Depression and other Neurotransmitter Related Conditions- the mercury connection

B.Windham (Ed.)

Introduction.

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(10). 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 (598). Several factors appear to be contributing to this:

1. 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, etc. Studies by the National Academy of Sciences indicate that these affect close to 30% of all children in the U.S., more in some populations than others.

2. changes in dietary habits resulting in nutrient, vitamin, and mineral deficiencies or imbalances and blood sugar imbalances(594), and increased consumption of inflammatory excitotoxins such as aspartame, MSG, and high fructose corn syrup.

3. 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(6). 71% of the sample were female. All patients filled in the Beck Depression Inventory (BDI). The prevalence of depressive disorders in the whole sample was 23.3%.

II. Causes of Depression

Depression appears 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 depressive disorders and other chronic neurological conditions (592,593,598, etc.). 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(13,596-599,etc.)

Mercury and other toxic metals inhibit astrocyte function in the brain and CNS(119), causing increased glutamate and calcium related neurotoxicity (119,333,416,496). Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage(142,13). 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(524,521).

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(598). 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, etc. (593,598,600,etc.)

Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions(599,43). 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 (43,196,338,597).

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(7). 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(11). 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(11a). 94 patients with subclinical hypothyroidism and a control group were evaluated to determine the prevalence of psychiatric disorders(11b). 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(8a). 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(8b). 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(9). 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(7b).

For a group of women with PPT, 46% had postpartum depression in one or more pregnancies(8b).

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 (600,602). 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 (602). Mercury in pregnant women is also documented to cross the placenta and accumulate in the fetus to levels higher than in the mother (603). 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(603). Young children also 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(602). 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 (604) . The top 3 toxic substances affecting large numbers of people in the U.S. adversely according to EPA/ATSDR are mercury, lead, and arsenic. (600,604).

IV. Toxic and immune reactive effects of mercury.

Mercury is neurotoxic (kills or damages brain and nerve cells): (19,27,34,36,43,69,70, 147,148,175,207, 211,273, 291,295,327,329,301,303,395,600/ 39,262,274,303); 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 (13,56, 98,102,126,145,169,170,184,213,218,219, 250, 257,259,286, 290,291,302,324,326,329,600); kills or inhibits production of brain tubulin cells (66,67,161,166, 207,300); inhibits production of neurotransmitters by inhibiting: calcium-dependent neurotransmitter release(372), dihydroteridine reductase(27,122,257),nitric oxide synthase(259), blocking neurotransmitter amino acids(438,601), and effecting phenylalanine, tyrosine and tryptophan transport to neurons) (34,122,126,257,285,288,333,438/255,333).

Numerous studies have found long-term chronic low doses of mercury cause neurological, memory, behaviour, sleep, and mood problems (5,72,74,107,109, 290,etc.). 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 (94,107,109,212,222,229,233,285c,294,317,320,322,372,374,453), schizophrenia (34,35,295,601), memory problems(70,94,212,222,600), and other more serious neurological diseases such as MS, ALS, Parkinson’s, and Alzheimer’s (13,33,66,98,207b,330, 331,424,438, 483,600). Some factors that have been documented in depression are low serotonin levels, abnormal glucose tolerance(hypoglycemia), and low folate levels(480-83), which mercury has also been found to be a cause of. Occupational exposure to mercury has been documented to cause depression and anxiety(534). Acute exposure to mercury vapor has been found to cause chronic depression, anxiety, and obsessive-compulsive behavior(487). 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 (175,451,465,254). Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior(481,482).

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(569). Melatonin has found to have a significant protective action against methyl mercury toxicity, likely from antioxidative effect of melatonin on the MMC induced neurotoxicity(567).

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_b-hydroxylase (DBH) enzyme (571). 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 (569).

There is evidence that mercury can block the dopamine-beta-hydroxylase (DBH) enzyme(571). 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(260) 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(285,404). 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.(460) Immune Th1 cells inhibit candida by cytokine related activation of macrophages and neutraphils. Development of Th2 type immune responses deactivate such defenses(404b,285). Mercury inhibits macrophage and neutraphil defense against candida by its affects on Th1 and Th2 cytokine effects(181,285). Candida overgrowth results in production of the highly toxic canditoxin and ethanol which are known to cause fatigue, toxicity, and depressive symptoms(460).

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 (280,294,333,33,56 ). Medical texts on neurology (27,295) 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 (158,34,207,etc.}

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, depression (294,375,408,438,601). 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 casein(411,412,602). Studies involving a large sample of 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(410). 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(5). Such populations have also been found to have high levels of mercury and to recover after mercury detoxification. (413,60,313,600). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs(5). Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes and neurotransmitter amino acids(33,114,438,5), enzymatic processes involving vitamins B6 and B12(418,5), effects on the cytochrome-C energy processes(232,35), along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, chromium, and lithium (43,96,198,333,386,427,432,484,38).

Studies have shown a significant association between hypothyrodism and mood disorders such as depression(391,8). Mercury from dental amalgam has been documented to cause hypothyroidism (50,91,212,222,369,382, 390,35ab). The majority of patients tested with hypothyroidism or thyroiditis and treated with dental amalgam replacement significantly improved after replacement(91,369).

Numerous studies have found long term chronic low doses of mercury cause neurological, memory, behavior, sleep, and mood problems (34,69,70,71,72,74,95,107,108,109,115,119,140,141,196,199,222,252, 255,257,258, 282,290]. Neurological effects have been documented at very low levels of exposure(urine Hg< 4 ug/L), levels commonly received by those with amalgam fillings(290). One of the studies at a German University(199) assessed 20,000 people. There is also evidence that fetal or infant exposure causes delayed neurotoxicity evidenced in serious effect at middle age(255). Studies of groups of patients with amalgam fillings found significantly more neurological, memory, mood, and behavioral problems than the control groups. (34,107,108,109,140,141,196,199,222,290]. Increased mercury levels from amalgam are documented to cause increased neurological problems related to lowered levels of neurotransmitters dopamine, serotonin, noreprenephrine,and acetylcholinesterase (35,107,140,141,175,251,254,288, 290,296,305,372,451,465,412). 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(141).

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 (35,94,95,107,222,271,294,212,229,230, 233,317,320,322, 376,407), schizophrenia (294,34,35), insomnia (94,95,212,222,271,317,322,376,407), anger(212,233,320,407,102), anxiety & mental confusion (94,95,212,222,229,233,271,317,320,322 ,407,57), memory disorders (94,95,222,407). 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(95).

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(600,601,552). Amalgam dental fillings have been found the most common source of such toxic exposures, with mercury thimerosal from vaccinations also affecting millions of children(600,601). 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(560,600). 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(560). Subnormal levels of zinc, for example, are associated with treatment resistant depression(561). And deficiencies of magnesium can provoke a wide range of psychiatric symptoms related to depression, ranging from apathy to psychosis(562). 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(563).

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(593,598,etc.) 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. (593,598,601,600, 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 (598).

Reducing glutamate levels and blocking glutamate receptors can significantly improve depression (598). Additionally, SAMe and Inositol have been found to be effective in treating depression with effectiveness at least as much as pharmaceutical antidepressants and much less adverse effects(590). Inositol has been found to be effective for treating OCD, panic disorders, and bipolar depression(591), with effectiveness at least as much as SSRIs and less adverse effects(591).

References

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