MercuryToxicity/Endochrinology

From AutismPedia

(Redirected from Mercury Endochrinology)
Jump to: navigation, search
Biomed Labs Poop Analysis Treatments Testimonials Etiology (Cause) Links Acronyms
http://tinyurl.com/Hg-Endocrine
This material was compiled and edited by Bernard Windham
Main Article: Childhood Neurological and Immune Reactive Conditions
Endocrine System
Endocrine System

Contents

Effects of Mercury Toxicity on the Endocrine System

Preface

Mercury Detox
ADHD populations have high levels of mercury and recover after mercury detoxification. As mercury levels are reduced, the protein binding is reduced and improvement in the enzymatic process occurs.

Introduction

It has been well documented that mercury is an endocrine system disrupting chemical in animals and people. Low levels of exposure disrupt many hormonal functions and function of the:

  • pituitary gland,
  • thyroid gland,
  • enzyme production processes.

People with high mercury levels in their bodies have more:

  • hormonal disturbances,
  • immune disturbances,
  • recurring fungal infections,
  • chronic bacterial infections, [1]
  • hair loss and allergies.
Endocrine Mercury Accumulation
Autopsy studies in 1975 revealed that, contrary to accepted belief that the kidney was the prime accumulator of inorganic mercury, the thyroid and pituitary retain and accumulate more inorganic mercury than the kidneys.

Endocrine glands secrete their products, hormones, directly into the blood stream. [2] Most hormones are steroid or amino acid based.[2] Hormones that are most often affected by mercury are:

  • insulin,
  • estrogen,
  • testosterone,
  • and adrenaline.

Almost all hormones have binding sights capable of connecting to metabolic cofactors, but mercury can bind here, too. Mercury frequently has a stronger affinity for these binding sites than the normal activators; even though the hormone is present in the bloodstream, it may not be able to act as it is supposed to act.


Endocrine Systems Impacts

The affinity of mercury for the pituitary gland was first identified by Stock in 1940.
The affinity of mercury for the pituitary gland was first identified by Stock in 1940.

Mercury (especially mercury vapor or organic mercury) rapidly crosses the blood-brain barrier and is stored in direct proportion to the number and extent of dental amalgam surfaces in the following locations:

  • the pituitary gland,
  • thyroid gland,
  • hypothalamus,
  • and occipital cortex.

Immune Activation

In general, immune activation from toxins such as heavy metals, resulting in cytokine release and abnormalities of the hypothalamus-pituitary-adrenal axis, can cause changes in the brain, fatigue, and severe psychological symptoms, such as:

  • depression,
  • profound fatigue,
  • muscular-skeletal pain,
  • sleep disturbances,
  • gastrointestinal and neurological problems
    • as are seen in CFS, fibromyalgia, and autoimmune thyroiditis.

Symptoms usually improve significantly after amalgam removal.

Enzymamatic Effects

A direct mechanism involving mercury's inhibition of hormones and cellular enzymatic processes by binding with the hydroxyl radical (SH) in amino acids, appears to be a major part of the connection to allergic/immune reactive/autoimmune conditions such as:

  • autism/ADHD,
  • schizophrenia,
  • lupus,
  • scleroderma,
  • eczema,
  • psoriasis and allergies.
Mercury inhibits the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein casein as well as xanthine oxidase.

Studies involving a large sample of autistic and schizophrenic patients found that over 90% of those tested had high levels of the neurotoxic milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein. Elimination of milk products from the diet improves the condition.

Additional cellular level enzymatic effects of mercury binding with proteins include:

  • blockage of sulfur oxidation processes,
  • enzymatic processes involving vitamins B6 and B12,
  • effects on cytochrome-C energy processes,
  • along with mercury's adverse effects on mineral levels of calcium, magnesium, zinc, and lithium.
The enzymatic effects of mercury intoxication may be overcome by the administration of the thyroid hormone thyroxine.

Thyroid

Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the most common problems of the thyroid gland.[3]

Hypothyroidism is a well-documented cause of mental retardation.
Mercury blocks thyroid hormone production by occupying iodine-binding sites and inhibiting hormone action even when the measured thyroid levels appears to be in the proper range.
Mercury blocks thyroid hormone production by occupying iodine-binding sites and inhibiting hormone action even when the measured thyroid levels appears to be in the proper range.

The thyroid is one of the largest endocrine glands in the body.[3] The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones.[3] The gland gets its name from the Greek word for "shield", after the shape of the related thyroid cartilage. [3]

The thyroid is controlled by the hypothalamus and pituitary. Through a feedback loop, the pituitary releases thyrotropin-releasing hormone, which in effect tells the thyroid how much thyroxine hormone to release into the blood.
The thyroid is controlled by the hypothalamus and pituitary.[3] Through a feedback loop, the pituitary releases thyrotropin-releasing hormone, which in effect tells the thyroid how much thyroxine hormone to release into the blood.[4][5]

Organic mercury causes severe damage to both the endocrine and neural systems. Studies have documented that mercury causes:

  • hypothyroidism,
  • damage of thyroid RNA,
  • autoimmune thyroiditis (inflammation of the thyroid),
  • and impairment of conversion of thyroid T4 hormone to the active T3 form.
Hypothyroidism
Large percentages of women have elevated levels of antithyroglobulin (anti-TG) or antithyroid peroxidase antibody (anti-TP).
Slight imbalances of thyroid hormones in expectant mothers can cause permanent neuropsychiatric damage in the developing fetus.
Maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children.
Studies have also established a clear association between the presence of thyroid antibodies and spontaneous abortions.
Hypothyroidism is a risk factor in spontaneous abortions and infertility.
In pregnant women who suffer from hypothyroidism, there is a four-time greater risk for miscarriage during the second trimester than in those who don't.


Thyroid Regulation

Both the pituitary and the thyroid display an affinity for accumulating mercury.

Mercury first stimulates and then suppresses the thyroid function.

Chronic intake of mercury for more than ninety days results in signs of mercury poisoning, together with decreased uptake of iodine and depression of thyroid hormonal secretion. The thyroid and hypothalamus regulate body temperature and many metabolic processes including enzymatic processes.

Mercury damage thus commonly results in poor body temperature control, in addition to many problems caused by hormonal imbalances such as depression. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested.

Blood Brain Barrier

Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances.

Cardiovascular Disease

Hypothyroidism is also a major factor in cardiovascular disease.

Nutritional Status and Methly-B12

The thyroid gland has four binding sites for iodine. When mercury attaches to one of these sites, the hormone activity is altered.

There is a relationship between thyroid function and the nutritional status of folate, vitamin B12, and methionine.
Mercury affects the nutritional status of folate, vitamin B12, methionine, and zinc, as well as protein.
There is also a strong association between lowered zinc intake, lowered basal metabolic rate, lowered thyroid hormones and lowered protein utilization.

Degenerative Disease

There is a fluid flow from the pulp chamber, through the dentin, through the enamel and into the mouth in people who have no dental decay. Thyroid is part of the endocrine function that controls the direction of this fluid flow. Low thyroid hormone production allows this fluid flow to run in the opposite direction--from the mouth, into the enamel, dentin, and pulp chamber. This fluid brings bacteria and debris from the mouth with it, leading to dental decay. When the teeth are susceptible to decay, the whole body is susceptible to degenerative disease.

Body Temperature Regulation

The thyroid is involved with maintenance of proper body temperature. Most mercury toxic patients have lower than optimum body temperatures.

The most toxic persons may have temperatures as low as 96.2.

When the amalgam fillings are removed, there is a trend for the temperature to approach 98.6, sometimes within 24 hours of removing all of the amalgams.

Psychological Effects

The thyroid gland is controlled by the pituitary gland. When the thyroid is influenced by mercury, there is a high incidence of unexplained depression and anxiety. A person may have adequate levels of T3 and T4 hormones, but if the hormones are contaminated, the person is functionally thyroid deficient.

Heart Failure

Thyroid imbalances cause chronic conditions such as clogged arteries and chronic heart failure. People who test hypothyroid usually have significantly higher homocysteine and cholesterol--documented risk factors in heart disease.

High Homocysteine

Fifty percent of those also have high levels of homocysteine, and 90% are either hyperhomocystemic or hypercholesterolemic.


Posterior Pituitary Gland

Emotions - The posterior pituitary hormone joins forces with the thyroid in influencing emotions. Posterior pituitary hormone is really two hormones, oxytocin and vasopressin.

The pituitary gland controls many of the body's endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive systems.
The pituitary gland controls many of the body's endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive systems.

One study found mercury levels in the pituitary gland ranged from 6.3 to 77 ppb, while another found the mean levels to be 30 ppb, levels found to be neurotoxic (toxic to nerves) and cytotoxic (kills cells).

Amalgam fillings, nickel and gold crowns are major factors in reducing pituitary function.


High Blood Pressure

High blood pressure is related to the function of the posterior pituitary hormone vasopressin. It is a short trip for mercury vapor to leave a filling, and travel into the sinus, and then travel an inch through very porous, spongy tissues to the pituitary gland.

Mercury is detected in the pituitary gland in less than a minute after placing amalgam in teeth of test animals.

Adrenal Glands

The adrenal glands (also known as suprarenal glands) are the star-shaped endocrine glands that sit on top of the kidneys. They are chiefly responsible for regulating the stress response through the synthesis of corticosteroids and catecholamines, including cortisol and adrenaline, respectively.

Mercury accumulates in the adrenal glands and disrupts adrenal gland function.  During stress, the adrenal glands increase in size as a normal reaction in order to produce more steroids (hormones). Both physical and physiological stress will stimulate the adrenal glands.
Mercury accumulates in the adrenal glands and disrupts adrenal gland function. During stress, the adrenal glands increase in size as a normal reaction in order to produce more steroids (hormones). Both physical and physiological stress will stimulate the adrenal glands.

[6]

The outer shell of the adrenal gland is called the cortex, and the inner core of the gland is called the medulla
The outer shell of the adrenal gland is called the cortex, and the inner core of the gland is called the medulla

Adrenal Cortex

The adrenal cortex (outer shell) produces several different types of corticosteroid hormones:

  • Glucocorticoids
  • Mineralocorticoids
  • Androgens
Glucocorticoids
The primary glucocorticoid released by the adrenal gland is cortisol. Its secretion is regulated by the hormone ACTH from the anterior pituitary. Upon binding to its target, cortisol enhances metabolism in several ways:
  • It stimulates the release of amino acids from the body
  • It stimulates lipolysis, the breakdown of fat
  • It stimulates gluconeogenesis, the production of glucose from newly-released amino acids and lipids
  • It increases blood glucose levels in response to stress, by inhibiting glucose uptake into muscle and fat cells
  • It strengthens cardiac muscle contractions
  • It increases water retention
  • It has anti-inflammatory and anti-allergic effects.[6]
Cortisone is a corticoid essential to life and functions to maintain stress reactions.
Mineralocorticoids
The primary mineralocorticoid is aldosterone. Aldosterone regulates the balance of blood electrolytes and also cause the kidneys to retain sodium and excrete potassium and hydrogen. [6] Mineral corticoids are also involved in gluconeogenesis, which is the process whereby your body converts glycogen to glucose (blood sugar). It also increased water retention and blood volume.[6]
Adrogens
Small amounts of corticoid sex hormones, both male and female, are also produced by the adrenal cortex. The most important androgens include:
  • Testosterone
  • Dihydrotestosterone (DHT): a metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors.
  • Androstenedione (Andro)
  • Dehydroepiandrosterone (DHEA): It is the primary precursor of natural estrogens. DHEA is also called dehydroisoandrosterone or dehydroandrosterone.

Nutrients

Two primary nutrients for the adrenal glands are:

  1. pantothenic acid
  2. and vitamin C.
Pantothenic acid: - A deficiency of pantothenic acid can lead to adrenal exhaustion (chronic fatigue) and ultimately to destruction of the adrenal glands. A deficiency of pantothenic acid also causes a progressive fall in the level of adrenal hormones produced.
Vitamin C - One of the largest tissue stores of vitamin C is the adrenals; it is exceeded only by the level of vitamin C in the pituitary. Physical and mental stress increase the excretion of adrenocorticotropic hormone (ACTH) from the pituitary, which is the hormone that tells the adrenals to increase their activity. The increased adrenal activity, in turn, depletes both vitamin C and pantothenic acid from the glands.
Humans cannot produce vitamin C. They therefore attempt to replenish the needs of the adrenals by taking the vitamin from other storage locations in the body.

If your overall ascorbate status is low, there may be an insufficient amount available to satisfy the needs of the adrenals. Under this condition, normal adrenal hormone response may become inadequate, leading to an inadequate immune function.

Cholesterol

All adrenocortical hormones are synthesised from cholesterol.[6] Cholesterol is transported into the inner mitochondrial membrane by steroidogenic acute regulatory protein (STAR), where it is converted into pregnenolone by the enzyme CYP11A1.[6] Accordingly, production of hormones in all three layers of the adrenal cortex is limited by the transportation of cholesterol into the mitochondria and by its conversion into pregnenolone.[6]

The major regulator of adrenocortical growth and secretion activity is the pituitary hormone ACTH (adreno-cortico-tropic hormone). ACTH attaches to receptors on the surface of the adrenal cortical cell and activates an enzymatic action that ultimately produces cyclic adenosine monophosphate (cAMP). cAMP, in turn, serves as a co-factor in activating key enzymes in the adrenal cortex.


The adrenal cortex is able to synthesize cholesterol and to also take it up from circulation.

All steroid hormones produced by the adrenal glands are derived from cholesterol through a series of enzymatic actions, which are all stimulated initially by ACTH.

Steroid biosynthesis involves the conversion of cholesterol to pregnenolone, which is then enzymatically transformed into the major biologically active corticosteroids.

cAMP is produced from adenosine triphosphate (ATP) by the action of adenylate cyclase. Adenylate cyclase activity in the brain is inhibited by micromolar concentrations of lead, mercury, and cadmium. One of the key biochemical steps in the conversion of adrenal pregnenolone to cortisol and aldosterone involves an enzyme identified as 21-hydroxylase.

Steroid Biosynthesis Blocked by Mercury

Mercury causes a defect in adrenal steroid biosynthesis by inhibiting the activity of 21a-hydroxylase. The consequences of this inhibition include:

  • lowered plasma levels of corticosterone, and
  • elevated concentrations of progesterone and dehydroepiandrosterone (DHEA, an adrenal male hormone.

Adrenal Hyperplasia

Hypothesis
The inhibition of the 21-hydroxylase system may be the mechanism behind the mercury-induced adrenal hyperplasia.
Because patients with 21a-hydroxylase deficiencies are incapable of synthesizing cortisol with normal efficiency, there's a compensatory rise in ACTH leading to adrenal hyperplasia, and excessive excretion of 17a-hydroxyprogesterone, which, without the enzyme 21-hydroxylase, cannot be converted to cortisol. The inhibition of the 21-hydroxylase system may be the mechanism behind the mercury-induced adrenal hyperplasia. Adrenal hyperplasia can stress the adrenal glands by their accelerated activity to produce steroids to the point that production begins to diminish and the glands will atrophy. The result is a subnormal production of corticosteroids.

Hypothalamus-Pituitary-Adrenal Axis

Both lead (Pb) and mercury (Hg) can precipitate pathophysiological changes along the hypothalamus-pituitary-adrenal and gonadal axis that may seriously affect:
  • reproductive function,
  • organs, and
  • tissues.

Leukocyte production, distribution, and function are markedly altered by glucocorticosteroid administration.

In Addison's disease (hypofunction of adrenal glands), neutrophilia occurs 4-6 hours after administration of a single dose of hydrocortisone, prednisone, or dexamethasone. Neutrophilia is an increase in the number of neutrophils in the blood. Neutrophils are also called polymorphonuclear leukocytes (PMNs).

Mercury not only causes a suppression of adrenocorticosteroids that would normally have stimulated an increase of PMNs, but at the same time also affects the ability of existing PMNs to perform immunity by inhibiting a reaction that destroys foreign substances.

Adrenal Mercury Toxicity

Mercury builds up in the pituitary gland and depletes the adrenals of both pantothenic acid and vitamin C. Stress and the presence of mercury will have a very negative effect on the adrenal production of critical steroids.

The ability of the adrenal gland to produce steroids is called steroidogenesis and is dependent upon reactions mediated by the enzyme Cytochrome P-450.

These adrenal functions are also affected by metal ions.

Other Effects

Suicide

Part of the reason for depression is related to mercury's effect of reducing the development of posterior pituitary hormone (oxytocin).

Low levels of pituitary function are associated with depression and suicidal thoughts, and appear to be a major factor in suicide of teenagers and other vulnerable groups.

As a profession, dentists rank highest in suicide.

Autopsy studies in Sweden showed that the pituitary glands of dentists held 800 times more mercury than people who were not in dentistry.

Braces

Suicidal thoughts are not limited to dental personnel though. Suicide is close to the number-one cause of death in teenagers.

Braces increase the electrical and toxic load people are carrying if they have amalgam in their mouths. Amalgam can create suicidal tendencies by itself, but the addition of braces, nickel crowns, or even gold crowns evidently increases the exit rate of mercury, and the glands react--or actually stop reacting. Suicidal tendencies tend to disappear within a few days of supplemental oxytocin extract, along with dental metal removal.

Menstrual cycle problems, also normalize and fertility increases and endometriosis symptoms subside.

Frequent Urination

The center that controls the need to get up several times each night to urinate is the posterior pituitary gland. There is a certain amount of solid material that must be disposed of daily in the urine.

  • If the concentration of these solids is high (yield a specific gravity of 1.022 to 1.025) then the proper volume of urine will be excreted in a day.
  • Should the concentration be half that, or yielding a specific gravity of 1.012 for instance, then it will take double the amount of urine to rid yourself of the same amount of solid. In other words, the solids remain the same.

If the concentration of the urine is reduced, the total volume of urine is increased substantially. This ability of the kidney is controlled by the posterior pituitary.

Enzymatic Impacts to Cellular Function

Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes such as cysteine dioxygenase, gamma-glutamyl transpeptidase (GGT), and sulfite oxydase, along with neurotransmitter amino acids which have been found to be significant factors in many autistics, plus enzymatic processes involving vitamins B6 and B12, with effects on the cytochrome-C energy processes as well. [7][8][9][10][11](36)[12][13][14][15][16][17][18] For example, the Vitamin B6 activating enzyme, B6-kenase, is totally inhibited in the intestine at extremely low (nanamolar) concentrations. [19]

Effective therapeutic methods of dealing with these enzymatic blockages
Epson salts (magnesium sulfate) baths
Supplementation with the p5p form of Vit B6, N-acetyl cysteine [20][21]
vit B12 shots

Mercury has also been found to have adverse effects on cellular mineral levels of:

Lithium
Supplementing with these minerals has also been found to be effective in the majority of cases(39,50), and lithium has even been found to cause regeneration of neurons in damaged areas of the brain such as the hippocampus.

Enzymatic Impacts on the Liver

Another of the results of these toxic exposures and enzymatic blockages is the effect on the liver and disfunction of the liver detoxification processes which autistic children have been found to have.[28][29][30](36)[31][32][33][34](500).

All of the autistic cases tested were found to have high toxic exposures/effects and liver detoxification profiles outside of normal.[28]

Digestive Enzymes and Lack of Pain Response

Lack of Pain Response
Mercury and toxic metals block enzymes required to digest milk casein and wheat gluten, resulting in dumping morphine like substances in the blood that are neurotoxic and psychotic, as a major factor in schizophrenia, autism, and ADHD.

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 these allergic/immune reactive conditions. [35][36][37][38] [39][40][41][16][17] [18][7][8][9][10][11][42] [43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58](36)[12][13][14][15][31][32][33][34][59]

DPP IV Activity

For example mercury has been found to strongly inhibit the activity of xanthine oxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein or wheat protein gluten [35][36][37][38][39][40][41][16][17][18][42][43][44][45][46][60][47](500)[53][54][55][56][57][58][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][59][77][78], and the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation.

CD26 or DPP IV is a cell surface glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain.
Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors.[35]

Bioactive Peptide Beta-casomorphin 7 (BCM-7)

Beta-casomorphine-7 is a morphine like compound that results in neural dysfunction [61][62][63][64][65][66][67][68][69][70][71][72], as well as being a direct histamine releaser in humans and inducing skin reactions. [79][48][72]

  1. Proteins in bovine milk are a common source of bioactive peptides.
    • The peptides are released by the digestion of caseins and whey proteins.[77][78]
  2. BCM-7 appears to play a significant role in the aetiology of human diseases.[77][78]
  3. Higher levels of BCM-7 is found in the blood of children with autism, most of whom have been exposed to high levels of toxic metals through:

In vitro the bioactive peptide beta-casomorphin 7 (BCM-7) is yielded by the successive gastrointestinal proteolytic digestion of bovine beta-casein variants A1 and B, but this was not seen in variant A2 or in goats milk.

  • In hydrolysed milk with variant A1 of beta-casein, BCM-7 level is 4-fold higher than in A2 milk.
  • Variants A1 and A2 of beta-casein are common among many dairy cattle breeds.
A1 Variant A2 Variant
A1 is the most frequent in
  • Holstein-Friesian (0.310–0.660),
  • Ayrshire (0.432–0.720) and
  • Red (0.710) cattle.
In contrast, a high frequency of A2 is observed in
  • Guernsey (0.880–0.970) and
  • Jersey (0.490–0.721) cattle.[77][78]
Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from ischaemic heart disease. It appears that the populations that consume milk containing high levels of beta-casein A2 have a lower incidence of cardiovascular disease and type 1 diabetes.

Immunosuppression Opioid

Beta-casomorphin-7 has opioid properties including immunosuppression, which account for the specificity of the relation between the consumption of some but not all beta-casein variants and diabetes incidence.

Autism, Schizophrenia, Mania Study

Studies involving large samples of patients with autism, schizophrenia, or mania found that over 90 percent 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.[61][62][63][64] [65][66] [67][68][69][70][71][72][80][81], and similarly for the corresponding enzyme needed to digest wheat gluten.[61][62][63][64][65][66][67][68][73][74][75][76]

Like casein, gluten breaks down into molecules with opioid traits, called gluteomorphine or gliadin. As with caseomorphin, it too can retain biological activity if the enzymes needed to digest it are not functioning properly.

SIDS Hypothesis

BCM-7 has also been suggested as a possible cause of sudden infant death syndrome (SIDS).

Neurological Disorders

In addition, neurological disorders, such as autism and schizophrenia, appear to be associated with milk consumption and a higher level of BCM-7.[77][78]

Casein Immunology

Similarly to BCM-7, a corresponding form of gluten protein has similar effects. [61][62][63][64][65][66][67][68][73][74][75][76]

The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein.

Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition. [82][83],etc.

Naltrexone Study

A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects.[83]

The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio.

The neurotoxic effects of such opioid mechanisms has also been found to be a factor in multiple sclerosis, and low dose naltrexone (LDN) has been found to often be effective in reducing MS symptoms and exerbations. [84]

T-cell Studies

Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors.[85][86]As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detoxification.[53][54][55][56][57][58][87][88](500)[28][29][30][89][90][91][82]

  • As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs. (500)[87][88] recently began testing children with autism. [92][93]

Glutathione Depletion

Studies have also found heavy metals to deplete glutathione and bind to protein-bound sulfhydryl SH groups, resulting in inhibiting SH-containing enzymes and production of reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl radical. [22][23][24][25][94][95][96][97][98][99][100][101][12][13][14][15][102][103][104][105][106][107][20][21][108] [109][110][82]

In addition to forming strong bonds with SH and other groups like OH, NH2, and Cl in amino acids which interfere with basic enzymatic processes, toxic metals exert part of their toxic effects by replacing essential metals such as zinc at their sites in enzymes.

An example of this is mercury’s disabling of the metallothionein protein, which is necessary for the transport and detoxification of metals.

Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions[111], thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function.

Matallothionein Detoxification Study

Another large study [31][32][33][34] found a high percentage of autistic and PDD children are especially susceptible to metals due to the improper functioning of their metallothionein detoxification process, and that with proper treatment most recover.

Mercury has also been found to play a part in neuronal problems through blockage of the P‑450 enzymatic process.[112][113][20][21]

Accelerated Lipofuscin Study

Another study found accelerated lipofuscin deposition--consistent with oxidative injury to autistic brain in cortical areas serving language and communication.(97) Compared with controls, children with autism had significantly higher urinary levels of lipid peroxidation.

Double-blind, placebo-controlled trials of potent antioxidants--vitamin C or carnosine--significantly improved autistic behavior.

Learn More

References

  1. Summers, A.O., Wireman, J., Vimy, M.J., Lorscheider, F.L., Marshall, B., Levy, S.B., Bennett, s., Billard, L., Mercury released from dental "silver" fillings provokes an increase in mercury and antibiotic resistant bacteria in primates oral and intestinal flora; Antimicrobial Agents and Chemotherapy, vol. 37, pp.825-834, 1993
  2. 2.0 2.1 WikiPedia Endocrine Gland
  3. 3.0 3.1 3.2 3.3 3.4 WikiPedia Thyroid
  4. John Cargill MA, MBA, MS; Susan Thorpe Vargas MS, Ph.D. Hypothyroidism link
  5. WikiPedia Thyroid Stimulating Hormone (TSH)
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 WikiPedia Adrenal Cortex
  7. 7.0 7.1 Mc Fadden SA, Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65
  8. 8.0 8.1 Markovich et al, Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1, Toxicol Appl Pharmacol, 1999,154(2):181‑7
  9. 9.0 9.1 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
  10. 10.0 10.1 T.L. Perry et al, Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase deficiency, Ann Neural, 1985, 18(4):482-489
  11. 11.0 11.1 Ceaurriz et al, Role of gamma-glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of inorganic mercury, J Appl Toxicol,1994, 14(3): 201-
  12. 12.0 12.1 12.2 12.3 Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism., Invest Clin 1996, 37(2):113-28;
  13. 13.0 13.1 13.2 13.3 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;
  14. 14.0 14.1 14.2 14.3 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;
  15. 15.0 15.1 15.2 15.3 Carlsson ML., Is infantile autsim a hypoglutamatergic disorer?, J Neural Transm 1998, 105(4-5): 525-35.
  16. 16.0 16.1 16.2 Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents: Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol 1978; 20(6): 729-35;
  17. 17.0 17.1 17.2 W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, In vitro effect of mercury on enzyme activities, Environ Res, 1992, 57(1):96-106;
  18. 18.0 18.1 18.2 Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT; Gastrointestinal abnormalities in children with autistic disorder. J Pediatr 1999, 135:559-63.
  19. Srikantaiah MV, Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine: Part III--purification and properties of monkey intestinal pyridoxal kinase., Indian J of Biochem 7:151-156 (1970).
  20. 20.0 20.1 20.2 Makani A, Gollapudi S, Yel L, Chiplunkar S, Gupta S; Biochemical and molecular basis for thimerosal-induced apoptosi in T-cells; a major role of mitochondrial pathway; Genes and Immunity, 2002, 3:270-278;
  21. 21.0 21.1 21.2 James S.J., Slikker W, Melnyk S, New E, Pogribna M, Jernigan S; Thimerosal neurotoxicity is associated with glutathione depletion: Protection with nutritional supplementation; Dept. of Pediatrics, College of Medicine, Univ. of Arkansas, and Arkansas Children’s Hospital Reserch Institute, Little Rock, Ark; Neurotoxicology Conference, Hawaii, February 2004
  22. 22.0 22.1 Pfieffer SI; Norton J; Nelson L; Shott S. Efficacy of vitamin B6 and magnesium in the treatment of autism. J Autism Dev Disord 1995 Oct;25(5):481‑93;
  23. 23.0 23.1 Chuang D. Et al, National Institute of Mental Health, Science News, Nov 11, 2000, 158:309;
  24. 24.0 24.1 Lithium Protects Against Neuron Damage by Glutamate, Science News, 3-14-98, p164;
  25. 25.0 25.1 Moore G.J.et al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276.
  26. B. Windham, Cognitive and Behavioral Effects of Toxic Metals, (over 150 medical study references) http://www.flcv.com/tmlbn.html;
  27. Prenatal and neonatal effects of mercury on infants, http://www.flcv.com/fetaln.html
  28. 28.0 28.1 28.2 Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63;
  29. 29.0 29.1 Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998. 3(3):187-98;
  30. 30.0 30.1 (copyright) HRI-Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001; http://www.hriptc.ort/Publish0900/index.html
  31. 31.0 31.1 31.2 Walsh, WJ, Health Research Institute, Autism and Metal Metabolism, http://www.hriptc.org/autism.htm, Oct 20, 2000;
  32. 32.0 32.1 32.2 Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning, 2000, http://www.hriptc.org/mhfres.htm;
  33. 33.0 33.1 33.2 HRI‑Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001;
  34. 34.0 34.1 34.2 Metal-Metabolism and Autism: Defective Functioning of Metallothionein Protein, Amy Holmes, MD; http://www.healing-arts.org/children/metal-metabolism.htm
  35. 35.0 35.1 35.2 Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology 1990; 29(5): 445-52.
  36. 36.0 36.1 Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. J Inorg Biochem 1996; 62(4): 271-9;
  37. 37.0 37.1 Lead and mercury mutagenesis: Role of H2O2, superoxide dismutase, and xanthine oxidase, Maria E. Ariza, Gautam N. Bijur, Marshall V. Williams, Environ. Mol. Mutagen. 31:352-361, 1998;
  38. 38.0 38.1 Naidu BV, Fraga C, Salzman AL, Szabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant 22:784-93;
  39. 39.0 39.1 Liaudet L, Szabó G, Szabó C. 2003. Oxidative stress and regional ischemia-reperfusion injury: the peroxynitrite – PARP connection. Coronary Artery Dis. 14:115-122;
  40. 40.0 40.1 Naidu BV, Fraga C, Salzman AL, Szabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant. 22: 784-93;
  41. 41.0 41.1 Virág L, Szabó E, Gergely P, Szabó C. 2003. Peroxynitrite- induced cytotoxicity: mechanisms and opportunities for intervention. Toxicology Letters 140:113-124;& Xanthine oxidase and neutrophil infiltration in intestinal ischemia. Grisham MB, Hernandez LA, Granger DN. Am J Physiol. 1986 Oct;251(4 Pt 1):G567-74 http://www.inotekcorp.com/content/xo_inhibitors.asp
  42. 42.0 42.1 Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996;10(6):435-40
  43. 43.0 43.1 Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993 Jul;44(1):13-8;
  44. 44.0 44.1 Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of dipeptidyl peptidase IV from human placenta', Eur J Biochem 1982 Aug;126(2):359-65;
  45. 45.0 45.1 Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92;
  46. 46.0 46.1 Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174,etc., http://www.autismndi.com/
  47. 47.0 47.1 Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure, 1998; 8(5): 278-84.
  48. 48.0 48.1 Crinnion WJ. Environmental toxins and their common health effects., Altern Med Rev 2000, 5(1):52-63.
  49. Immunological findings in autism. Int Rev Neurobiol. 2005;71:317-41, Cohly HH, Panja A;
  50. Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis). Toxicol Lett. 1996 Dec;89(1):19-28
  51. Ilbäck NG, Wesslén L, Fohlman J, Friman G; & Trace element distribution in heart tissue sections studied by nuclear microscopy is changed in Coxsackie virus B3 myocarditis in methyl mercury-exposed mice. Biol Trace Elem Res. 2000 Winter;78(1-3):131-47
  52. Crompton P, Ventura AM, de Souza JM, Santos E, Strickland GT, Silbergeld E., Assessment of mercury exposure and malaria in a Brazilian Amazon riverine community. Environ Res. 2002 Oct;90(2):69-75
  53. 53.0 53.1 53.2 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 http://www.autism.com/ari/mercurylong.html
  54. 54.0 54.1 54.2 Dr. A Holmes, Autism Treatment Center, Baton Rouge, La; http://www.healing-arts.org/children/holmes.htm#wethink
  55. 55.0 55.1 55.2 Jaquelyn McCandless, M.D., Autism Spectrum Treatment Center, Woodland Hills, CA, & Jaquelyn McCandless, M.D, Children with Starving Brains, A Medical Treatment Guide for Autism Spectrum Disorder, 2003 http://www.autism‑rxguidebook.com/DesktopDefault.aspx?tabindex=11&tabid=15
  56. 56.0 56.1 56.2 L. Redwood, Mercury and Autism, Vitamin Research News, May 2001, 15(5):1-12
  57. 57.0 57.1 57.2 Andrew H. Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996, http://www.noamalgam.com/
  58. 58.0 58.1 58.2 Dr. R. Buttar, Autism, the Misdiagnosis of Our Future Generations, Congressional Testimony: Government Reform and Oversight Committee, U.S. House of Representatives, May 2004, http://www.hyperbaricmedicalassociation.org/docs/0_BUTTAR1.PDF
  59. 59.0 59.1 Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism. Vojdani A, Pangborn JB, et al, Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):189-99.
  60. Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics., Kidney Int. 1993 Jul;44(1):13-8
  61. 61.0 61.1 61.2 61.3 61.4 61.5 J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999. http://news.ufl.edu/1999/03/15/autism/
  62. 62.0 62.1 62.2 62.3 62.4 62.5 Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000.http://www.feingold.org/Research/cade.html
  63. 63.0 63.1 63.2 63.3 63.4 63.5 http://www.paleodiet.com/autism/
  64. 64.0 64.1 64.2 64.3 64.4 64.5 Beta-casomorphin induces Fos-like immunoreactivity in discrete brain regions relevant to schizophrenia and autism Autism March 1999 vol 3(1) 67-83; Sun, ZJ, Cade JR, et al
  65. 65.0 65.1 65.2 65.3 65.4 65.5 A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats, J.R. Cade, Z. Sun , Univ of Florida, USA , Autism, Vol. 3, No. 1, 85-95 (1999) DOI: 10.1177/1362361399003001007 (copyright) 1999 The National Autistic Society, SAGE Publications http://aut.sagepub.com/cgi/content/abstract/3/1/85
  66. 66.0 66.1 66.2 66.3 66.4 66.5 Opiate hypothesis in infantile autism - Therapeutic trials with naltrexone, Leboyer M, et al., Encephale 1993 Mar-Apr;19(2):95-102;
  67. 67.0 67.1 67.2 67.3 67.4 67.5 Food allergy and infantile autism. Lucarelli S, et al., Panminerva Med 1995 Sep;37(3):137-41; http://www.feingold.org/Research/autism.html
  68. 68.0 68.1 68.2 68.3 68.4 68.5 Application of the Exorphin Hypothesis to Attention Deficit Hyperactivity Disorder: A Theoretical Framework, by Ronald Hoggan A Thesis Submitted To The Faculty Of Graduate Studies In Partial Fulfillment Of The Requirements For The Degree Of Master Of Arts, Graduate Division Of Educational Research,Calgary, April, 1998 University of Calgary
  69. 69.0 69.1 69.2 69.3 Reichelt KL., Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4;
  70. 70.0 70.1 70.2 70.3 Reichelt KL et al, Biologically active peptide-containing fractions in schizophrenia and childhood autism., Adv Biochem Psychopharmocol 1981; 28: 627-43;
  71. 71.0 71.1 71.2 71.3 Lucarelli S, Cardi E, et al, Food allergy and infantile autism., Panminerva Med 1995; 37(3):137-41;
  72. 72.0 72.1 72.2 72.3 72.4 Shel L, Autistic disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5):413-4.
  73. 73.0 73.1 73.2 73.3 Huebner FR, Lieberman KW, Rubino RP, Wall JS. Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Peptides 1984; 5(6):1139-47;
  74. 74.0 74.1 74.2 74.3 Wheat gluten as a pathogenic factor in schizophrenia. Singh MM, Kay SR, Science 1976 Jan 30;191(4225):401-2;
  75. 75.0 75.1 75.2 75.3 Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates. Huebner FR, Lieberman KW, Rubino RP, Wall JS. Peptides. 1984 Nov-Dec;5(6):1139-47;
  76. 76.0 76.1 76.2 76.3 Naloxone antagonises effect of alpha-gliadin on leucocyte migration in patients with coeliac disease. Horváth K, Gráf L, Walcz E, Bodánszky H, Schuler D. Lancet. 1985 Jul 27;2(8448):184-5
  77. 77.0 77.1 77.2 77.3 77.4 Polymorphism of bovine beta-casein and its potential effect on human health, J Appl Genet 48(3), 2007, pp. 189–198, Stanis³aw Kamiñski1, Anna Cieoeliñska1, El¿bieta Kostyra2;
  78. 78.0 78.1 78.2 78.3 78.4 Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia 1999 Aug;42(8):1032; Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE.
  79. Kurek M, Przybilla B, Hermann K, Ring J., An opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy immunol 1992; 97(2): 115-20
  80. Willemsen-Swinkels SH, Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H. Plasma beta-endorphin concentrations in people with learning disability and self-injurious and/or autistic behavior., Br J Psychiary 1996; 168(1):105-9;
  81. Leboyer M, Launay JM et al. Difference between plasma N- and C-terminally directed beta-endorphin immunoreactivity in infantile autism. Am J Psychiatry 1994; 151(12): 1797-1801.
  82. 82.0 82.1 82.2 Annotated Bibliography: Adverse health effects related to mercury and amalgam fillings and clinically documented recoveries after amalgam replacement. Windham, B. (over 3000 peer-reviewed references); http://www.flcv.com/amalg6.html
  83. 83.0 83.1 Scifo R, Marchetti B, et al. Opioid-immune interactions in autism: behavioral and immunological assessment during a double-blind treatment with naltexone., Ann Ist Super Sanita 1996; 32(3): 351-9.
  84. LDN for MS Trials/Experience http://www.ldnresearchtrust.org/default.asp?page_id=77
  85. Eedy DJ, Burrows D, Dlifford T, Fay A., Elevated T cell subpopulations in dental students. J prosthet Dent 1990; 63(5):593-6;
  86. Yonk LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341-5.
  87. 87.0 87.1 V.D.M. Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden, Lymphocyte Immuno-Stimulation Assay - MELISA, paper presented at International Autism Conference, San Diego, 2002 http://www.melisa.org/autism.php
  88. 88.0 88.1 Mercury-specific Lymphocytes: an indication of mercury allergy in man, J. Of Clinical Immunology, 1996, Vol 16(1);31-40; see: http://www.melisa.org
  89. Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers;
  90. Dr. SB Edelson, http://www.edelsoncenter.com
  91. (copyright) Eppright TD, Sanfacon JA, Horwitz EA. ADHD, infantile autism, and elevated blood-lead: a possible relationship. (case study) Mo Med 1996; 93(3):136-8.
  92. A clinical trial of combined anti-androgen and anti-heavy metal therapy in autistic disorders. Geier DA, Geier MR. Neuro Endocrinol Lett. 2006 Dec;27(6):833-8;
  93. A prospective assessment of androgen levels in patients with autistic spectrum disorders: biochemical underpinnings and suggested therapies. Geier DA, Geier MR. Neuro Endocrinol Lett. 2007 Oct;28(5):565-73
  94. Rodier P.M., Developing brain as a target of toxicity., Environ Health Perspect 1995; 103(Supp 6): 73-76;
  95. Rice DC, Barone S, Critical Periods of Vulnerability for the Developing Nervous System: Evidence from human and animal models. Environ Health Persect 2000, 108(supp 3):511-533.
  96. Grandjean P; Jurgensen PJ; Weihe P., Milk as a Source of Methylmercury Exposure in Infants. Environ Health Perspect 1994 Jan;102(1):74‑7.
  97. Science News, Methylmercury’s toxic toll. July 29, 2000, Vol 158, No.5, p77
  98. National Research Council, Toxicological Effects of Methylmercury, National Acadamy Press, Wash, DC, 2000
  99. U.S. CDC, Second National Report on Human Exposure to Environmental Chemicals, http://www.cdc.gov/exposurereport/
  100. U.S. Centers for Disease Control, Mar 2001, Blood and Hair Mercury Levels in Young Children and Women of Childbearing Age ‑‑‑ United States, 1999 http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.htm
  101. Grandjean P, 2000, Health effects of seafood contamination with methylmercury and PCBs in the Faroes, Atlantic Coast Contaminants Workshop, June 22-25, 2000, Bar Harbor Maine; & Environ Res, 1998; 77: 165-72
  102. P.Bulat, Activity of Gpx and SOD in workers occupationally exposed to mercury, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9;
  103. Stohs SJ, Bagchi D., Oxidative mechanisms in the toxicity of metal ions., Free Radic Biol Med 1995; 18(2): 321-36.
  104. Spivey-Fox MR., Nutritional influences on metal toxicity. Environ Health Perspect 1979; 29: 95-104;
  105. Pfeiffer SI et al, Efficacy of vitamin B6 and magnesium in the treatment of autism., J Autism Dev Disord 1995, 25(5):481-93.
  106. Govani S, Memo M., Chronic lead treatment differentially affects dopamine synthesis, Toxicology 1979, 12:343-49;
  107. Scheuhammer AM. Cherian MG. Effects of heavy metal cations and sulfhydyl reagents on striatal D2 dopamine receptors. Biochem Pharmacol 1985, 34(19):3405-13.
  108. The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8;
  109. Šterzl I, Procházková J, Hrdá P, Matucha P, Bártová J, Stejskal VDM: Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis. Neuro Endocrinol Lett, 2006, 27(Suppl.1): 25-30 http://www.melisa.org/pdf/Mercury-and-autoimmunity.pdf
  110. Mechanisms by which mercury and toxic metals are factors in Multiple Sclerosis and other neurological and autoimmune conditions, and by which mercury detoxification commonly brings improvement; B Windham (Ed), http://www.flcv.com/ms.html
  111. Lars Landner and Lennart Lindestrom. Swedish Environmental Research Group(MFG), Copper in society and the Environment, 2nd revised edition. 1999.
  112. J.C.Veltman et al, Alterations of heme, cytochrome P‑450, and steroid metabolism by mercury in rat adrenal gland, Arch Biochem Biophys,1986, 248(2):467‑78
  113. A.G.Riedl et al, Neurodegenerative Disease Research Center, King's College,UK, P450 and hemeoxygenase enzymes in the basal ganglia and their role's in Parkinson's disease, Adv Neurol, 1999; 80:271‑86
Personal tools