Mercury-Caused Endocrine Conditions Causing Widespread Adverse Health
Effects, Cognitive Effects, and Fertility Effects B.Windham(Ed.)
I. Introduction.
As will be documented in this paper, the majority
of the population receives significant mercury exposures and significant
adverse health effects are common.
Mercury has been found to be an endocrine system disrupting chemical in
animals and people, disrupting function of the pituitary gland, thyroid gland,
parathyroid gland, thymus gland, adrenal gland, pineal gland, enzyme production
processes, and affecting many hormonal and enzymatic functions at very low
levels of exposure . The main factors
determining whether chronic conditions are induced by metals appear to be
exposure and genetic susceptibility, which determines individuals immune
sensitivity and ability to detoxify metals(405). Very low levels of exposure have been found
to seriously affect
large groups of individuals who are immune sensitive to toxic
metals, or have an inability to detoxify metals due to
such as deficient sulfoxidation or metallothionein function or other
inhibited enzymatic processes related to detoxification or excretion of metals.
Toxic metal exposures are common and they often have additive or synergistic adverse effects.
Thyroid conditions are extremely common
and adversely affect the health of millions of people, though most cases are
undiagnosed (580,581). The thyroid gland
secretes hormones which control the body’s metabolic rate, using iodine to
create thyroid hormone. So iodine
deficiency is a common cause of hypothyroid condition (395). The hypothalamus secretes a hormone which
triggers thyroid-stimulating hormone (TSH) from the pituitary gland to cause
the thyroid gland to produce thyryroxine (T4) and triiodothyronine (T3) (produces
mostly T4). T4 is then converted in the body to the active thyroid hormone
T3. A problem with any of these steps
can cause hypothyroidism. As will be seen, toxic metal exposures such as
mercury can accumulate and block or inhibit any of these necessary processes,
as can other factors. The hypothalamus also controls hormone secretions by the
pituitary gland. Mercury has been found to commonly accumulate in the hypothalamus(303), affecting hormone secretions of the
pituitary or thyroid gland and many bodily functions. Calcitonin is another hormone secreted by the
thyroid gland that maintains blood calcium levels and prevents hypercalcemia
and which can be affected.
Effects and Symptoms of Thyroid
Deficiency: fatigue, nervousness,
depression, increased allergies, cold sensitivity, skin problems, brittle
nails, weight problems, constipation, infertility, memory problems, low immune
function, carpal tunnel syndrome.
Tests for thyroid deficiency (580)) : Standard
test is blood test for TSH level (concentrations chronically above 2..0
mU/L indicate thyroid problem and cause long term health effects).
Another
sensitive thyroid function test is the TRH stimulation test. Another test is the Achilles tendon reflex
test. A good
home test is the Barnes Basal Temperature Test (put a thermometer in
reach of bed, before getting up take temperature under arm shoulder joint
(holding tight for at least 3 minutes). Below
97.8 degrees indicates you are T3 deficient. Repeat several times.
Hashimoto’s thyroiditis is chronic
inflammation of thyroid caused by an autoimmune reaction to environmental
factors such as mercury or toxic metals or gluten sensitivity or milk casein
sensitivity (which is commonly caused by toxic metals blocking enzymatic
process needed to digest gluten or
milk casein). (see later documentation)
Other common hormone problems are
related to the adrenal glands.
The adrenal medulla manufactures epinephrine and norepinephrine
(adrenaline and noradrenaline) – the fight or flight hormones. Prolonged stress
and anxiety commonly cause imbalances of these hormones, and also can be a
factor in causing mercury to accumulate in the endocrine gland. Mercury tends
to accumulate in body areas that are stressed or inflamed due to various factors(303). The
adrenal cortex makes steroid hormones (cortisone, hydrocortisone, testosterone,
estrogen, DHEA, pregnenolone, aldosterone, androstenedrone, progesterone. Some of these are also made in other parts of
the body. The hormone aldosterone, together with the kidneys, regulates the
balance of sodium and potassium in the body, which is commonly out of balance. Mercury can accumulate in the adrenal gland
and inhibit proper function of any of these hormones. Both mercury and stress
commonly cause imbalances that result in adrenal fatigue, which is a factor in
chronic fatigue(303)
Besides imbalances of the various
adrenal hormones that can cause effects, there are common chronic conditions
that have been identified. Addison’s Disease is chronic adrenal failure, usually
related to autoimmune attack on the adrenal glands, commonly caused by toxic
exposures such as mercury (see more later). It usually results in chronic hypocortisolism,
resulting in inability to properly deal with stress. This also affects blood
pressure, insulin regulation, inflammatory response, and metabolism of
proteins, carbohydrates, and fats. (580) Symptoms of Addison’s Disease include:
skin changes such as dark tanning on scars, skin folds, toes, lips, elbows,
knees, knuckles.
Cushing’s
Syndrome is overproduction of cortisol, usually
related to tumor of pituitary or other organs.
It is also common caused by prescription drug effects of steroid
hormones, etc. Symptoms include: stomach fat, thin extremeties, moon face,
buffalo hump, excessive hair growth, irregular menstrual periods, infertility.
Adrenal fatigue can be caused by chronic
anxiety or stress, poor nutrition, toxic metal accumulation, etc. The adrenals
can become depleted leading to fatigue, weakening of immune response, disrupted
sugar metabolism, etc. (580) Environmental toxic exposure such as mercury can
block or inhibit any of the adrenal hormone processes and contribute to such
conditions.
II. Common Exposures to Significant Levels of Mercury and
Distribution in the Body
Most people with several amalgam fillings get
daily exposure of mercury at levels well above U.S. government health guidelines (16,19,20,49,199,
211,501), which amount to about 4 to 8 micrograms per day(217). Mixed metals in the mouth such as amalgam
dental fillings, metal crowns, and metal braces have been found to result in
galvanic currents in the metals which drive the metals into the saliva and
tissues of the oral cavity at high levels as well as systemically, with
accumulations in the brain and hormonal glands (14,19,84,85,183,192,348,369,
381,500). Additionally, electric and electromagnetic fields from appliances,
computer monitors, power lines, etc. cause electric currents in metals in the
mouth which further increase exposures to mercury and other metals(28). Mercury and nickel, which are highly
neurotoxic (19,84,217,372, 500) and immunotoxic
(181,91,114ab,380b,369,383ab,405), are often found at high levels in tests of
those with mixed metals in the mouth and are known to commonly cause DNA
damage(296,458,114), immune reactivity (234,330,331,342,369,375, 383,405,91),
and hormonal effects in animals and humans (50,84,104,105,369,382,459),
including related reproductive effects.
Government health agencies in other countries such as Health Canada and amalgam
manufacturers have warned against using amalgam near other metals(209,500), but
this is still common in the U.S. and several other countries. Children typically also get high levels of
exposure to highly toxic organic mercury compounds such as ethyl mercury
through thimerosal, used as a preservative in vaccines (160,409,476,555),
and to methyl mercury from fish(2). Warnings to ban or limit
consumption of fish have been issued for over 30 percent of all U.S. lakes,
including all Great Lakes, as well as U.S. river miles and bays(2).
Studies
have documented that mercury causes hypothyroidism (50,84,390,392,407),
damage of thyroid RNA(458), autoimmune thyroiditis (369,382,91), and impairment
of conversion of thyroid T4 hormone to the active T3 form(369,382,390,392,407,50d).
The thyroid gland has iodine binding sites where the iodine needed for its
function is obtained. For those with
chronic mercury exposure the mercury occupies some of the iodine binding sites,
blocking full utilization of iodine by the thyroid(394,395), in addition to the
direct damage to the thyroid since mercury is highly cytotoxic (392,394,500,etc.). These studies and clinical experience
indicate that mercury and toxic metal exposures appear to be the most common
cause of hypothyroidism and the majority treated by metals detoxification
recover or significantly improve (503,303).
Infants
of women with hypothyroxinemia at 12 weeks' gestation had significantly lower
scores on the Neonatal Behavioral Assessment Scale orientation index compared
with subjects(10b). Regression analysis showed that
first-trimester maternal free thyroid hormone T4 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.
Mercury
(especially mercury vapor from dental amalgam or organic mercury) rapidly
crosses the blood brain barrier and is stored preferentially in the pituitary
gland, thyroid gland, hypothalamus, and
occipital cortex in direct proportion to the number and extent of dental
amalgam surfaces (14,19,85,99,273,274,407), and likewise rapidly crosses the
placenta and accumulates in the fetus including the fetal brain and hormone
glands at levels commonly higher than the level in the mother(20,22-27). Milk from
mothers with 7 or more mercury amalgam dental fillings was found to have levels
of mercury approximately 10 times that of amalgam free mothers(22b).
The milk sampled ranged from 0.2 to 57 ug/L. In a population of German women, the
concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L (26).
A Japanese study found that the average mercury level in samples tested
increased 60% between 1980 and 1990[25].
The study found that prenatal Hg exposure is correlated with lower
scores in neurodevelopmental screening, but more so in the linguistic pathway(25). The
level of mercury in umbilical cord blood, meconium, and placenta is usually
higher than that in mother's blood[23-25].
Alterations
of cortical neuronal migration and cerebellar Purkinje cells have been observed
in autism. Neuronal migration, via reelin regulation, requires triiodothyronine
(T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases(407). Experimental animal models have shown that
transient intrauterine deficits of thyroid hormones (as brief as 3 days) result
in permanent alterations of cerebral cortical architecture reminiscent of those
observed in brains of patients with autism. Early maternal hypothyroxinemia
resulting in low T3 in the fetal brain during the period of neuronal cell
migration (weeks 8-12 of pregnancy) may produce morphological brain changes
leading to autism. Insufficient dietary iodine intake and a number of
environmental antithyroid and goitrogenic agents such as mercury, soy, and
peanuts can affect maternal thyroid function during pregnancy (395).
Mercury can have significant effects
on thyroid function even though the main hormone levels remain in the normal
range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely
affects the activity of selenoenzymes,
including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases(5-Di and
5'-DI) in the fetal brain, even though thyroxine(T4) levels are normal(390de). Another
mechanism by which mercury exerts such effects is mercury’s effects on selenium
levels which are required for conversion of T4 to T3(392,390d).
Gpx activity is severely inhibited,
while 5-DI levels are decreased and 5'-DI increased in the fetal brain, similar
to hypothyroidism. Thus normal thyroid
tests will not pick up this condition.
Mercury reduces the bloods ability
to transport oxygen to fetus and transport of essential nutrients including
amino acids, glucose, magnesium, zinc, selenium, and Vit B12
(43,96,198,263,264,338, 339,347,392,427); depresses enzyme isocitric
dehydrogenase (ICD) in fetus, causes reduced iodine uptake, autoimmune
thyroiditis, & hypothyroidism.
(50,91,212,222,369,382,394,407,459,35). Because of
the evidence of widespread effects on infants,
the American
Assoc. of Clinical Endocrinologists advises that all women considering becoming
pregnant should get a serum thyrotropin test so that hypothyroidism can be
diagnosed and treated early(558,7b).
Since mercury and toxic metals are common causes of hypothyroidism,
another test that should be considered is a hair element test for mercury or
toxic metal exposures and essential mineral imbalances.
Studies have also established a “clear
association” between the presence of thyroid antibodies and spontaneous abortions(511).
Levels of recurrent abortions in a population with positive levels of
thyroid antibodies in one study were 40%, 5 times the normal rate(511). Hypothyroidism is a well documented risk
factor in spontaneous abortions and infertility(9,511). Another study of pregnant women who suffer
from hypothyroidism (underactive thyroid) found a four-times greater risk for miscarriage during the second
trimester than those who don’t(511), and women with untreated thyroid
deficiency were four-times more likely to have a child with a developmental
disabilities(509f-h). Mercury through
its affects on the endocrine system is also documented to cause other
reproductive effects including infertility, low sperm counts, abnormal sperm,
endometriosis, PMS, adverse effects on reproductive organs, etc. (9,50,104,105,390,500,559).
Mercury blocks thyroid hormone
production by occupying iodine binding sites and inhibiting hormone action even
when the measured thyroid level appears to be in proper range(390,394,35). The thyroid and hypothalamus regulate body
temperature and many metabolic processes including enzymatic processes that
when inhibited result in higher dental decay(35) .
Mercury damage thus commonly results in poor bodily 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 (50,390,84), as previously
confirmed by hormonal/reproductive problems in animal populations
(104,381c,50d). Mercury also damages the
blood brain barrier and facilitates penetration of the brain by other toxic
metals and substances(311). Hypothyroidism is also known to be a major
factor in cardiovascular disease(510,509h).
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(85), while
another(348) found the mean level to be 30ppb- levels found to be neurotoxic
and cytotoxic in animal studies. Some of
the effect on depression is related to mercury’s effect of reducing the level
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. The pituitary glands of a group of dentists
had 800 times more mercury than controls(99). This may explain why dentists have much
higher levels of emotional problems, depression, suicide, etc(500,Section
VIII.). Amalgam fillings, nickel and
gold crowns are major factors in reducing pituitary function(35,50,369,etc.). Supplementary oxytocin extract has been found
to alleviate many of these mood problems(35), along
with replacement of metals in the mouth(107,500-Section VI.). The normalization of pituitary function also
often normalizes menstrual cycle problems, endometriosis, and increases fertility(35,9,500).
Mercury accumulates in the adrenal
gland and disrupts adrenal gland function(84,369,381).
In general immune activation from
toxics 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(369,375,379-383,107)
such as depression, profound fatigue,
muscoskeletal pain, sleep disturbances, gastrointestinal and neurological
problems as are seen in CFS, Fibromyalgia, and autoimmune thyroiditis. Such
symptoms usually improve significantly after amalgam removal (503,303). Such hypersensitivity has been found most
common in those with
genetic predisposition to heavy metal sensitivity
(342,369,375,382) such as found more
frequently in patients with HLA-DRA antigens(375,381,383). A significant
portion of the population appears to fall in this category and adrenal problems
have been increasing significantly in recent years(570).
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 has effects on conditions like
depression, mood disorders, ADHD, etc. 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.
Thyroid imbalances, which are documented to be commonly caused by
mercury (369,382,459,35,50,91,212), have been found to play a major role in chronic heart conditions such as
clogged arteries, mycardial infarction, and chronic heart failure(510). In a recent study, published in the Annals of
Internal Medicine, researchers reported that subclinical hypothyroidism is highly prevalent in elderly women and is
strongly and independently associated with cardiac atherosclerosis and
myocardial infarction(510c). People who tested hypothyroid usually have
significantly higher levels of homocysteine and cholesterol, which are
documented factors in heart disease. 50%
of those testing hypothyroid, also had high levels of homocysteine
(hyperhomocysteinenic) and 90% were either hyperhomocystemic or hypercholesterolemic(510a). These are also known factors in
developing arteriosclerotic vascular disease. Homocysteine levels are significantly increased in
hypothtyroid patients and normalize with treatment(510efg).
The
thymus gland plays a significant part in the establishment of the immune system
and lymphatic system from the 12th week of gestation until
puberty. Inhibition of thymus function
can thus affect proper development of the immune and lymphatic systems. Lymphocyte differentiation, maturation and
peripheral functions are affected by the thymic protein hormone thymulin.
Mercury at very low concentrations has been seen to impair some lymphocytic
functions causing subclinical manifestations in exposed workers. Animal studies
have shown mercury significantly inhibits thymulin production at very low
micromolar levels of exposure(513a). The metal allergens mercuric chloride and
nickel sulfate were found to stimulate DNA synthesis of both immature and
mature thymocytes at low levels of exposure, so chronic exposure can have long
term effects(513b). Also, micromolar levels of
mercuric ions specifically blocked synthesis of ribosomal RNA, causing
fibrillarin relocation from the nucleolus to the nucleoplasm in epithelial
cells as a consequence
of the blockade of ribosomal RNA synthesis.
This appears to be a factor in deregulation of basic cellular events and
in autoimmunity caused by mercury.
There were specific immunotoxic and biochemical alterations in lymphoid
organs of mice treated at the lower doses of mercury. The immunological defects
were consistent with altered T-cell function as evidenced by decreases in both
T-cell mitogen and mixed leukocyte responses. Mercury caused increased immunoreactivity for glial
fibrillary protein at 1 nanamole (0.2 ppb) concentration, and microglial response at even
lower levels(175). There was a particular association between
the T-cell defects and inhibition of thymic pyruvate kinase, the rate-limiting
enzyme for glycolysis(513c). Pyruvate and glycolysis problems are often
seen in mercury toxic children being treated for autism(409).
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(409-411,439,464,468,476,33,160), schizophrenia(409,410),
lupus(113,126,234,330,331,33,468), Scleroderma(468), eczema and psoriasis (323,375,385,419,33),
and allergies (271,313,330,331, 369,375,468).
Mercury and
other toxic metals also form inorganic compounds with OH, NH2, CL, in addition
to the SH radical and thus inhibits many cellular enzyme processes, coenzymes,
hormones, and blood cells(405,409,500,555). 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) as well as of xanthine oxidase(439). 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(410). Elimination of milk products from the diet
has been found to improve the condition. Similar results have been seen in
similarly but lesser affected patients with other pervasive developmental
conditions such as ADHD. Such
populations have also been found to have many with high levels of mercury who
recover after mercury detox (409,413,369,160).
As mercury levels are reduced the protein binding is reduced and improvement
in the enzymatic process occurs. Additional cellular level enzymatic effects of
mercury’s binding with proteins include blockage of sulfur oxidation processes
(33,114,194,330,331,412), enzymatic processes involving vitamins B6 and
B12(418), effects on the cytochrome-C energy processes (43,84,338c,35), along
with mercury’s adverse effects on cellular mineral levels of calcium,
magnesium, zinc, and lithium (43,96,333,338,160,500). Thus some of the main mechanisms of toxic
effects of metals include cytotoxicity; changes in cellular membrane
permeability; inhibition of enzymes, coenzymes, and hormones; and generation of
lipid peroxides or free radicals- which
result in neurotoxicity, immunotoxicity, impaired cellular respiration,
gastrointestinal/metabolic effects, hormonal effects, and immune reactivity or autoimmunity.
Mercury has been found to cause hormonal
changes which cause hair loss and greying of hair. In a large German study where 20,000 were
tested, allergies and hair-loss were found to be 2-3 times as high in a group
with large numbers of amalgam fillings compared to controls(199,9). Levels of mercury in
follicular fluid was significantly higher for those with amalgam
fillings (9,146). Based on this finding, a Gynecological Clinic that sees a
large number of women suffering from alopecia/hair loss that was not responding
to treatment had amalgams replaced in 132 women who had not responded to
treatment. 68 % of the women then
responded to treatment and alopecia was alleviated(187). In other studies involving amalgam removal,
the majority had significant improvement (40,317,503). Higher levels of hormone disturbances, immune
disturbances, infertility, and recurrent fungal infections were also found in
the amalgam group. The results of hormone tests, cell culture studies, and
intervention studies agree(9,146). Other clinics have also found alleviation of
hair loss/alopecia after amalgam removal and detox(40,317).
Another study in Japan found significantly higher levels of mercury in gray
hair than in dark hair(402).
III. Treatment of thyroid conditions.
As previously documented, for those with
amalgam fillings or toxic metal exposure amalgam replacement and detoxification
usually bring about significant improvement in thyroid function, including
thyroiditis.
Conventional treatment of hypothyroidism is Synthroid or Unithroid or Levoxyl (synthetic T4). Clinical experience has found Armour Thyroid (desiccated thyroid gland of pig) and Cytomel (synthetic T3) and Thyrolar (synthetic T4/T3 mix) to often be more effective than the conventional treatments. (580)
Nutrient supplementation found by
clinical experience to benefit hypothyroidism include complex vit B, vit C, E,
A, CoQ10, and minerals magnesium, manganese, selenium, and zinc. Deficiencies of any of these can prevent
conversion of T4 to T3 and should be corrected.
(580,581).
Iodine is the primary mineral
requirement for thyroid function and deficiency can cause hypothyroidism and
other problems. It is found in kelp, seaweeds, sea salt, and iodized salt . Iodoral is an iodine supplement that commonly cures
or improves hypothyroidism. (395) Selenium
assists in removing toxins from the body and deficiency has been found to
result in some cases of hypothyroidism.
Found in asparagus, grains, garlic, mushrooms- except the soil in some
areas is deficient. Tyrosine is a necessary precursor of thyroid hormone and
the neurotransmitters dopamine, norepinephrine, epinephrine. A deficiency can lead to hypothyroidism and
low adrenal function as well as mood disorders. DHEA is a hormone that affects other
hormone levels and metabolic function and is commonly found low in
hypothyroidism. Levels can be determined by blood test. Raw cabbage, cauliflower, or turnips contain
low levels of goitrogens, though cooking inactivates them. (580)
Natural treatments for adrenal fatigue
include vit C (3 gm/day),DHEA (50 gm/day) L-theanine (100-400 mg/day, vit B5
(1500 mg/day), Phosphatidylserine (300 mg/day), Licorice (no more than 1000
mg), Melatonin (300 mcg to 6 mg at bedtime). Limit processed foods, alcohol,
smoking. (580)
Natural treatments of Addison’s
Disease or hypocortisolism includes DHEA, Licorice, pantothenic
acid (B5), and L-Theanine (green tea extract).
A physician should be consulted to test for DHEA levels and high doses
of licorice should be used long term only under care of a doctor. DHEA deficiency is common in the aging
population, and chronic conditions like Addison’s make this more likely. Clinical studies found significant benefit in
the majority. Licorice helps to break down the amount of hydrocortisone broken
down by the liver, reducing the workload of the adrenal glands. Vit B5 activates the adrenal glands. L-Theanine works by increasing GABA levels,
which helps modulate stress and mood. (580)
Natural treatments for Cushing’s Syndrome
that have demonstrated benefits include DHEA, Vit C, Phosphatidylserine (PS),
and Melatonin (nightly) (580).
References
(2) United States Environmental
Protection Agency, Office of Water, Novermber 2000, The
National Listing of Fish and Wildlife Advisories:, EPA‑823‑F‑00‑20,
http://www.epa.gov/ost/fish/advisories/general.html
www.dep.state.pa.us/dep/deputate/watermgt/Wqp/WQStandards/FishAdvis/fishadvisory‑Hg.htm &
The Conference of New England Governors and Eastern Canadian
Premiers, New England Governors/ Eastern
Canadian Premiers Mercury Action Plan- 1998;
http://www.cmp.ca/neg/reports/mercury.htm#anchor1
; & U.S. EPA, FDA, Advisory on Fish
Consumption by Women of Child Bearing Age and Children, http://www.epa.gov/mercury/fishadv.pdf
(3) The
Third National Health and Nutrition Examination Survey (NHANES III)
(6) The study of the prevalence of depressive disorders
in primary care patients in Poland], Wiad Lek.
2007;60(3-4):109-13. Drózdz W,
Wojnar M, Araszkiewicz A, Nawacka-Pawlaczyk D, Urbański R, Cwiklińska-Jurkowska M, Rybakowski J
(9)(a)
Dr.I.Gerhard, Dr. E.Roller,et al, Tubingen Univ. Gynecological Clinic, Heidelberg,1996; & (b)Gerhard I, Monga B, Waldbrenner A,
Runnebaum B “Heavy Metals and
Fertility”, J of Toxicology and Environmental Health,Part A, 54(8):593-611,
1998; & (c) Gerhard I, Waibel S, Daniel V, Runnebaum B “Impact of heavy metals on hormonal and
immunological factors in women with repeated miscarriages”, Hum Reprod Update
1998 May;4(3):301‑309; & (d) Gerhard I, “Ganzheitiche Diagnostik un
Therapie bie Infertilitat”,
Erfahrungsheilkunde,1993, 42(3): 100-106; & (e)“Hormonal conditions
affecting women caused by environmental poisons” in Pravention, Diagnose und
Therapie von Umwelterkrankungen, JD Kruse-Jarres(Ed.), 1993, p51-68; & (f)
Gerhard I, Waldbrenner P, Thuro H, Runnebaum B, Diagnosis of heavy metal
loading by the oral DMPS and chewing gum tests. Klinisches Labor 1992,
38:404-411.
(14) (a) Mercury accumulation in tissues from dental staff and
controls in relation to exposure. Nylander M, Friberg L, Eggleston D,
Björkman L. Swed Dent J. 1989;13(6):235-43; & (b) Mercury burden of human
fetal and infant tissues. Drasch G, Schupp I, Höfl H, Reinke R, Roider G. Eur J
Pediatr. 1994 Aug;153(8):607-10; & (c ) Dental amalgam and mercury levels
in autopsy tissues: food for thought. Guzzi G,
Grandi M, Severi G et al. Am J
Forensic Med Pathol. 2006 Mar;27(1):42-5
(16) Lichtenberg H,
"Mercury vapor in the oral cavity in relation to number of amalgam
surfaces and the classic symptoms of chronic mercury poisoning", J
Orthomol Med (1996), v11, n.2, 87-94 http://www.lichtenberg.dk/symptoms_before_and_after_proper.htm
(20)(a) Vimy MJ,
Takahashi,Y, Lorscheider FL; Maternal ‑Fetal
Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine
and Medical Physiology , faculty of
Medicine, Univ. of Calgary, Calgary Alberta Canada, Amer.J.Physiol.,1990, 258:R939-945; & (b) Hahn LJ, Kloiber R, Leininger RW, Vimy MJ,
Lorscheider FL. Distribution of mercury released from amalgam fillings into monkey tissues”, FASEB J.,1990, 4:5536
(21)
R.A.Goyer,”Toxic effects of metals”in: Caserett and Doull’s Toxicology-
TheBasic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; &(b)
Goodman, Gillman, The Pharmacological Basis of Therapeutics, Mac Millan
Publishing Company, N.Y. 1985; &(c) Encyclopedia of Occumpational Health
and Safety, International Labour Office, Geneva, Vol 2, 3rd Edition.
22. Oskarsson
A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Mercury in breast
milk in relation to fish consumption and amalgam. Arch Environ Health, 1996,51(3):234‑41;&(b) Drasch G, Aigner S, Roider G, Staiger F,
Lipowsky G. Mercury
in human colostrum and early breast milk. J Trace Elem Med Biol 1998; 12:23‑27;
&(c) Paccagnella B, Riolfatti M.
Total mercury levels in human milk from Italian mothers. Ann Ig 1989:
1(3-4):661-71;
23. Yang J, Jiang Z,Wang
Y, Qureshi IA, Wu XD. Maternal‑fetal transfer of metallic mercury via placenta and
milk. Ann Clin Lab Sci 1997; 27(2):135‑141; & (b) Soong YK, Tseng R, Liu C, Lin PW. J of Formosa Medical Assoc 1991; 90(1): 59‑65;
& (c ) Sundberg J, Ersson B, Lonnerdal B,
Oskarsson A. Protein
binding of mercury in milk and plasma
from mice and man‑‑a comparison between methylmercury and inorganic
mercury. Toxicology 1999 Oct 1;137(3):169‑84.
24. Kuhnert PM, Kuhnert BR, Erhard P. Comparison of mercury levels in maternal
blood, fetal blood, fetal cord blood, and placental tissues. Am J Obstet
Gynecol, 1981, 139(2): 209-13, & Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund
M, "Longitudinal study of methylmercury and inorganic mercury in blood and
urine of pregnant and lactating women, as well as in umbilical cord
blood", Environ Res 2000 Oct;84(2):186-94;
& Kuntz WD, Pitkin RM, Bostrom AW,
Hughes MS. Maternal and chord blood mercury background
levels; a longitudinal surveillance. Am J Obstet and Gynecol 1982; 143(4): 440‑443.
25. Ramirez GB, Cruz MC, Pagulayan O, Ostrea E,
Dalisay C. The Tagum study I: analysis
and clinical correlates of mercury in maternal and cord blood, breast milk,
meconium, and infants' hair. Pediatrics
2000 Oct;106(4):774‑81; & (b) Ramirez GB, Pagulayan O, Akagi H,
Francisco Rivera A, Lee LV, Berroya A, Vince Cruz MC, Casintahan D. Tagum study II: follow-up study at two years
of age after prenatal exposure to mercury.
Pediatrics. 2003 Mar;111(3):e289-95;
&(c) Warfvinge K, Berlin M, Logdberg
B. The effect on
pregnancy outcome and fetal brain development of prenatal exposure to mercury
vapour. Neurotoxicology 1994; 15(4).
26. Drexler H, Schaller KH. The mercury concentration
in breast milk resulting from amalgam fillings and dietary habits. Environ Res 1998; 77(2): 124-9.
27. Mottet NK, Shaw CM,
Burbacher, TM, Health Risks from
Increases in Methylmercury Exposure, Health Perspect 1985; 63: 133‑140;
& (b) P.Grandjean et al, “MeHg and neurotoxicity in children”, Am J
Epidemiol, 1999; & Sorensen N, et al; Prenatal mercury exposure raises
blood pressure, Epidemiology 1999, 10:370-375; & Grandjean P; Jurgensen
(33) (a) 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; &
(b)2S.A.McFadden, “Xenobiotic metabolism and adverse environmental response:
sulfur-dependent detox pathways”,Toxicology, 1996, 111(1-3):43-65;
&(c) S.C. Langley-Evans et al, “SO2:
a potent glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol
Endocrinol, 114(2):89-98; & (d)Alberti A, Pirrone
P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children.
Biol Psychiatry 1999, 46(3):420-4.
(35) Huggins HA, Levy,TE, Uniformed Consent:
the hidden dangers in dental care, 1999, Hampton Roads Publishing Company
Inc; & Hal Huggins, Its All in Your Head,
1997; & Center for Progressive Medicine, 1999, www.hugnet.com
(38) Sensitization
to inorganic mercury could be a risk factor for infertility; Podzimek S,
Prochazkova J, Bultasova L, Bartova J, Ulcova-Gallova Z, Mrklas L, Stejskal
VD., Neuro Endocrinol Lett. 2005 Aug;26(4):277-82; & S.Ziff and M.Ziff, Infertility
and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause?,
Bio-Probe, Inc. ISBN: 0-941011-03-8.1987
(40) F.Perger, Amalgamtherape, in Kompendiu
der Regulationspathologie und Therapie, Sonntag-Verlag, 1990; &
“Belastungen durch toxische Schwermetalle”, 1993, 87(2): 157-63; & K.H.Friese, ”Homoopathische
Behandlung der Amalgamvergiftung”,
Allg.
Homoopathische Z, 241(5); 184-187, & Erfahrungsheikunde, 1996, (4):
251-253; & “Amalgamvergiftung_moglicher”Der Naturazt,1995,135(8):13-15;
& “Schnupfen-Was tun?”, Therapeutikon, 1994, 8(3): 62-68;
(43) (a)Knapp LT; Klann
E. Superoxide‑induced stimulation
of protein kinase C via
thiol modification and
modulation of zinc content. J Biol Chem 2000 May 22; &
(b)B.Rajanna et al, “Modulation of protein kinase C by heavy metals”,
Toxicol Lett, 1995,
81(2-3):197-203.
(49) A.Kingman et al, National Institute of
Dental Research, “Mercury concentrations in urine and blood associated with
amalgam exposure in the U.S. military population”, Dent Res, 1998,
77(3):461-71.
(50) Sin YM, Teh WF, Wong MK, Reddy PK -
"Effect of Mercury on Glutathione and Thyroid Hormones" Bulletin of
Environmental Contamination and Toxicology 44(4):616-622 (1990); & (b) J.Kawada et al, “Effects of
inorganic and methyl mercury on thyroidal function”, J Pharmacobiodyn, 1980,
3(3):149-59; & (c) Ghosh N.
Thyrotoxicity of cadmium and mercury. Biomed Environ Sci 1992, 5(3): 236-40;
&(d) Goldman, Blackburn, The Effect of Mercuric Chloride on Thyroid Function of the Rat, Toxicol and
Applied Pharm 1979, 48: 49-55; &(e)Kabuto M - "Chronic effects of
methylmercury on the urinary excretion of catecholamines and their responses to
hypoglycemic stress" Arch Toxicol 65(2):164-7 (1991) ; & Assoc. for Birth Defect Children,
Birth Defect News, March 2001;
(61) (a)E.Lutz
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;
& (b)G.Drasch et al, “Mercury Burden of Human Fetal and Infant
Tissues”, Eur J Pediatr 153:607-610,1994;
(84) (a)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;
&(b) 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; &(c) Alfred V.
Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance. J. Orthmol. Med. v6#2
pp67-77 (1991); & (d)
Nishida M, Muraoka K, et al, Differential effects of methylmercuric
chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase
and the thyroid peroxidase activity of isolated pig thyroid cells. J Histochem Cytochem. 1989 May;37(5):723-7; & (e) Khayat A, Dencker L. Whole body
and liver distribution of inhaled mercury vapor in the mouse: influence of
ethanol and aminotriazole pretreatment. J Appl Toxicol.
1983 Apr;3(2):66-74;
(85) Weiner JA,
Nylander M; The relationship between
mercury concentration in human organs and different predictor variables. Sci Total Environ 1993 Sep 30;138(1‑3):101‑15 ; & (b) Falnoga I,
Tusek-Znidaric M, Horvat M, Stegnar P.
Mercury, selenium, and cadmium in human autopsy samples from Idrija
residents and mercury mine workers. Environ Res. 2000 Nov;84(3):211-8
(91) B.Lindqvist et al, "Effects of
removing amalgam fillings from patients with diseases affecting the immune
system", Med Sci Res
24(5): 355-356, 1996.
(96) A.F.Goldberg
et al, “Effect of Amalgam restorations on whole body potassium and bone mineral
content in older men”,Gen Dent, 1996,
44(3): 246-8; & (b) K.Schirrmacher,1998, “Effects of lead, mercury, and methyl
mercury on gap junctions and [Ca2+]I in bone cells”, Calcif Tissue Int 1998
Aug;63(2):134‑9.
(99) M. Nylander et al, Mercury accumulation in
tissues from dental staff and
controls”, Swedish Dental Journal, 13:235-243, 1989; & (b) Nylander M, “Mercury in pituitary glands of dentists”,
Lancet,442, Feb 26, 1986.
(104) (a)C.F.Facemire et al, “Reproductive
impairment in the Florida Panther”, Health Perspect,1995, 103 (Supp4):79-86;
&(b)Yang JM, Jiang XZ, Chen QY, Li PJ, Zhou YF, Wang YL. , “The distribution of HgCl2 in rat body and
its effect on fetus”, Environ Sci , 1996, 9(4):
437-42; & (c) M.Maretta et al, “Effect of mercury on the epithelium of the
fowl testis”, Vet Hung 1995, 43(1):153-6.
(105) (a)T.Colborn(Ed.),Chemically Induced Alterations
in Functional Development,
Princeton Scientific Press,1992;
&(b) Colborn T, ” Developmental Effects of Endocrine-Disrupting
Chemicals",Environ Heath Perspectives, V 101, No.5, Oct 1993; &
(c)B.Windham, "Health, Hormonal, and Reproductive Effects of Endocrine
Disrupting Chemicals" (including mercury), Annotated Bibliography ,2000; &(d)
Giwercman A, Carlsen E, Keiding N, Skakkabaek NE, Evidence for increasing
incidence of abnormalities of the human testis: a review. Environ Health Perspect 1993; 101 Suppl(2): 65-71.
(107) R.L.Siblerud et al,”Psychometric evidence that
mercury from dental fillings may be a factor in depression,anger,and
anxiety", Psychol Rep,
v74,n1,1994; & Amer. J. Of
Psychotherapy, 1989; 58: 575-87; Poisoning and Toxicology compendium,
Leikin & Palouchek, Lexi-Comp,1998, p705.
(113) (a)T.A.Glavinskiaia et al, “Complexons in the
treatment of lupus erghematousus”,
Dermatol Venerol, 1980, 12: 24-28;
& (b)A.F.Hall, Arch Dermatol 47, 1943, 610-611; & Panasiuk J , Peripheral blood
lymphocyte transformation test in various skin diseases of allergic origin. (nickel &
lupus) Przegl Dermatol 1980;67(6):823‑9 [Article in Polish] ; & S Moore,
Lupus: Alternative Therapies That Work; www.shirleys‑wellness‑cafe.com/amalgam.htm
(114) (a)M.Aschner et al,
“Metallothionein induction in fetal rat brain by in utero exposure to elemental
mercury
vapor”, Brain Research, 1997, dec 5, 778(1):222-32; &
(b) O’Halloran TV, “Transition metals in control
Of gene
expression”, Science, 1993, 261(5122):715-25; & (c)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; &
(d) Boot JH. Effects
of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct 1995; 20(3): 233-8.
(122) B.Ono et al, “Reduced tyrosine uptake in
strains sensitive to inorganic mercury”, Genet, 1987,11(5):399-
(126) Noda M, Wataha JC, Lockwood PE,
Volkmann KR, Kaga M, Sano H. Sublethal, 2-week exposures of dental material components alter
TNF-alpha secretion of THP-1 monocytes Dent Mater. 2003;19(2):101-5; & Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production
but activates proinflammatory cytokine expression in murine macrophage:
differential modulation of NF- kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002
Aug;7(1):67-74; & Chen L, Nordlind K, Liden S, Sticherling M., Increased
expression of keratinocyte interleukin-8 in human contact eczematous reactions
to heavy metals. APMIS. 1996
Jul-Aug;104(7-8):509-14; & & Feighery L, Collins
C, Feighery C, Mahmud N, Coughlan G, Willoughby R, Jackson J.
Anti-transglutaminase antibodies and the serological diagnosis of coeliac disease. Br J Biomed Sci. 2003;60(1):14-8.
(146) (a) Gerhard
I, Runnebaum B, The limits of hormone
substitution in pollutant exposure and fertility disorders Zentralbl Gynakol, 1992, 114, 593-602:
&(b)Gerhard, I.: Fortpflanzungsstörungen durch Umweltgifte? Therapeutikon
7, 478‑491 (1993).;
&(c)Roller, E., Vallon, U. und Clédon, Ph.: Einfluß von
Schwermetallen auf die Progesteronsynthese von Leydig‑Zellen. J Fert Reprod 3, 33 (1995).
&(d) Vallon U, Roller E, und Clédon, Ph.: Schwermetallionen beeinflussen
die Progesteronsynthese von humanen Granulosazellen bei IVF‑Patientinnen:
Anwendung eines alternativen in‑vitro‑Zytotoxizitätstests. J Fert Reprod 3, 31 (1995).
(160) B. Windham, Cognitive and Behavioral
Effects of Toxic Metals, 2001. (over 200 medical study references) www.flcv.com/tmlbn.html
(175) Monnet-Tschudi F, Zurich MG, Honegger
P. Comparison of the developmental effects of two mercury compounds on glial
cells and neurons in aggregate cultures of rat telencephalon.. Brain Res. 1996 Nov 25;741(1-2):52-9.
(181) Mathieson PW,
“Mercury: god of TH2 cells”,1995, Clinical Exp
Immunol.,102(2):229-30; & Heo Y, Parsons PJ, Lawrence DA, Lead
differentially modifies cytokine production in vitro and in vivo. Toxicol Appl Pharmacol,
196; 138:149-57; & Murdoch RD, Pepys J; Enhancement of antibody and IgE
production by mercury and platinum salts. Int Arch
Allergy Appl Immunol 1986 80: 405-11.
(183) World Health Organization(WHO),1991,
Environmental Health Criteria 118,
Inorganic Mercury, WHO, Geneva, Switzerland.
(187) (a)Klobusch J, Rabe T, Gerhard I, Runnebaum B, "Alopecia and environmental
pollution" Klinisches Labor 1992, 38:469‑ 476; &
(b)“Schwermetallbelastungen bei Patientinnen mit Alopezie” Arch Gynecol.
Obstet., 1993,254(1-4):278-80;& (c)G. Kunzel et al, “Arch Gynecol. Obstet.,
1993, 254:277-8; & Schrallhammer-Benkler K, et al, Acute
mercury intoxication with lichenoid drug eruption followed by mercury
contact allergy and development of antinuclear antibodies. Acta Derm Venereol. 1992 Aug;72(4):294-6.
(192) (a)N.Nogi, “Electric current around dental
metals as a factor producing allergic metal ions in the oral cavity”, Nippon
Hifuka Gakkai Zasshi, 1989, 99(12):1243-54;
& J. Bergdahl, A.J.Certosimo et al, National Naval Dental Center,
“Oral Electricity”, Gen Dent, 1996, 44(4):324-6; & B.M.Owens et al,
“Localized galvanic shock after insertion of an amalgam restoration”,
Compendium, 1993, 14(10),1302,1304,1306-7
& (b)M.D.Rose et al, Eastman Dental Institute, “The tarnished
history of a posteria restoration”, Br Dent J 1998;185(9):436;& & R.D.Meyer et al, “Intraoral galvanic
corrosion”,Prosthet Dent, 1993,69(2):141-3
R.H.Ogletree et al, School of Materials Science, GIT, Atlanta,”Effect of
mercury on corrosion of eta’ Cu-Sn phase in dental amalgams”, Dent Mater, 1995,
11(5):332-6; &(c) Johansson E, Liliefors T, "Heavy elements in root
tips from teeth with amalgam
fillings", Department of Radiation Sciences, Division of Physical Biology,
Box 535, 751 21 Uppsala, Sweden
(198)
B.R.G.Danielsson et al,”Ferotoxicity of inorganic mercury: distribution and
effects of nutrient uptake by placenta and fetus”, Biol Res Preg Perinatal.
5(3):102-109,1984; & Danielsson et al, Neurotoxicol. Teratol., 18:129-134
(199) Dr. P.Kraub & M.Deyhle, Universitat
Tubingen- Institut fur Organische Chemie, “Field Study on the Mercury Content of
Saliva”, 1997
http://www.uni‑tuebingen.de/KRAUSS/amalgam.html;
(20,000 people
tested for mercury level in saliva and health status/symptoms compiled)
(211) Mercury from maternal "silver" tooth
fillings in sheep and human breast milk. A source of
neonatal exposure. Vimy MJ, Hooper DE, King WW,
Lorscheider FL. Biol Trace Elem Res. 1997 Feb;56(2):143-52; & Maternal-fetal distribution of
mercury (203Hg) released from dental amalgam fillings. Vimy MJ, Takahashi Y,
Lorscheider FL. Am J Physiol. 1990 Apr;258(4 Pt 2):R939-45; & R.Schiele et al,
Institute of Occupational Medicine, Univ. Of Erlamgem- Nurnberg, “Studies of
organ mercury content related to number of amalgam fillings”,Symposium paper, March 12,
1984, Cologne, Germany; (in 38);
(217) Agency for Toxic Substances and Disease
Registry, U.S. Public Health Service, Toxicological
Profile for Mercury , 1999; & (b)Apr 19,1999 Media Advisory, New MRLs
for toxic substances, MRL:elemental mercury vapor/inhalation/chronic &
MRL: methyl mercury/ oral/acute; &
http://www.atsdr.cdc.gov/mrls.html
(234) P.E. Bigazzi, “Autoimmunity and Heavy Metals”,
Lupus, 1994; 3: 449-453;(b) & Pollard KM, Pearson Dl, Hultman P.
Lupus-prone mice as model to study xenobiotic-induced
autoimmunity. Environ Health
Perspect 1999; 107(Suppl 5): 729-735; &(c) Nielsen JB; Hultman P. Experimental studies on genetically
determined susceptibility to mercury‑induced autoimmune response. Ren Fail 1999 May‑Jul;21(3‑4):343‑8; &(d) Hultman P, Enestrom S,
Mercury induced antinuclear antibodies in mice,
Clinical and Exper Immunology, 1988, 71(2): 269-274.
(260) J.S. Woods et
al, “Urinary
porphyrin profiles as biomarker of mercury exposure: studies on dentists”, J
Toxicol Environ Health, 40(2-3):1993, p235-;
& “Altered porphyrin metabolites as a biomarker of mercury exposure
and toxicity”, Physiol Pharmocol, 1996,74(2):210-15
(263) Kumar
AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase
activity: a common pathway in central nervous system disorders. J Assoc Physicians India.
2002 Mar;50:400-6
(264) B.R.
Danielsson et al, “ ”Behavioral effects of prenatal
metallic mercury inhalation exposure in rats”, Neurotoxicol
Teratol, 1993, 15(6):
391-6;& A. Fredriksson et
al,”Prenatal exposure to metallic mercury vapor
and methyl mercury produce interactive
behavioral changes in adult rats”, Neurotoxicol Teratol, 1996, 18(2): 129-34
(271) B.A.Weber,
“The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases) & (b) “Amalgam and Allergy”, Institute for
Naturopathic Medicine, 1994;
(40 MS
cases), http://home,t‑online.de/home/Institut_f._Naturheilverfahren/patinf.htm"
(273) Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). H V Aposhian ; Environ
Health Perspect. 1998 August; 106(Suppl
4): 1017–1025, www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1533322; &(b) R.Schiele et
al, Mercury Mobilization by DMPS in
persons with and without amalgam fillings ”,
Zahnarztl. Mitt, 1989, 79(17): 1866-1868;
(274) L.Friberg et al, “Mercury in the brain and CNS
in relation to amalgam fillings”, Lakartidningen, 83(7):519-521,1986(Swedish Medical Journal), http://home.swipnet.se/misac/research6.html
(287) Warvinge K, Mercury distribution in the
neonatal and adult cerebellum after mercury vapor exposure of pregnant squirrel
monkeys, Environ Res 2000, 83(2): 93-101;
(296)
L.Bucio et al, Uptake, cellular distribution and DNA damage produced by
mercuric
chloride in a
human fetal hepatic cell line. Mutat Res 1999 Jan
25;423(1‑2):65‑72;
& (b) Ho PI,
Ortiz D, Rogers E, Shea TB.
Multiple aspects of
homocysteine neurotoxicity: glutamate excitotoxicity, kinase
hyperactivation
and DNA damage. J Neurosci Res.
2002 Dec 1;70(5):694-702;
&(c) Snyder RD; Lachmann PJ; Thiol involvement
in
the
inhibition of DNA repair by metals in mammalian cells. Source Mol
Toxicol,
1989 Apr‑Jun, 2:2, 117‑28 ;
& L.Verschaeve et al, “Comparative
in vitro
cytogenetic
studies in mercury-exposed human lymphocytes”, Muta Res, 1985,
157(2-3):221-6; &
L.Verschaeve,“Genetic damage induced by low level mercury
exposure”,
Envir Res,12:306-10,1976.
(317) S.Zinecker,
“Amalgam: inorganic mercury in the brain”, der Kassenarzt, 1992, 32(4):23; “Praxiproblem Amalgam”, Der
Allgermeinarzt, 1995,17(11):1215-1221. (1800 patients)
(323) (a)Dr. Kohdera, Faculty of Dentistry, Osaka Univ., International
Congress of Allergology and Clinical Immunology, EAACI, Stockholm, June
1994; & Heavy Metal Bulletin, Vol 1, Issue 2, Oct
1994. (160 cases cured-eczema);
(b) Tsunetoshi Kohdera, MD, dermatology,
allergology, 31 Higashitakada‑cho
Mibu Nakagyo‑ku Schimazu Clinics
Kyoto 604 Japan e‑mail:smc‑inet@mbox.kyoto‑inet.or.jp &(c) P.Dallmann,”Dermatalogical
conditions caused by amalgam? PeDa_Eigenverisg, 1995; & (d)G.
Ionescu, Biol Med, 1996, (2): 65-68; & (e) Ionescu G.: Tooth alloys.
Electro‑chemical and biological processes. Materialprueuefung..
Komplementaeaermed. , 3, 72-77, 1996; & (f) Ionescu
G; Heavy metal load by Dental materials. Experience with Neurodermitis and Psoriasis
patients.. Zeitung f. Umweltmedizin, 3, 163-171, 1997
(327) Danscher G; Horsted‑Bindslev P;
Rungby J. Traces of mercury in organs
from primates with amalgam fillings. Exp Mol Pathol 1990;52(3):291‑9;
(330) (a) Wilkinson LJ, Waring RH. Cysteine dioxygenase:
modulation of expression in human cell lines by cytokines and control of
sulphate production. Toxicol In Vitro. 2002 Aug;16(4):481-3;
& (b) C.M. Tanner et al,“Abnormal Liver Enzyme Metabolism in
Parkinson’s”,Neurology, 1991, 41(5):
Suppl 2, 89-92; & M.T.Heafield
et al, "Plasma cysteine and sulphate levels in patients with Motor neurone
disease, Parkinson's Disease, and Alzheimer’s's Disease", Neurosci Lett,
1990, 110(1‑2), 216,20; &
A.Pean et al, "Pathways of cysteine metabolism in MND/ALS", J
neurol Sci, 1994, 124, Suppl:59‑61;
& Steventon GB, et al; Xenobiotic metabolism in motor neuron
disease, The Lancet, Sept 17 1988, p
644-47; & Neurology 1990,
40:1095-98.
(331) C.Gordon et
al, “Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE)”,
Lancet,
1992,339:8784,25-6; & P.Emory et al, “Poor sulphoxidation in
patients with rheumatoid arthitis”, Ann Rheum Dis, 1992,
51:3,318-20; & Bradley H,et al, Sulfate metabolism is abnormal in patients
with rheumatoid arthritis. Confirmation by in vivo biochemical findings. J Rheumatol. 1994
Jul;21(7):1192-6; & T.L. Perry et al, “Hallevorden-Spatz
Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann
Neural, 1985,
18(4):482-489.
(333)
(a)A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat
brain”, Brain Research, 1996, 738(2): 257-64; &
(b)P.R.Yallapragoda et al,“Inhibition of calcium transport by Hg salts” in rat
cerebellum and cerebral cortex”, J
Appl toxicol, 1996, 164(4): 325-30;
& (c) E.Chavez et al,
“Mitochondrial calcium release by
Hg+2",J Biol Chem, 1988, 263:8, 3582-;&(d) A. Szucs et al, Cell Mol Neurobiol,
1997,17(3): 273-8; & (e)
D.Busselberg, 1995, “Calcium channels as target sites of heavy metals”,Toxicol
Lett, Dec;82‑83:255‑61; & Cell Mol Neurobiol 1994 Dec;14(6):675‑87; & (f) Rossi AD, et al, Modifications
of Ca2+ signaling by inorganic
mercury in PC12 cells. FASEB J 1993,
7:1507-14.
(337) H.G.
Abadin, et al, U.S. ATSDR, “Breast-feeding exposure of infants to mercury,
lead, and cadmium: A Public Health Perspective”, Toxicol Ind Health, 1997,
13(4): 495-517.
(338) (a)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 and its accumulation in the first-trimester human placenta”,
Environ Res, 1992, 57(1):96-106;& “In vitro exposure to mercury and
cadmium alters term human placental
membrane fluidity”, Pharmacol, 1992, 116(1): 17-23; & (b)J.Urbach et al, Dept. of Obstetrics
& Gynecology, Rambam
Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro
placental nutrient transfer and oxygen consumption”, Reprod Toxicol,
1992,6(1):69-75;& © Karp W, Gale TF
et al, Effect of mercuric
acetate on selected enzymes of maternal and fetal hamsters”
Environmental Research, 36:351-358; &
W.B. Karp et al,
“Correlation of human placental enzymatic
activity with trace metal
concentration in placenta”, Environ
Res. 13:470- 477,1977; & (d)
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;
& Semczuk M, Semczuk‑Sikora
A. New data on toxic metal intoxication
(Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit 2001 Mar;7(2):332‑340
(342)
Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et
al. Metal- specific
memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999; 20: 289-98.
(348)(a)
Kistner A, “Mercury poisoning by amalgam:
Diagnosis and therapy” ZWR, 1995,104(5):412-417;
&(b) Mass C, Bruck W. “Study on the significance of mercury
accumulation in the brain from dental amalgam fillings through direct mouth-nose-brain
transport”, Zentralbl Hyg Umweltmed 1996; 198(3): 275-91.
(363) J.W.Reinhardt, Univ. Of Iowa
College of Dentistry, “Side effects: mercury contribution to
body burden from dental amalgam”, Adv Dent Res, 1992,
6: 110-3.
(366) (a)“Tooth amalgam and
pregnancy”, Geburtshilfe Frauenheikd. 1995, 55(6): M63-M65; &(b)
T. Zinke, “There are new realizations to
the Amalgam problem”, in Status Quo and perspectiveves of Amalgam and Other
Dental Materials, L.F. Friberg(Ed.), Georg=Thieme-Verlag, Stuttgart, New
York, 1995, p1-7.
(367)(a)
Gerhard I, “Amalgam from gynacological view”, Der Frauenarzt, 1995,36(6):
627-28; & (b)“Schdstoffe und
Fertillitatsstorungen”, Schwermetalle und Mineralstoffe, Geburtshilfe
Frauenheikd, 1992, 52(7):383-396; & (c) Gerhard I, “Reproductive risks of heavy
metals and pesticides in women”, in: Reproductive Toxicology, M.Richardson(ed.), VCH
Weinhelm, 1993, 167-83; & (d)Gerhard I, “Infertility with women
by
environmental illnesses, JD. Kruse-Jarres(Ed.),
1993, 51-68.
(369) Sterzl I,
Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in
fatigue and autoimmunity. Neuroendocrinology Letters
1999; 20:221-228.
www.melisa.org
(372) (a)Atchison WD. Effects of neurotoxicants on synaptic transmission.
Neurotoxicol Teratol 1998, 10(5):393- 416;
& 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; &(b) 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; &(c)Brouwer
M et al, Functional changes induced by heavy metal ions. Biochemistry, 1982, 21(20): 2529-38.
(375) (a) Stejskal VDM, Danersund A, Lindvall A. Metal-specific memory
lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters 1999; &(b) Stejskal V,
Hudecek R, Mayer W, "Metal-specific lymphocytes: risk factors in CFS and other related diseases",
Neuroendocrinology Letters, 20: 289-298, 1999
www.melisa.org
(379)(a)
MacDonald EM, Mann AH, Thomas HC. Interferons as mediators of
psychiatric morbidity. The Lancet 1978; Nov 21,
1175-78; & (b) Hickie I, Lloyd A.
Are cytokines associated with neuropsychiatric syndrome in humans?
Int J Immunopharm 1995; 4:285-294.
(380) (a) Komaroff AL, Buchwald DS. Chronic fatigue syndrom: an update. Ann Rev Med 1998; 49: 1-13; &
(b) Buchwald DS, Wener MH, Kith P.
Markers of inflamation and immune activation in CFS. J Rheumatol 1997; 24:372-76.
(381) (a) Demitrack MA, Dale JK. Evidence for impaired
activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metabol 1991; 73:1224-1234;
& (b)Turnbull AV, Rivier
C. Regulation of the
HPA axis by cytokines. Brain
Behav Immun 1995; 20:253-75; & (c)Ng TB, Liu WK. In
Vitro Cell Dev Biol 1990 Jan;26(1):24‑8. Toxic effect of heavy metals on cells
isolated from the rat adrenal and
testis.
(382) Sterzl I, Fucikova T,
Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44:
456-60.
www.melisa.org ; &(b) 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 ; & &
(c)Kolenic J, Palcakova D, Benicky L, Kolenicova M - "The frequency of
auto-antibody occurrence in occupational
risk (mercury)" Prac Lek 45(2):75-77 (1993), & ; &(c) 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. www.melisa.org
; & (d) Removal of dental
amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with
autoimmune thyroiditis, Ivan Sterzl , Jarmila P,
Pavlina H, Petr M, Jirina B & Vera
D.M. , Neuroendocrinol
Lett 2006; 27(Suppl
1):101–000
(383)(a) Saito K. Analysis of a genetic
factor of metal allergy-polymorphism of HLA-DR-DO gene. Kokubyo Gakkai
Zasschi 1996; 63: 53-69; &(b) Prochazkova J,
Ivaskova E, Bartova J, Stejskal VDM.
Immunogentic findings in patients
with altered tolerance to heavy metals.
Eur J Human Genet 1998; 6: 175.
(385)(a)
Kohdera T, Koh N, Koh R. Antigen-specific lymphocyte stimulation test on patients with
psoriasis vulgaris. XVI International Congress of Allergology and
Clinical Immunology, Oct 1997, Cancoon, Mexico; & (b)Ionescu
G,. Heavy metal load with atopic Dermatitis and Psoriasis, Biol Med 1996; 2:65-68; &
(c) A subset of patients with common variable immunodeficiency. Blood 1993, 82(1): 192-20.
(390) (b) 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 20(6):483-9
(2000)
www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=11180271&form=6&db=m&Dopt=r; &(c) Barregard L, Lindstedt G, Schutz A,
Sallsten G - "Endocrine function in mercury exposed chloralkali
workers" Occup Environ Med 51(8):536-40 (1994) www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=
7951778&form=6&db=m&Dopt=r ; & (d) Watanabe C - "Selenium
deficiency and brain functions: the significance for methylmercury
toxicity" Nippon Eiseigaku Zasshi 55(4):581-9 (2001); & (e) Watanabe
C, Yoshida K, Kasanuma Y, Kun Y, Satoh H.
In
utero methylmercury exposure differentially affects the activities of
selenoenzymes in the fetal mouse brain.. Environ Res
1999 Apr;80(3):208-14; &(f) Li MX, Tan ZQ, Qin SZ, Zhong LP, Li FH,
Wang HZ, [Three cases of hypothyroidism
induced by cosmetics containing mercury], Zhonghua Lao Dong Wei Sheng Zhi Ye
Bing Za Zhi. 2004 Aug;22(4):312-3. Chinese.
(394) Amalgam Illness Diagnosis and Treatment, Andrew Hall Cutler, PhD, PE, http://www.noamalgam.com/; & Heavy
Metals and Halogens Displace and Block Utilization of Essential Minerals- Iodine and Chelation, International Medical Veritas Association http://www.alkalizeforhealth.net/Liodine2.htm;
& The effect of mercuric chloride on thyroid function in the rat., Goldman
M, Blackburn P. Toxicol Appl Pharmacol.
1979 Mar 30;48; & THE
EFFECT OF CERTAIN METALLIC CATIONS ON THE IODIDE UPTAKE IN THE THYROID GLAND OF
MICE. Acta Endocrinol (Copenh). 1964 Aug;46:643-52.ANBAR M, INBAR M.
(395) Iodine: Why You Need It, Why You Can't Live Without It (4th Edition), Dr. David Brownstein, 2008; & Overcoming Thyroid Disorders, Dr. David Brownstein,
(402) Ando T, Wakisaka I, Hatano H. Mercury
concentration in gray hair.
Nippon Eiseigaku Zasshi 1989; 43(6):1063-8.
(405) Jenny Stejskal, Vera Stejskal. The role of metals
in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345‑358,
1999.
(409) (a)Autism: a unique form of mercury poisoning. www.autism.com/ari/mercurylong.html
; & (b) Yazbak
FE(MD,FAAP) Autism 99: A National
Emergency, &www.garynull.com/documents/autism_99.htm; & (c) Dr. A Holmes, Autism
Treatment Center,Baton Rouge, La, http://www.healing‑arts.org/children/holmes.htm
; & (c)Jaquelyn McCandless, M.D.,
Autism Spectrum Treatment Center,
Woodland Hills, Ca www.flcv.com/kidshg.html
(410) J.R. Cade et al, Autism and
schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism,
Mar 1999.
(411) (a) 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;
&(b) Kar NC, Pearson CM. Dipeptyl
Peptidases in human muscle
disease. Clin Chim Acta 1978; 82(1-2): 185-92; &(c) Seroussi K,
Autism and Pervasive Developmental Disorders , 1998,
p174, etc.
(412) (c) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in
autism. Invest Clin 1996,37(2): 113-28; &
(b)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;
& (c)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; &(d) Carlsson ML. Is infantile autism a hypoglutamatergic
disorder? J Neural Transm 1998, 105(4-5):
525-35.
(413) (a) Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; & (b) Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998.
3(3):187-98; & (c)
www.edelesoncenter.com
(418) 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.
(419) Lipozencic J; Milavec‑Puretic V; Pasic
A. Contact allergy and psoriasis. Arh Hig Rada
Toksikol 1992 Sep;43(3):249‑54; & Roujeau JC et al, Acute generalized exanthematous pustulosis.
Analysis of 63 cases; Arch Dermatol 1991
Sep;127(9):1333‑8; & Yiannias
JA; Winkelmann RK; Connolly SM. Contact sensitivities in
palmar plantar pustulosis
(acropustulosis). Contact Dermatitis 1998 Sep;39(3):108‑11
(427)
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; & Bara M, Guiet-Bara A, Durlach J.
Comparison of the effects of taurine and magnesium on electrical
characteristics of artificial and natural membranes. V. Study on the human
amnion of the antagonism between magnesium, taurine and polluting metals. [ French] Magnesium. 1985;4(5-6):325-32.
(439) (a) Mercuric chloride intoxication. Part 1, Bull Environ Contam
Toxicol 1978; 20(6): 729-35; & (b) Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by
Hg2+ and other metal ions. J Inorg
Biochem 1996; 62(4): 271-9; & (c)
Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by
heavy metals and their reversal by
chelating agents:
(458) Dowling AL, Iannacone
EA, Zoeller RT. Maternal
Hypothyroidism Selectively Affects the Expression of Neuroendocrine‑Specific Protein A Messenger Ribonucleic
Acid in the Proliferative Zone of the Fetal Rat Brain Cortex.
Endocrinology 2001 Jan 1;142(1):390‑399
(459) Isny Clinic(South Germany) Kurt Muller ,
MD, member of Editorial board for
Ganzheitliches Medicine Journal. Wassertornstrasse 6 ,
Isny, BRD fax: 0049 7562 550 52
(464) (a) Walsh,
WJ, Health Research Institute, Autism and Metal Metabolism, www.hriptc.org/autism.htm, Oct 20, 2000;
& (b) Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and
Human Functioning, 2000, www.hriptc.org/mhfres.htm;
(468) Overzet K,
Gensler TJ, Kim SJ, Geiger ME, van Venrooij WJ, Pollard KM, Anderson P, Utz PJ.
Small nucleolar RNP Scleroderma
autoantigens associate with phosphorylated serine/arginine
splicing factors during apoptosis.
Arthritis Rheum 2000 Jun;43(6):1327‑36
(476) (a) Dr Thomas
Verstraeten, US
Centres for Disease Control and
Prevention, Summary Results: Vaccine Safety
Datalink Project ‑ a database of 400,000 children , May 2000;
& (b) Halsey, NA.
Limiting Infant Exposure to Thimerosal in vaccines. J. of the Amer. Medical Assoc., 282:
1763-66; & (c) The
Center for Biologics Evaluation and Research (CBER), Review of the Use of
Thimerosal in Vaccines, The US Food and Drug Administration(FDA),
Jul 4, 2000.
(500) B.Windham, Common Exposure Levels and
Adverse Health Effects from Mercury/Amalgam Dental Fillings, and Results of
Replacement of Amalgam Fillings, Review, 2001. (over
3000 peer-reviewed studies documenting
common exposures more
than Gov’t health guidelines and mechinisms of causality of 40 chronic
conditions, and 60,000 clinical cases of recovery or significant improvement
after amalgam replacement as followed by doctors) www.flcv.com/amalg6.html
(501) Review: Documentation of
common mercury exposure levels from amalgam by medical labs, Government agency
studies, peer-reviewed studies. B Windham (Ed), www.flcv.com/damspr1.html &
www.flcv.com/amalno1.html
(502) Effects of prenatal and neonatal mercury exposure on children, B
Windham(Ed), over 150 peer-reviewed studies, www.flcv.com/fetaln.html
(503) Summary of results of treatment of chronic health conditions by
amalgam replacement, as reported to the FDA and treatment clinics, www.flcv.com/hgrecovp.html & www.flcv.com/hgremove.html
(508)(a) Bonar DB, McColgan B,
Smith DR, Darke C, Guttridge MG, Williams HSmyth PPA, Hypothyroidism and aging: The Rosses’ Survey. Thyroid 2000, 10(9):821-827;&
(b) Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid
disease prevalence study. Arch Tntern Med 2000, 160(4):526-34; &(c)
GS Connection 11(12): Prevelence of Thyroid Imbalance, Thyroid in Pregnancy,
GSDL, www.gsdl.com
(509)(a) Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE,
Mitchell ML, Relation of severity of maternal hypothyroidism to cognitive
development of offspring. J Med Screen
2001: 8:18-20; &(b) de Escobar DM, Orbregon MF,
del Rey FE, Is neuropsychological development related to maternal
hypothyroidism or to maternal hypothyroxinemia?
J Clin Endocrin Metab 2000; 3975-3987; &(c) Thyroid Imbalances in
Pregnancy Linked to Poor Child Neurodelopment, Great Smokies Diagnostic Lab,
www.gsdl.com/news/connections/vol11/conn20010228.html
&(d) J. E. Haddow et al, Babies Born to
Mothers with Untreated Hypothyroidism Have Lower I.Q.'s, New
England Journal of Medicine, Aug 19, 1999; & (e) Lavado-Autric et al.
Early maternal hypothyroxinemia alters histogenesis and cerebral cortex
cytoarchitecture of the progeny. JCI 111:1073-1082 (2003); & (f)Pop VJ,
Vader HL et al, Low maternal free thyroxine during early pregnancy is
associated with impaired psychomotor development in infancy, Clin
Endocrinol(Oxf), 50:149-55, 1999; & Man EB, Brown JF, Serunian SA. Maternal
hypothyroxinemia: psychoneurological deficits of progeny. Ann Clin Lab Sci
1991;21(4):227-39; & Pharoah POD, Connolly KJ et al, Maternal thyroid
hormone levels in pregnancy and cognitive and motor performance of the
children, Clin Endocrinol(Oxf), 1984, 21:265-70; & (g) Pop VJ, de Vries E,
et al, Maternal thyroid peroxidase antibodies during pregnancy: and impaired
child development, J Clin Endocrinol Metab., 1995, 80:3561-3566 & Connors
MH, Styne DM, Neonatal athyreosis resulting from thyrotropin-binding inhibitory
immonoglobulins, Pediatrics, 1986, 78:287-290; & (h) Asami T, Suzuki H, Effects of thyroid
hormone deficiency on electrocardiogram findings of congenenitally hypothyroid
neonates. Thyroid 11: 765-8, 2001; & Kumar R, Chaudhuri BN. Altered
maternal thyroid function: fetal and neonatal heart cholesterol and
phospholipids, .Indian J Physiol
Pharmacol 1993 Jul;37(3):176-82
(510) (a)Morris MS,
Bostom AG, Jacques PJ, Selhub J, Rosenberg IH, Hyperhomocysteinemia and hypercholesterolemia associated with
hypothyroidism in the third U.S. National Health and Nutrition Examination Survey, Artherosclerosis 2001,
155:195-200; & (b) Shanoudy H. Soliman A, Moe S, Hadian D, Veldhuis F,
Iranmanesh A, Russell D, Early
manifestations of “sick eythyroid syndrome” in patients with compensated
chronic heart failure, J Card Fail 2001, 7(2):146-52; & (c)AE. Hak, HAP. Pols, TJ. Visser, et al., The Rotterdam Study., Subclinical
hypothyroidism is an independent risk factor for atherosclerosis and myocardial
infarction in elderly women, Ann Int Med, 2000, vol.
132, pp. 270--278 &(d)Thyroid Dysfunction Linked to Elevated
Cardiac Risk, GSDL,
www.gsdl.com/news/connections/vol12/conn20010411.html.; &(e) Biondi
B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002 Dec 3;137(11):904-14; & (f) B.G.
Nedreboe, O. Nygard, et al, Plasma Total
Homocysteine of hypothyroid patients during 12 months of treatment, Haukeland
Univ. Hospital, Bergen, Norway, bjoern.gunnar.nedreboe@haukeland.no (references 7 other studies with similar
findings); & (g) Hussein, WI, Green, R, Jacobsen, DW, Faiman, C.
Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann
Intern Med 1999; 131:348;
(511) (a) Abramson J, Stagnaro-Green A, Thyroid antibodies and fetal
loss, Thyroid 2001, 11(1): 57-63; &(b) Thyroid
Antibodies May Spur Pregnancy Loss, GSDL,
www.gsdl.con/news/connections/vol12/conn20010411.html
& (c)Allan W.(MD), Maternal Hypothyroidism During Pregnancy Linked to
Increased Risk for Miscarriage, Journal of Medical Screening, November 22,
2000; & (d)
Abstract # 274: Wolfberg, Adam J. and David
A. Nagey, "Thyroid Disease During Pregnancy and Subsequent
Congenital Anomalies."St Johns Univ.,
kblum@jhmi.edu ; & Birth Defect News, Jan
2002, p2; & (e)Emerson, C.H. (1996). Thyroid Disease During and
After Pregnancy. In L.E.
Braverman & R.D. Utiger (Eds.), The Thyroid, A Fundamental and Clinical
Text (pp. 1021-1031; & (f) Man EB, Jones WS, Thyroid function in human
pregnancy: retardation in 8-month old infants, Am J Obstet Gynecol, 1969,
104:898-908; & Brent GA, Maternal hyrothyroidism: recognition and
management, Thyroid, 1999, 9:661-5.
(513) (a) Valentino M, Santarelli L, Pieragostini E, Soleo L,
Mocchegiani E. In
vitro inhibition of thymulin production in mercury-exposed thymus of young
mice. Sci Total Environ 2001 Apr 10;270(1-3):109-112
; &
(b) Nordlind K. Stimulating effect of
mercuric chloride and nickel sulfate on DNA synthesis of thymocytes and
peripheral lymphoid cells. Int
Arch Allergy Appl Immunol 1983;72(2):177-179;
& Chen M, von Mikecz A. Specific inhibition of rRNA
transcription and dynamic relocation of fibrillarin induced by mercury. Exp Cell Res 2000 Aug 25;259(1):225‑238;
& © Dieter MP, Luster MI, Boorman GA, Jameson CW, Dean JH, Cox JW.
Immunological and biochemical responses in mice treated with mercuric chloride.. Toxicol Appl
Pharmacol 1983 Apr;68(2):218‑228.
(555) 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; Bellabarba D, and Tremblay R;
Effect of thimerosal on serum binding of thyroid hormones, Can J Physsiol
Pharmacol,173, 51:156-159: & Hokkfen B, Kodding R, Hesch RD; Regulation of
thyroid hormone metabolism in rat liver fractions, Biochim Biophys Acta 1978,
539:(1): 114-24.
(558)
American Assoc. of Clinical Endocrinologists and American College of
Endocrinolog. AACE clinical practice
guidelines for the evaluation and treatment of hyperthyroidism and
hypothyroidism. Endocr Pract.,
1995, 1: 54-62.
(559) Choy CM, Lam
CW, et al, 2002, Infertility, blood mercury concentrations, and dietary seafood
consumption: a case control study, BJOG: An International Journal of Obstetrics
and Gynaecology, 109: 1121-1125.
(560) Nath J, Safar R. Late-onset bipolar disorder
due to hyperthyroidism. Acta Psychiatr Scand 2001;104:72-75.
(561) Muller AF, Drexhage HA,
Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of
childbearing age: recent insights and consequences for antenatal and postnatal
care. Endocrine Reviews 2001;22(5):605-30.
(567) 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; & 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.
(568) Bemis JC, Seegal RF; 2000, PCBs and methylmercury alter
intracellular calcium concentrations in rat cerebellar granule cells.
Neurotoxicology, 21(6): 1123-1134.
(569) 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
(570) 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.
(571) 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 Suppl 1:, S20-35.
(580)
Life Extension Foundation (MDs), Disease Prevention and Treatment,
Expanded 4th Edition, 2003; &
(b) American Journal of Clinical Nutrition, 2008 & Life Extension Foundation, Life Extension, Jan 2009, , http://www.life-enhancement.com/
(581) Vitamin Research News, weekly journal (several editions), 2003-2009, www.vrp.com
***********
(395)