 Jan 10; 62(1): 55-65.
  76. Bapu C, Purohit RC, Sood PP, West ES, et al. Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994 Dec;13(12): 815-23.
  77. Pendergrass JC, Haley BE. The toxic effects of mercury on CNS proteins: Similarity to observations in Alzheimer’s Disease. IAOMT symposium paper. 1997.
  78. Pendergrass JC. Mercury vapor inhalation inhibits binding of GTP: Similarity to lesions in Alzheimer’s disease brains. Neurotoxicology. 1997; 18(2): 315-24.
  79. Ziff, MF. Documented clinical side effects to dental amalgams. Adv Dent Res. 1992; 1(6):131-134.
  80. Ziff, S. Dentistry Without Mercury. 8th ed. Bio-Probe, Inc., 1996.
  81. Daunderer M. Improvement of nerve and immunological damages after amalgam removal. Amer J Of Probiotic Dentistry and Medicine. 1991.
  82. Rogers SA. Depression: Cured at Last! Sarasota, FL: SK Publishing, 1997.
  83. Omura, Y. Abnormal deposits of Al, Pb, and Hg in the brain, particularly in the hippocampus, as one of the main causes of decreased cerebral acetylcholine, electromagnetic field hypersensitivity, pre-Alzheimer’s disease, and autism in children. Acupuncture & Electro-Therapeutics Research. 2000; 25(3/4): 230.
  84. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cellular glutathione content. Immunopharmacol Immunotoxicol. 1993, 15(2-3): 273-90.
  85. al-Saleh I, Shinwari N. Urinary mercury levels in females: influence of dental amalgam fillings. Biometals. 1997; 10(4): 315-23.
  86. Smith I, et al. Pteridines and mono-amines: Relevance to neurological damage. Postgrad Med J. 1986; 62(724):113-123.
  87. Kay AD, et al. Cerebrospinal fluid biopterin is decreased in Alzheimer’s disease. Arch Neurol. 1986; 43(10):996-9.
  88. Yamiguchi T, et al. Effects of tyrosine administration on serum bipterin in patients with Parkinson’s disease and normal controls. Science. 1983; 219(4580): 75-77.
  89. Nagatsu T, et al. Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s. Neurol. 1984; 40: 467-73.
  90. Ely, JTA. Mercury induced Alzheimer’s disease: Accelerating incidence? Bull Environ Contam Toxicol Clinical Management of Poisoning. 3rd Ed. Philadelphia: Haddad, Shannon, and Winchester, W.B. Sounders and Company, 1998.
  91. Mittal, CK. et al, Interaction of heavy metals with the nitric oxide synthase. Mol Cell Biochem. 1995; 149(150): 263-5.
  92. Woods JS, et al. Urinary porphyrin profiles as biomarker of mercury exposure: Studies on dentists. J Toxicol Environ Health. 1993; 40(2-3): 235.
  93. Woods, JS. Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity. Physiol Pharmocol. 1996; 74(2): 210-15.
  94. Nonaka, S et al, Lithium treatment protects neurons in CNS from glutamate induced excitibility and calcium influx. Neurobiology. 1998; 95(5): 2642-2647.
  95. Clarkson TW, et al. Transport of elemental mercury into fetal tissues. Biol Neonate. 1972; 21: 239-244.
  96. Greenwood MR, et al. Transfer of metallic mercury into the fetus. Experientia. 1972; 28:1455-1456.
  97. Perlingeiro RC, et al. Polymorphonuclear phagentosis in workers exposed to mercury vapor. Int J Immounopharmacology. 1994; 16(12):1011-7.
  98. Albers JW, et al. Neurological abnormalities associated with remote occupational elemental mercury exposure. Ann Neurol. 1988; 24(5): 651-9.
  99. Soleo L, Urbano ML, Petrera V, Ambrosi L. Effects of low exposure to inorganic mercury on psychological performance. Br J Ind Med. 1990 Feb; 47(2):105-9.
  100. Hua MS, et al. Chronic elemental mercury intoxication. Brain Inj. 1996, 10(5): 377-84.
  101. Gunther W, et al. Repeated neurobehavioral investigations in workers. Neurotoxicology. 1996; 17(3-4): 605-14.
  102. Rajanna B, 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.
  103. Hobson M, Rajanna B. Influence of mercury on uptake of dopamine and norepinephrine. Toxicol Letters. 1985; 27: 7-14.
  104. 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.
  105. Scheuhammer AM; Cherian MG. Effects of heavy metal cations, sulfhydryl reagents and other chemical agents on striatal D2 dopamine receptors. Biochem Pharmaco1. 1985 Oct 1; 34(19): 3405-13.
  106. 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.
  107. Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.
  108. Echeverria D, et al. Neurobehavioral effects from exposure to dental amalgam. FASEB J. Aug 1998; 12(11): 971-980.
  109. Hock C, et al. Increased blood mercury levels in patients with Alzheimer’s disease. J Neural Transm. 1998; 105(1): 59-68.
  110. Kidd RF. Results of dental amalgam removal and mercury detoxification. Alternative Therapies. 2000; 6(4): 49-55.
  111. Soderstrom S, Fredriksson A, Dencker L, Ebendal T. The effect of mercury vapor on cholinergic neurons in the fetal brain. Brain Res. 1995; 85: 96-108.
  112. 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 Mar; 26(4):733-7.
  113. Stejskal VDM, et al. Mercury-specific Lymphocytes: An indication of mercury allergy in man. J of Clinical Immunology. 1996; 16(1): 31-40.
  114. Zinecker S. Amalgam: Quecksilberdamfe bis ins Gehirn der Kassenarzt. 1992; 32(4): 23.
  115. Malt UF, et al. Physical and mental problems attributed to dental amalgam fillings. Psychosomatic Medicine. 1997; 59: 32-41.
  116. Engel P. Beobachtungen uber die gesundheit vor und nach amalgamentfernug. Separatdruck aus Schweiz Monatsschr Zahnm. 1998; 108(8).
  117. Gordon C, et al. Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE). Lancet. 1992; 339: 8784.
  118. Emory P, et al. Poor sulphoxidation in patients with rheumatoid arthritis. Ann Rheum Dis. 1992; 51(3): 318-20.
  119. Steventon GB, et al. Xenobiotic metabolism in motor neuron disease. Neurology. 1990; 40:1095-98.
  120. Freitas AJ, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Res. 1996; 738(2): 257-64.
  121. 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.
  122. Chavez E, et al. Mitochondrial calcium release by Hg+2&quot. J Biol Chem. 1988; 263:8.
  123. Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.
  124. Rossi AD, et al. Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J. 1993; 7:1507-14.
  125. 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.
  126. Boadi WY. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity. Pharmacol. 1992, 116(1): 17-23.
  127. Urbach J, et al. Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Reprod Toxicol. 1992, 6(1): 69-75.
  128. Karp W, Gale TF, et al. Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters. Environ Research. 2008; 36: 351-358.
  129. Karp WB, et al. Correlation of human placental enzymatic activity with trace metal concentration in placenta. Environ Res. 1977; 13:470-477.
  130. Boot JH. Effects of SH-blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct. 1995 Jun; 20(3): 233-8.
  131. Sterzl I, Prochazkova J, Stejskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.
  132. 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 Jun; 25(3): 211-8.
  133. Atchison WD. Effects of neurotoxicants on synaptic transmission. Neurotoxicol Teratol. 1998, 10(5): 393-416.
  134. Sidransky H, Verney E. Influence of lead acetate and selected metal salts on tryptophan binding to rat hepatic nuclei. Toxicol Pathol. 1999; 27(4): 441-7.
  135. Shukla GS, Chandra SV. Effect of interaction of Mn2+withZn2+, Hg2+, and Cd2+ on some neurochemicals in rats. Toxicol Lett. 1982; 10(2-3):163-8.
  136. Brouwer M, et al. Functional changes induced by heavy metal ions. Biochemistry. 1982; 21(20): 2529-38.
  137. Benkelfat C, et al. Mood lowering effect of tryptophan depletion. Arch Gen Psychiatry. 1994, 51(9): 687-97.
  138. Young SN, et al. Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology. 1985; 87(2):173-77.
  139. Smith KA, et al. Relapse of depression after depletion of tryptophan. Lancet. 1997; 349(9056): 915-19.
  140. Delgado PL, et al. Serotonin function, depletion of plasma tryptophan, and the mechanism of antidepressant action. Arch Gen Psychiatry. 1990; 47(5): 411-18.
  141. Stejskal VDM, Danersund A, Lindvall A. Metal-specific memory lymphocytes: Biomarkers of sensitivity in man. Neuroendocrinology Letters. 1999.
  142. Stejskal V, Hudecek R, Mayer W. Metal-specific lymphocytes: Risk factors in CFS and other related diseases. Neuroendocrinology Letters. 1999; 20: 289-298.
  143. Melchart D, Wuhr E, Weidenhammer W, Kremers L. A multicenter survey of amalgam fillings and subjective complaints in non-selected patients in the dental practice. Eur J Oral Sci. 1998; 106: 770-77.
  144. Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.
  145. Sterzl I, Hrda P, Prochazkova J, Bartova J. Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek. 1999 Sep; 45(9): 527-31.
  146. Kolenic J, Palcakova D, Benicky L, Kolenicova M. The frequency of auto-antibody occurrence in occupational risk (mercury). Prac Lek. 1993; 45(2):75-77.
  147. Doctors Data Lab. http://www.doctorsdata.com. Accessed December 31, 2014.
  148. Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI. Effects of low mercury vapour exposure on the thyroid function in chloralkali workers. J Appl Toxicol. 2000; 20(6):483-9.
  149. Barregard L, Lindstedt G, Schutz A, Sallsten G. Endocrine function in mercury exposed chloralkali workers. Occup Environ Med. 1994; 51(8):536-40.
  150. Almeida C, Brasil MA, Costa AJ, Vaisman M. Subclinical hypothyroidism: Psychiatric disorders and symptoms. Rev Bras Psiquiatr. 2007 Jun; 29(2):157-9.
  151. Filipci I, Popovi-Grle S, Hajnaek S, Aganovi I. Screening for depression disorders in patients with chronic somatic illness. Coll Antropol. 2007 Mar; 31: 139-43.
  152. Davis JD, Tremont G. Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrinol. 2007 Mar; 32(1): 49-65.
  153. Godfrey ME. Candida, dysbiosis, and amalgam. J Adv Med. 1996; 9(2).
  154. Romani L. Immunity to Candida Albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol. 1999; 2(4): 363-7.
  155. Zamm, AV. Candida albicans therapy: Dental mercury removal, an effective adjunct. J Orthmol Med. 1986; 1(4): 261-5.
  156. Ciacci, C. Depressive symptoms in adult celiac disease. Scand J Gastroenterol. 1998; 33(3): 247-50.
  157. Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J Prosthet Dent. 1990; 63(5): 593-6.
  158. Yonk LJ, et al. CD+4 helper T-cell depression in autism. Immunol Lett. 1990; 25(4): 341-5.
  159. Jaffe JS, Strober W, Sneller MC. Functional abnormalities of CD8+ T cells define a unique subset of patients with common variable immunodeficiency. Blood. 1993; 82(1): 192-20.
  160. Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: A novel form of mercury poisoning. Med Hypotheses. 2001 Apr; 56(4): 462-71.
  161. Cade JR, et al. Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism. Mar 1999.
  162. Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptyl peptidase IV from human placenta. Eur J Biochem. 1982 Aug; 126(2): 359-65.
  163. Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta. 1978; 82(1-2): 185-92.
  164. Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V. Plasma excitatory amino acids in autism. Invest Clin. 1996; 37(2):113-28.
  165. Carlsson ML. Is infantile autism a hypoglutamatergic disorder? J Neural Transm. 1998; 105(4-5): 525-35.
  166. Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of autistic children. Acta Psychiatr Scand. 1993; 87(5): 312-6.
  167. Naruse H, Hayashi T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment. No To Hattatsu. 1989, 21(2):181-9.
  168. Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health. 1998; 14(4): 553-63.
  169. Liska, DJ. The detoxification enzyme systems. Altern Med Rev. 1998; 3(3):187-98.
  170. Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes. Yonsei Med J. 1995; 36(3): 299-305.
  171. Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology. 1992; 76(3): 245-56.
  172. Albrecht J, Matyja E. Glutamate: A potential mediator of inorganic mercury toxicity. Metab Brain Dis. 1996; 11:175-84.
  173. 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.
  174. Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine. Purification and properties of monkey intestinal pyridoxal kinase. Indian J Biochem. 1970 Sep; 7(3): 151-6.
  175. Spivey-Fox MR. Nutritional influences on metal toxicity. Environmental Health Perspectives. 1979; 29: 95-104.
  176. McCarty MF. High-dose pyridoxine as an ‘anti-stress’ strategy. Med Hypotheses. 2000 May; 54(5): 803-7.
  177. Munch G, Gerlach M, Sian J, Wong A, Riederer P. Advanced glycation end products in neurodegeneration: More than early markers of oxidative stress? Ann Neurol. 1998 Sep; 44(3 Suppl 1): S85-8.
  178. Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Arch Int Physiol Biochem. 1990; 98(5): 261-7.
  179. Stefanovic V, et al. Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem. 1998; 8(5): 278-84.
  180. Miszta H, Dabrowski Z. Effect of mercury and combined effect of mercury on the activity of acetylcholinesterase of rat lymphocytes during in vitro incubation. Folia Haematol Int Mag Klin Morphol Blutforsch. 1989; 116(1):151-5.
  181. Bear, D, Rosenbaum, J, Norman, R. Aggression in cat and human by a cholinesterase inhibitor. Journal Psychosomatics. 1986; 27(7): 535-536.
  182. Devinsky O, Kernan J Bear D. Aggressive behavior following exposure to cholinesterase inhibitors. Journal of Neuropsychiatry. 1992; 4(2): 189-199.
  183. Edwards AE. Depression and Candida. JAMA. 1985; 253(23): 3400.
  184. Crook WG. Depression associated with Candida albicans infections. JAMA. 1984; 251: 22.
  185. Crook, WG. The Yeast Connection Handbook. Jackson, TN: Professional Books, Inc., 1997.
  186. Walsh WJ, Health Research Institute. Biochemical treatment of mental illness and behavior disorders. Minnesota Brain Bio Assoc. 1997.
  187. Salzer HM. Relative hypoglycemia as a cause of neuropsychiatric illness. J National Med Assoc. 1996; 58(1): 12-17.
  188. Heninger GR, et al. Depressive symptoms, glucose tolerance, and insulin tolerance. J Nervous and Mental Dis. 1975; 161(6): 421-32.
  189. Winokur A, et al. Insulin resistance in patients with major depression. Am J Psychiatry. 1988; 145(3): 325-30.
  190. Virkkunen M, Huttunen MO. Evidence for abnormal glucose tolerance among violent offenders. Neuropsychiobilogy. 1982; 8: 30-40.
  191. Markku I, Virkkunen L. Aggression, suicidality, and serotonin. J Clinical Psych. 1992; 53(10): 46-51.
  192. Pranjic N, Sinanovic O, et al. Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers. Bosn J Basic Med Sci. 2002 Dec; 2(1-2): 29-34.
  193. Linnoila M et al. Low serotonin metabolite differentiates impulsive from non-impulsive violent behavior. Life Sciences. 1983; 33(26): 2609-2614.
  194. Lopez-Ibor JJ. Serotonin and psychiatric disorders. Int Clinical Psychopharm. 1992, 7(2): 5-11.
  195. Thomas DE, et al. Tryptophan and nutritional status in patients with senile dementia. Psychological Med. 1986, 16: 297-305.
  196. Yaryura-Tobias JA, et al. Changes in serum tryptophan and glucose in psychotics and neurotics. Nutrition. 4557: 1132.
  197. Urberg M, Zemel MB. Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans. Metabolism. 1987; 36(9): 896-899.
  198. Anderson RA, et al. Effects of supplemental chromium on patients with reactive hypoglycemia. Metabolism. 1987; 36(4): 351-355.
  199. Haut MW, Morrow LA, Pool D, Callahan TS; Haut JS, Franzen MD. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999; 6(4): 193-200.
  200. Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S-adenosyl L-methionine. Psychiatry Res. 1995 Apr 28; 56(3): 295-7.
  201. Rosenbaum JF, Fava M, Falk WE, et al. The antidepressant potential of oral S-adenosyl l-methionine. Acta Psychiatr Scand. 1990 May; 81(5): 432-6.
  202. Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol. 1997 May; 7(2): 147-55.
  203. Fux, M. Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive-compulsive disorder: A double-blind cross-over study. Int J Neuropsychopharmcol. 1999 Sep; 2(3): 193-195.
  204. Palatnik A, Frolov K, Fux M, Benjamin J. Double-blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder. J Clin Psychopharmacol. 2001 Jun; 21(3): 335-9.
  205. Chengappa KN, Levine J, Kupfer DJ. Inositol as an add-on treatment for bipolar depression. Bipolar Disord. 2000 Mar; 2(1): 47-55.
  206. Narang RL, Gupta KR. Levels of copper and zinc in depression. Indian J of Physiol Pharmacol. 1991; 35(4): 272-4.
  207. McLoughlin IJ, Hodge JS. Zinc in depressive disorder. Acta Psychiatr Scand. 1990; 82(6): 451-3.
  208. Miller HL, et al. Acute tryptophan depletion: A method of studying antidepressant action. J Clin Psychiatry. 1992; 53: 28-35.
  209. Boman B. L-tryptophan: A rational anti-depressant and a natural hypnotic? Aust N Z J Psychiatry. 1988; 22(1): 83-97.
  210. Young SN. The use of diet and dietary components in the study of factors controlling affect in humans: A review. J Psychiatry Neurosci. 1993; 18(5): 235-44.
  211. Doble A. The role of excitotoxicity in neurodegenerative disease: Implications for therapy. Pharmacol Ther. 1999 Mar; 81(3): 163-221.
  212. 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 Oct; 60(4): 838-46.
  213. 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 Sep; 36(5): 687-97.
  214. Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: The role of peroxynitrite. Brain Res. 1999 Aug; 30(2): 153-63.
  215. 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 Apr; 47(4): 524-7.
  216. Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite is differentially prevented by antioxidants. Mol Pharmacol. 2001 Oct; 60(4): 838-46.
  217. Birdsall TC. 5-Hydroxytryptophan: A clinically-effective serotonin precursor. Altern Med Rev. 1998 Aug; 3(4): 271-80.
  218. Tirado V, Garcia MA, Franco A. Pneuropsychological disorders after occupational exposure to mercury vapors. Rev Neurol. 2000 Oct; 31(8): 712-6.
  219. Powell TJ. Chronic neurobehavioural effects of mercury poisoning on a group of chemical workers. Brain Inj. 2000 Sep; 14(9): 797-814.
  220. Laks, DR. Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999–2006. Biometals. Aug 2009.
  221. Laks, DR et al. Mercury has affinity for pituitary hormones. Medical Hypotheses: An Investigation of Factors Related to Levels of Mercury in Human Hair. Environmental Quality Institute. 2009.
  222. Maes M, Vandoolaeghe E, Neels H, et al. Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry. 1997; 42(5): 349-358.
  223. Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med. 1989; 19(1): 57-63.
  224. Levine J, Stein D. High serum and cerebrospinal fluid Ca/Mg ratio in recently hospitalized acutely depressed patients. Neuropsychobiology. 1999; 39(2): 63-70.
  225. Naylor GJ, Smith AH, Bryce, Smith D, Ward NI. Elevated vanadium content of hair and mania. Biol Psychiatry. 1984; 19(5): 759-764.
  226. McIntyre IM, Judd FK, Marriott PM, et al. Plasma melatonin levels in affective states. Int J Clin Pharmacol Res. 1989; 9(2): 159-64.
  227. Riemann D, Klein T, Rodenbeck A, et al. Nocturnal cortisol and melatonin secretion in primary insomnia. Psychiatry Res. 2002 Dec 15; 113(1-2): 17-27.
  228. Wade AG, Ford I, Crawford G, et al. Efficacy of prolonged release melatonin in insomnia patients aged 55-80 years: Quality of sleep and next-day alertness outcomes. Curr Med Res Opin. 2007 Oct; 23(10): 2597-605.
  229. Kim CY, Satoh H, et al. Protective effect of melatonin on methylmercury-induced mortality in mice. Tohoku J Exp Med. 2000 Aug; 191(4): 241-6.
  230. Olivieri G, Hock C, et al. Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. J Neurochem. 2000 Jan; 74(1): 231-6.
  231. Bemis JC, Seegal RF. PCBs and methylmercury alter intracellular calcium concentrations in rat cerebellar granule cells. Neurotoxicology. 2000; 21(6): 1123-1134.
  232. Baccarelli A, Pesatori AC, Bertazzi PA. Occupational and environmental agents as endocrine disruptors: experimental and human evidence. J Endocrinol Invest. 2000 Dec; 23(11): 771-81.
  233. Libe R, Baccarelli A, et al. Long-term follow-up study of patients with adrenal incidentalomas. Eur J Endocrinol. 2002 Oct; 147(4): 489-94.
  234. Manzo L, Candura SM, Costa LG, et al. Biochemical markers of neurotoxicity. A review of mechanistic studies and applications. Hum Exp Toxicol. 1996 Mar; 15(1): S20-35.
  235. Life Extension Foundation. http://www.life-enhancement.com/. Accessed December 31, 2014.
  236. Volz HP. Controlled clinical trials of hypericum extracts in depressed patients—An overview. Pharmacopsychiatry. 1997 Sep; 30(Suppl 2):72-6.
  237. Melzer J, Brignoli R, Keck ME, et al. A hypericum extract in the treatment of depressive symptoms in outpatients: An open study. Forsch Komplementmed. 2010; 17(1): 7-14.
  238. Starck G, Carlsson ML, et al. 1H magnetic resonance spectroscopy study in adults with obsessive compulsive disorder: Relationship between metabolite concentrations and symptom severity. J Neural Transm. 2008 Jul; 115(7):1051-62.
  239. Carlsson ML. On the role of prefrontal cortex glutamate for the antithetical phenomenology of obsessive compulsive disorder and attention deficit hyperactivity disorder. Biol Psychiatry. 2001 Jan; 25(1): 5-26.
  240. Chikani V, Reding D, Gunderson P, et al. Wisconsin rural women’s health study psychological factors and blood cholesterol level: Difference between normal and overweight rural women. Clin Med Res. 2004 Feb; 2(1): 47-53.
  241. Räikkönen K, Matthews KA, Kuller LH. Trajectory of psychological risk and incident hypertension in middle-aged women. Hypertension. 2001 Oct; 38(4): 798-802.
  242. Matthews KA, Owens JF, Kuller LH, et al. Are hostility and anxiety associated with carotid atherosclerosis in healthy postmenopausal women? Psychosom Med. 1998 Sep-Oct; 60(5): 633-8.
  243. Horsten M, Ericson M, Perski A, et al. Psychosocial factors and heart rate variability in healthy women. Psychosom Med. 1999 Jan-Feb; 61(1): 49-57.
  244. Vlastelica M. Emotional stress as a trigger in sudden cardiac death. Psychiatr Danub. 2008 Sep(3): 411-4.
  245. Birkmayer JGD, Birkmayer W. The coenzyme nicotinamide adenine dinucleotide (NADH) as a biological antidepressive agent. New Trends in Clinical Neuropharmacology. 1992; 6:1-7.
  246. László KD, Janszky I, Ahnve S. Anger expression and prognosis after a coronary event in women. Int J Cardiol. 2010 Apr 1; 140(1): 60-5.
  247. Olson MB, Krantz DS, Kelsey SF, et al. Hostility scores are associated with increased risk of cardiovascular events in women undergoing coronary angiography: A report from the NHLBI-Sponsored WISE Study. Psychosom Med. 2005 Jul-Aug; 67(4): 546-52.
  248. Stallones L, Beseler C. Pesticide poisoning and depressive symptoms among farm residents. Ann Epidemiol. 2002 Aug; 12(6): 389-94.
  249. Rehner TA, Kolbo JR, Trump R, Smith C, Reid D. Depression among victims of south Mississippi’s methyl parathion disaster. Health Soc Work. 2000 Feb; 25(1): 33-40.
  250. Maizlish NA, Parra G, Feo O. Neurobehavioral evaluation of Venezuelan workers exposed to inorganic lead. Occu Environ Med. 1995; 52: 408-414.
  251. Bouchard MF, van Wijngaarden. Major depressive disorder and panic disorder related to lead exposure. Arch Gen Psychiatry. 2009; 66: 1313-1319.
  252. Chang Y, Wang SJ. Hypericin as glutamate control. Eur J Pharmacol. 2010, 634:53-61.
  253. Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S-adenosyl L-methionine. Psychiatry Res. 1995 Apr 28; 56(3): 295-7.
  254. Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS. The antidepressant potential of oral S-adenosylmethionine. Acta Psychiatr Scand. 1990 May; 81(5): 432-6.
  255. Kagan BL, et al. Oral S-adenosylmethionine in depression: a randomized, double blind, placebo-controlled trial. Am J Psychiatry 1990; 147(5): 591-5.
  256. Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol. 1997 May; 7(2): 147-55.
  257. Fux, M. Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive-compulsive disorder: a double-blind cross-over study. Int J Neuropsychopharmcol. 1999; 2(3): 193-195.
  258. Palatnik A, Frolov K, Fux M, Benjamin J. Double-blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder. J Clin Psychopharmacol. 2001 Jun; 21(3): 335-9.
  259. Chengappa KN, Levine J, Kupfer DJ. Inositol as an add-on treatment for bipolar depression. Bipolar Disord. 2000 Mar; 2(1): 47-55.
  260. McIntyre RS, Soczynska JK, Kennedy SH, et al. Should Depressive Syndromes Be Reclassified as “Metabolic Syndrome Type II? Ann Clin Psychiatry. 2007 Oct-Dec; 19(4):257-64.
  261. Leonard BE. Inflammation, depression and dementia: Are they connected? Neurochem Res. 2007 Oct; 32(10): 1749-56.
  262. Blaylock, RL. Immunoexcitotoxicity. Alt Ther Health Med. 2008; 14: 46-53.
  263. Cordain, L. Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat. John Wiley & Son, 2010.
  264. Barnes DM, Kircher EA. Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005 Mar; 19(2): 207-14.
  265. Barnes DM, Hanlon PR, Kircher EA . Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003 Oct; 75(2): 368-77.
  266. Iturri, SJ. 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.
  267. Klip A, Grinstein S, Biber J, Semenza G. Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980 May; 8(1):100-14.
  268. 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 Dec;19(4):237-43.
  269. 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 Nov; 84(5):1062-9.
  270. Guerrero-Romero F, Rodríguez-Morán Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome. Diabetes Metab Res Rev. 2006; 22(6): 471-6.
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