Depression and other Neurotransmitter Related
Conditions- the mercury connection
B.Windham (Ed.)
Introduction.
According to Dr. Gerald Klerman,
based on National Institute of Health studies there has been a huge increase(over 500 %) in the rate of depression and chronic
neurological problems over the last 3 decades. A random sample of Oregon high
school students found that over 16% had been diagnosed with depression (10).
According to ECA samples, otherwise healthy people born in recent decades face
a 10 fold increase in incidence of major depressive episodes compared to those
sampled who were born in earlier decades. Over 6 million Americans over 65
suffer from major depression while another 5 million suffer from depressive
symptoms (598). Every year, 230 million prescriptions for antidepressants are
filled, making them one of the most prescribed drugs in the United States. The
psychiatric industry itself is a $330 billion industry.
Several
factors appear to be contributing to this:
1. neurological birth defects and
developmental conditions due to increased levels of vaccinations, fetal
exposure to alcohol, tobacco smoke, drugs, toxic metals such as lead, mercury,
cadmium, etc., other neurotoxic chemicals such as
pesticides (552,585),nitrates, etc., and other endocrine system/hormonal system
disrupting chemicals such as dioxins, etc.
Studies by the National Academy
of Sciences indicate that these affect close to 40% of all children in the
U.S., more in some populations than others
2. changes
in dietary habits resulting in nutrient, vitamin, and mineral deficiencies or
imbalances and blood sugar imbalances(594), and increased consumption of
inflammatory excitotoxins such as aspartame, MSG, and
high fructose corn syrup.
3.
stress in family and workplace environments.
Groups of primary care patients aged 18-65 years from 333 randomly chosen
public or private clinics throughout the whole country of Poland, totaling
7289, coming for a regular visit were asked to participate in a study of the prevalence of depressive disorders(6).
71% of the sample were female. All patients filled in the Beck Depression
Inventory (BDI). The prevalence of depressive disorders in the whole sample was
23.3%.
The number of people with anxiety
disorders is close to the number with mood disorders (584). The primary types of anxiety disorders are
phobias, panic attacks, generalized anxiety disorder (GAD), and
obsessive-compulsive disorder (OCD). At least 20 million people are affected at
some time by these conditions. Similar large numbers are affected by attention
disorders, including attention deficit hyperactive disorder (ADHD), dyslexia,
and schizophrenia (580,584).
Twenty-plus years of research on
antidepressants, from the old tricyclics to the newer
selective serotonin reuptake inhibitors (SSRIs) show that their benefit is
hardly more than what patients get when they take a placebo(30,31,etc.) In
Britain, the agency that assesses which treatments are effective enough for the
government to pay for stopped recommending antidepressants as a first-line
treatment, especially for mild or moderate depression. A spokesperson for Pfizer, which makes
Zoloft, added that the fact that antidepressants "commonly fail to
separate from placebo" is "a fact well known by the FDA, academia,
and industry." Antidepressants are
significantly more effective than a placebo in patients suffering only from the
most severe depression(31). The
serotonin-deficit theory of depression is built on a hypothesis that has little
support. And a new drug, tianeptine, which is sold in
France and some other countries (but not the U.S.), turns out to be as
effective as Prozac-like antidepressants that keep the synapses well supplied
with serotonin even though the mechanism of the new drug is to lower brain levels of
serotonin. "If depression can be equally affected by drugs that increase
serotonin and by drugs that decrease it," says Kirsch(30c),
"it's hard to imagine how the benefits can be due to their chemical
activity."
II. Causes of Depression and Anxiety
There appears to be both a
psychological/mind basis as well as physical/chemical basis for depression and
anxiety. Nutritional deficiencies, environmental factors, methylation
deficiencies, hormonal imbalances, and stress clearly can lead to depression
and anxiety, but they also facilitate psychological factors(386,580,etc.). Based on clinical experience, anxiety and
hyperventilation and panic attacks appear to often be related to a person
burying their feelings about their circumstances (583). Depression often occurs
where a person has suppressed anger, anger turned inward. Chronic anger has
been found to be linked to increased risk of recurrent heart attacks and
cardiac death(583b). Other
heart risks have also been linked to depression, anxiety, repressed anger and
isolation or infrequent social interactions(582b).
These factors, which lead to increased risks of heart disease, have been
correlated with elevated cholesterol, blood pressure, variable heart rate plus
increased arterial thickness and plaque accumulation. And studies estimate that
20 to 40 percent of all sudden cardiac deaths will be triggered by some type of
acute emotional stressor (582c). Dealing with nutritional deficiencies and
environmental factors, along with being honest with yourself, acknowledging
anger or feelings rather than assigning blame, and doing what makes you feel
good usually leads to reduced depression or anxiety (583a).
The
levels of brain neurotransmitters such as dopamine, norepinephrine,
and serotonin, appear to be major factors in controlling moods, and appear to
be affected by lifestyle, diet, philosophy, and environmental factors. Some are
more susceptible to depression than others, and thus more affected by diet and
environmental factors(580).
Chronic or acute brain inflammation
appears to be a primary factor in depression. The brain is very sensitive to
inflammation. Disturbances in metabolic
networks: e.g., immuno-inflammatory processes, insulin-glucose
homeostasis, adipokine
synthesis and secretion, intra-cellular signaling cascades, and mitochondrial
respiration have been shown to be major factors in depressive disorders and
other chronic neurological conditions (592,593,598, etc.).
Inflammatory chemicals such as mercury,
aluminum, and other toxic metals as well as other excitotoxins
including MSG and aspartame cause high levels of free radicals, lipid peroxidation, inflammatory cytokines, and oxidative stress in
the brain and cardiovascular systems(13,596-599,etc.) Overexposure
to heavy metals like lead and mercury have been shown to induce anxiety or
depression (386a,586). Accumulation of mercury in the brain limbic system with
resulting oxidative stress and inflammation has been found to commonly be a
factor in depression(303).
Studies
have found that oxidative stress from reactive oxygen species (such as caused
by mercury and toxic metals) causes increased insulin resistance, whereas
reducing reactive oxygen species lowers insulin resistance. (15). Insulin
resistance has been found to be a significant factor in metabolic syndrome,
cognitive decline, cardiovascular disease, depression, cancer, etc. Mercury
and cadmium inhibit magnesium and zinc levels as well as inhibiting glucose
transfer. Reduced levels of magnesium and zinc are related to metabolic
syndrome, insulin resistance, and brain inflammation and are protective against
these conditions(599,43). These are additional mechanisms by which mercury
and toxic metals are factors in metabolic syndrome and insulin resistance and
conditions such as diabetes, depression, etc. (43,196,338,597,15a). As documented later, for those who have
several amalgam fillings, replacement of the amalgam greatly lowers mercury and
toxic metal exposure, lowers reactive oxygen species and related damage, and
brings significant improvement in the health of people with conditions caused
by oxidative damage and insulin resistance.
It has also been documented that supplementation with antioxidants such
as green tea extract, bilberries, curcumin, N-acetyl-cysteine, etc. and supplements such as DHEA, Goat’s Rue,
cinnamon, quercetin, and vanadyl
sulfate reduces inflammatory cytokine effects and lowers insulin resistance (15a).
Many
studies have found toxic metal exposure such as mercury, lead, cadmium, and
manganese commonly causes depression and other mood and neurological disorders(586). Young adults with higher blood lead levels
are more likely to have major depressive disorder (MDD) or panic disorder, even
if they have exposure to lead levels generally considered safe(586b)
Mercury and other toxic metals inhibit astrocyte function in the brain and CNS(119),
causing increased glutamate and calcium related neurotoxicity
(119,333,416,496). Mercury and increased glutamate activate free radical
forming processes like xanthine oxidase
which produce oxygen radicals and oxidative neurological damage(142,13). Nitric oxide related toxicty
caused by peroxynitrite formed by the reaction of NO
with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD)
has been found to cause inhibition of the mitochondrial respiratory chain,
inhibition of the glutamate transporter, and glutamate-induced neurotoxicity
involved in ALS(524,521).
These inflammatory processes damage cell
structures including DNA, mitochondria, and cell membranes. They also activate microglia cells in the
brain, which control brain inflammation and immunity. Once activated, the microglia secrete large
amounts of neurotoxic substances such as glutamate,
an excitotoxin, which adds to inflammation and
stimulates the area of the brain associated with anxiety(598).
Inflammation also disrupts brain neurotransmitters resulting in reduced levels
of serotonin, dopamine, and norepinephrine. Some of the main causes of such disturbances
that have been documented
include vaccines, mercury, aluminum, other toxic metals, MSG,
aspartame, etc. (593,598,600,etc.)
Hormone
imbalance has been found to be a common factor in depression (488). Imbalances
in DHEA and cortisol may underlie depression,
particularly when stress and obesity are present, and thyroid imbalances have
also been found to cause depression(386a). Estrogen imbalances in post-menapausal women, low testosterone levels in some men, low
DHEA levels, and hypothyroid conditions have been found to be common factors in
depression. Subclinical hypothyroidism
and/or the presence of thyroid peroxidase antibodies
(TPOAb) has been found to be associated with subfertility, infertility, spontaneous abortion, placental
abruption, preterm delivery, gestational hypertension, preeclampsia, postpartum
thyroid dysfunction, depression (including postpartum depression), and impaired
cognitive and psychomotor child development(7).
It is recommended to suspect thyroid pathology if such conditions are
present.
Most studies support a relationship
between thyroid state and cognition, particularly slowed information processing
speed, reduced efficiency in executive functions, and poor learning(11).
Furthermore, hypo-thyroidism is associated with an
increased susceptibility to depression and reductions in health-related quality
of life. Controlled studies suggest that cognitive and mood symptoms improve
with thyroid treatment, though the data are limited by diverse treatment methodologies.
Functional neuroimaging data provide support for the
mood and cognitive findings and treatment reversibility for both overt and subclincial hypothoidism(11a). 94 patients
with subclinical hypothyroidism and a control group were evaluated to determine
the prevalence of
psychiatric disorders(11b).
The prevalence of depressive symptoms based on Beck's Scale among
subclinical hypothyroidism patients was about 2.3 times higher than among controls
(45.6% vs 20.9%, p = 0.006). Anxiety symptoms were
also more frequent in the hypothyroid group.
In a study of effects of hypothyroid
or thyroiditis during pregnancy, infants of women
with hypothyroxinemia at 12 weeks' gestation had
significantly lower scores on the Neonatal Behavioral Assessment Scale
orientation index compared with normal subjects(9). Regression analysis showed
that first-trimester maternal free thyroid hormone was a significant predictor
of orientation scores. This study confirmed that maternal hypothyroxinemia
constitutes a serious risk factor for neurodevelopmental
difficulties that can be identified in neonates as young as 3 weeks of age
Because of such evidence, in November 2002, the American
Association of Clinical Endocrinologists (AACE) recommended screening all women
considering conception and/or all pregnant women in the first trimester for
thyroid dysfunction(7b).
As will be shown,
there is considerable evidence that depression/neurological problems can be
caused by many physiological problems related to past toxic exposures or
combinations of these. Where
physiological problems are contributing factors, determination of the
underlying cause from assessing the persons past medical history, diet, blood
tests, hair tests, etc. can be useful to identifying and correcting any
nutritional deficiencies or imbalances(386a) or
identifying other problems to be dealt with. There is considerable evidence mercury exposure
is among the most common significant
exposures that commonly cause such effects, although many are also exposed to
lead(586), arsenic, and pesticides(552,585) that have similar effects and
effects are synergistic or
cumulative.
III. Mercury exposure levels from amalgam and
other sources.
Amalgam
fillings have been documented to leak significant levels of mercury
continuously due to high vapor pressure of mercury and galvanic action between
mixed metals in the mouth (600,602).
The average person with several fillings gets significant exposure of
mercury daily, much more than from
any other source and more than that prescribed by U.S. Government health
guidelines (602). Mercury in pregnant
women is also documented to cross the placenta and accumulate in the fetus to levels higher than in the
mother (603). Since mercury from amalgam
fillings of a mother is also transmitted to nursing infants in significant
amounts, mercury from their mom’s dental fillings has been found to be the largest source of mercury to the
fetus and a significant source of mercury in infants, which has produced
developmental problems that affect children later in life(603). Young children also have been receiving significant
levels of mercury (thimerasol which is used as a preservative in vaccines)
and large numbers have been found to be significantly adversely affected
because of receiving larger numbers of vaccinations, especially at very early
ages before the blood-brain barrier matures(602). People also get significant prenatal and
postnatal exposures to other toxic metals such as lead, arsenic, cadmium,
aluminum, etc. which have also been found to commonly cause significant
neurological effects (586,604) . The
top 3 toxic substances affecting large numbers of people in the U.S. adversely
according to EPA/ATSDR are mercury, lead, and arsenic. (600,604).
A 2009 study found that inorganic mercury
levels in people have been increasing
rapidly in recent years(543b). It used data
from the U.S. Centers for Disease Control
and Prevention’s National Health
Nutrition Examination Survey (NHANES) finding that
while inorganic mercury was detected in
the blood of 2 percent of women aged 18 to
49 in the 1999-2000 NHANES survey,
that level rose to 30 percent of women by
2005-2006. Surveys in all states
using hair tests have found dangerous levels of
mercury in an average of 22 % of the
population, with over 30% in some states like
Florida and New York(543c).
A
large U.S. Centers for Disease Control epidemiological
study, NHANES
III, found that those with more amalgam
fillings(more mercury
exposure) have
significantly higher levels of chronic health conditions(543). The
conditions in which
the number of dental amalgam surfaces were most highly
correlated with
disease incidence were MS, epilepsy, migraines, mental disorders,
diseases of the
nervous system, disorders of the thyroid gland, cancer, and infectious
diseases
(543).
IV.
Toxic and immune reactive effects of mercury.
Mercury is neurotoxic
(kills or damages brain and nerve cells): (19,27,34,36,43,69,70, 147,148,175,207,211,273,
291,295,327,329,301, 303,395,600/ 39,262,274,303); generates high levels of reactive oxygen
species (ROS) and oxidative stress, depletes gluatathione
and thiols causing increased neurotoxicity from
interactions of ROS, glutamate, and
dopamine (13,56,98,102, 126,145,169,170,184,213,218,219, 250,
257,259,286,290,291,302,324,326, 329,600); kills or inhibits production of
brain tubulin cells (66,67,161,166, 207,300); inhibits production of neurotransmitters by
inhibiting: calcium-dependent
neurotransmitter release(372), dihydroteridine reductase(27,122,257),nitric
oxide synthase(259), blocking neurotransmitter amino
acids(438,601), and effecting
phenylalanine, tyrosine and tryptophan transport to neurons) (34,122,126,257,285,288,333,438/255,333). Toxic metals as well as genetic factors
commonly cause systemic methylation deficiencies
(88), which are documented to commonly be a factor in chronic conditions such
as depression, autism, etc. (386a)
Numerous
studies have found long-term chronic low doses of mercury cause neurological,
memory, behaviour, sleep, and mood problems
(5,72,74,107,109, 290,etc.). Neurological
problems are among the most common and serious effects of mercury, and include
memory loss, moodiness, depression, anger and sudden bursts of anger/rage,
self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or
resist obsessions or compulsions, etc. Many studies of patients with major
neurological diseases have found evidence amalgam fillings may play a major
role in development of conditions such
as depression (94,107,109,212,222,229,233,285c, 294,317,320,322,372,374,453),
schizophrenia (34,35,295,601), memory problems (70,94,212,222,600), and other
more serious neurological diseases such as MS, ALS, Parkinson’s, and
Alzheimer’s (13,33,66,98,207b,330, 331,424,438, 483,600). Some factors that have been documented in
depression are low serotonin levels, abnormal glucose tolerance(hypoglycemia),
and low folate levels(480-83), which mercury has also
been found to be a cause of. Occupational
exposure to mercury has been documented to cause depression and anxiety(534). Acute
exposure to mercury vapor has been found to cause chronic depression, anxiety,
and obsessive-compulsive behavior(487). One mechanism by which mercury has been found
to be a factor in aggressiveness and violence is its documented inhibition of
the brain transmitter
acetylcholinesterase (175,451,465,254). Low serotonin levels and/or hypoglycemia have
also been found in the majority of those with impulsive and violent behavior(481,482).
Mercury(and
other toxic metals) has been found to accumulate in the pineal gland and
reduce melatonin levels, which is
thought to be a significant factor in mercury’s toxic effects(569). Melatonin
has found to have a significant protective action against methyl mercury
toxicity, likely from antioxidative effect of
melatonin on the MMC induced neurotoxicity(567). Disrupted sleep from low
melatonin, or ‘Seasonal Affective Disorder’ with excessive melatonin
production, can result in depression(386a). Melatonin is important in regulating
mood and improving sleep and increasing quality of life by regulating your
body’s circadian rhythms—while scientific evidence indicates that it has
helpful anti-inflammatory and antioxidant properties that can support your
heart, too. (564)
There is
also evidence that mercury affects neurotransmitter levels which have effects
on conditions such as depression, mood disorders, ADHD, etc..
There is evidence that mercury can block the dopamine_b-hydroxylase (DBH) enzyme (571). This enzyme synthesizes
noradrenaline, and low noradrenaline
can cause fatigue and depression. Mercury molecules can block all copper-catalysed dithiolane oxidases, such as coproporphyrin oxidase and DBH. Mercury and other toxic metals have been
found to accumulate in the pineal gland and reduce melatonin
levels, which is thought to be a significant factor in mercury’s toxic
effects (569).
There is evidence that mercury can block the
dopamine-beta-hydroxylase (DBH) enzyme(571). DBH is used to make the noradrenaline neurotransmitter and low noradrenaline can cause fatigue and depression. Mercury
molecules can block all copper catalyzed dithiolane oxidases, such as coproporphyrin oxidase(260) and DBH.
Workers occupationally exposed to
mercury at levels within guidelines have been found to have impairment of lytic activity of neutrophils and
reduced ability of neutraphils to kill invaders such
as candida(285,404). The balance of yeasts found in the intestine can
be a factor in neurological conditions such as depression(386a,404).
Evidence suggests Candida albicans may activate
depressive symptoms and fatigue by promoting ethanol production, a known
central nervous system depressant. Behavior changes are also associated with Candida's inherent toxin– canditoxin‑‑and/or
by its tendency to compete with the host organism for essential dietary
nutrients.(460) Immune Th1 cells inhibit candida by cytokine related activation of macrophages and neutraphils.
Development of Th2 type immune responses deactivate such defenses(404b,285). Mercury inhibits macrophage and neutraphil defense against candida
by its affects on Th1 and Th2 cytokine effects(181,285). Candida overgrowth results in production of
the highly toxic canditoxin and ethanol which are
known to cause fatigue, toxicity, and depressive symptoms(460).
Mercury causes decreased lithium levels, which is a factor in
neurological diseases such as depression and Alzheimer’s. Lithium protects brain cells against excess
glutamate and calcium, and low levels cause abnormal brain cell balance and
neurological disturbances (280,294,333,33,56 ). Medical texts on neurology (27,295) point out
that chronic mercurialism is often not recognized by
diagnosticians and misdiagnosed as dementia or neurosis or functional psychosis
or just “nerves”. “Early manifestations
are likely to be subtle and diagnosis difficult: Insomnia, nervousness, mild
tremor, impaired judgment and coordination, decreased mental efficiency,
emotional lability, headache, fatigue, loss of sexual
drive, depression, etc. are often mistakenly ascribed to psychogenic
causes”. Very high levels of mercury are
found in brain memory areas such as the cerebral cortex and hippocampus of
patients with diseases with memory related symptoms (158,34,207,etc.}
A
direct mechanism involving mercury’s inhibition of cellular enzymatic processes
by binding with the hydroxyl radical(SH) in amino acids appears to be a major
part of the connection to neurological conditions such as autism, schizophrenia,
manic-depressive,ADD, depression
(294,375,408,438,601). For example mercury has been found to strongly inhibit
the activity of dipeptyl peptidase (DPP IV) which is
required in the digestion of the milk protein casein(411,412,602).
Studies involving a large sample of schizophrenic or autistic patients
found that over 90 % of those tested had high levels of the milk protein
beta-casomorphin-7 in their blood and urine and defective enzymatic processes
for digesting milk protein(410). Similar findings have been confirmed for ADD
and mania patients. Elimination of milk
products from the diet has been found to improve these conditions in large
numbers of patients(5). Such populations have also been found to have
high levels of mercury and to recover after mercury detoxification. (413,60,313,600). As
mercury levels are reduced the protein binding is reduced and ment in the
enzymatic process occurs(5). Additional cellular level enzymatic effects of
mercury’s binding with proteins include blockage of sulfur oxidation processes
and neurotransmitter amino acids(33,114,438,5), enzymatic processes involving
vitamins B6 and B12(418,5), effects on the cytochrome-C
energy processes(232,35), along with mercury’s adverse effects on cellular
mineral levels of calcium, magnesium, zinc, chromium, and lithium (43,96,198,333,386,427,432,484,38).
When a pathological state exists, the
body’s finely balanced symbiosis may be damaged and cease to function normally.
Beneficial essential bacteria may be damaged, causing the malabsorption
of critical vitamins and minerals. If the damage is extensive and/or long
lasting, pathogens including pathogenic yeast and gram negative bacilli will
begin to fill the vacuum left by the healthy bacteria. The metabolism of these
pathogens is different and foods are no longer broken down in the same way.
Proteins that previously would be broken down to their constituent amino acids
are only partially digested, leaving long chains of amino acids called
peptides. Our entire body is built from proteins, which are themselves built
from chains of peptides. Certain peptides are extremely bioactive i.e they interact strongly with other proteins in the body.
Mercury and toxic metals cause dysbiosis and inhibits the function of the enzymes needed
to digest gluten and casein, resulting in peptides in the blood which have
significant neurological effects including depression, anxiety, and schizophrenia(404,405). A side effect of dysbiosis
(incorrect gut microorganisms) is that the gut becomes leaky i.e it passes larger molecules than would normally be the
case. Thus peptides, which should normally be broken down to amino acids, leave
the gut and enter the blood stream intact, where they are delivered to other
organs. Casein and Gluten, proteins and
mixture of proteins common in many foods break down to form very potent opio-peptides when acted on by certain pathogenic bacteria.
These peptides have a narcotic action and act on opiate receptors in the brain,
triggering major changes in brain function including depression, anxiety,
schizophrenia, etc. Certain pathogens
more plentiful during dysbiosis also have been found
to methylate mercury to its organic form which is
more readily taken up by the blood and redistributed. Taking antibiotics is
another cause of such dysbiosis.
Studies
have shown a significant association between hypothyrodism
and mood disorders such as depression(391,8). Mercury from dental amalgam has been
documented to cause hypothyroidism (50,91,212,222,369,382,
390,35ab). The majority of patients
tested with hypothyroidism or thyroiditis and treated
with dental amalgam replacement significantly improved after replacement(91,369,303).
Numerous
studies have found long term chronic low doses of mercury cause neurological,
memory, behavior, sleep, and mood problems
(34,69,70,71,72,74,95,107,108,109,115,119,140,141,196,199,222,252, 255,257,258,
282,290,303,304]. Neurological effects have been documented at very low levels
of exposure(urine Hg< 4 ug/L),
levels commonly received by those with amalgam fillings(290). One of the
studies at a German University(199) assessed 20,000
people. There is also evidence that
fetal or infant exposure causes delayed neurotoxicity evidenced in serious
effect at middle age(255). Studies of groups of patients with amalgam
fillings found significantly more neurological, memory, mood, and behavioral
problems than the control groups. (34,107,108,109,140,141,196,199,222,290].
Increased mercury levels from amalgam are documented to cause increased
neurological problems related to lowered levels of neurotransmitters dopamine,
serotonin, noreprenephrine,and
acetylcholinesterase (35,107,140,141,175,251,254,288, 290,296,305,372, 451,465,412). The
reduced neurotransmitter levels in those with amalgam appear to be a factor
encouraging smoking since nicotine increases these neurotransmitter levels and
a much higher percentage of those with amalgam smoke than in those without amalgam(141).
Based on thousands of clinically followed
cases by doctors, replacement of amalgam fillings resulted in the cure or
significant improvement in the majority of cases for: depression
(35,94,95,107,222,271,294,212,229,230,233,303,317,320,322, 376,407),
schizophrenia (294,34,35), insomnia (94,95,212,222,271,304,317,322,376,407), anger(212,233,320,407,102), anxiety &
mental confusion (94,95,212,222,229,233,271,304,317,320,322,407,57), memory
disorders (94,95,222,304,407). For
example, in a study of amalgam replacement for 56 persons who suffered from
chronic depression, 16 had the condition eliminated and 34 had significant
improvement after a year or 4 years(95).
One of the most common causes of depression and
mood disorders has been documented to be past toxic exposures such as mercury
or pesticides(585), and the majority treated for these
at clinics that deal with such conditions have either recovered or shown
significant improvement(600,601,552).
Amalgam dental fillings have been found the most common source of such
toxic exposures, with mercury thimerosal from vaccinations also affecting
millions of children(600,601). Many
doctors treating depression and mood disorder conditions related to toxic
exposures also usually recommend supplementing the deficient essential minerals
that mercury affects by affecting cell membrane permeability and blocking
cellular enzymatic processes, often obtaining a hair element test to determine
imbalances and needs(560,600). The body requires adequate, but not
excessive, amounts of trace minerals and nutrients for proper functioning.
Under certain conditions, excesses or deficiencies of many of these elements
can set off symptoms of depression(560). Subnormal
levels of zinc, for example, are associated with treatment resistant depression(561). And deficiencies of magnesium can provoke a
wide range of psychiatric symptoms related to depression, ranging from apathy
to psychosis(562).
Research on manic patients, on the other hand, has revealed elevated
vanadium in the hair‑‑significantly higher levels than those
measured in both a control group and a group of recovered manic patients(563).
V.
The Danger of Vaccinations
Chronic over activation of the immune system
has been found to be a major factor in neurological and cardiovascular conditions(593,598,etc.)
Immune adjuvants in vaccines including aluminum,
mercury, special lipids, and even MSG in some cause activation of the immune
system which can last for months. This
causes inflammation of the brain that is magnified by each additional vaccination
with more immune adjuvants. The high number of vaccinations in a short
period of time has been found to be a major cause of autism spectrum and other
inflammatory conditions in children, and also to be major factors in
inflammatory conditions of older adults such as depression, Alzheimer’s,
Parkinson’s, etc. (593,598,601,600, etc.) Flu vaccinations in those over 55 years of age
have been found to increase the risk of Alzheimer’s by over 500%, along with
increased risk of major depression (598).
VI.
Treatment of Depression
Anyone with depression should be
examined and tested for toxic metal exposure or exposures to other toxics. Detoxification should be carried out as
appropriate. Those with several amalgam
fillings or metal crowns over amalgam are getting high exposures of extremely
toxic substances that are highly inflammatory so should have the problematic dental work replaced. Everyone should also be checked for
problematic root-canal teeth and jawbone cavitations, which likewise are highly
inflammatory and can have major impacts on the immune system and health (605,303). Reducing glutamate
levels and blocking glutamate receptors can significantly improve depression
(598).
Diet and lifestyle are important
factors in preventing or controlling depression. One should avoid alcohol,
sugar, caffeine, and inflammatory substances such as MSG, high-fructose corn
syrup, etc. (580,598). Reduce stress and get regular
exercise. Yoga and meditation have been
found to be helpful for many. Properly
formulated nutritional supplements have been found to be effective in treating
ADHD and depression(522).
Studies
and clinical experience have found that diet plays a role in depression and
diet measures commonly avoid, cure, or significantly improve depression
(565,566,580,583,591). B Vitamins and
magnesium deficiencies have been found to be factors in depression and anxiety.
Supplementaion to assure proper levels is beneficial
in treatment (565,566,583). Many
people, particularly women over 65, have B-12 deficiencies and respond
dramatically to injections of the vitamin. But all B vitamins can boost mood;
they work by facilitating neurotransmitter function. Other pluses: B vitamins
are critical for preventing other maladies, including heart disease, cancer,
and Alzheimer’s. Suggested Dosage: Take at least 800
micrograms of folate, 1,000 mcg of B-12, and 25 to 50
milligrams of B-6. A B-complex vitamin should do the trick, says Hyman,
and if you’re depressed, take more. Take them in combination because otherwise
one can mask another B vitamin deficiency(565).
The supplement 5-HTP has been shown by many studies and
clinical experience to often be effective in treating or controlling depression(530). Double
blind studies have found 5-HTP to be as effective as SSRIs and other types of antidepressives at treating depression. But studies have
also cast doubt on serotonin levels as the main cause in depression and found
both 5-HTP and SSRIs have limited effect on many with depression. SSRIs appear to be attempting to suppress
symptoms related to one type of imbalance found in many with depression rather
than the underlying causes.
SAMe
(400-1600 mg) and Inositol have been found to be effective in
treating depression and anxiety with effectiveness at least as much as
pharmaceutical antidepressants and much less adverse effects(565,566,580,590). SAMe is an amino acid combination produced by humans, animals, and
plants. Supplements come from a synthetic version produced in a lab that has
shown a lot of promise in European studies. May affect the
synthesis of neurotransmitters. Has fewer side
effects than 5-HTP and fewer drug interactions than Saint-John’s-wort. Dosage: Can range from 400 to 1,200 mg a day, though
high doses can cause jitteriness and insomnia. Risks: People with bipolar
disorder shouldn’t use it without supervision because it can trigger mania.
(566) Inositol has been found to be effective for treating OCD,
panic disorders, and bipolar depression(591), with effectiveness at least as
much as SSRIs and less adverse effects(591).
St. Johns Wort (300 mg x 3) also has been found effective for many (565,580)
and is one of the best-known remedies. Best for mild to moderate depression. Suggested Dosage(566): Start on a dose of 300 mg (standardized to 0.3
percent hypericin extract) two to three times a day,
depending on severity of depression; it can take three weeks to show benefits.
Risks: It may interfere with up to half of all drugs, prescription and
over-the-counter.
Amino acids are
the building blocks of neurotransmitters; 5-HTP is the most popular. Taking it
can elevate mood in cases of depression, anxiety, and panic attacks, and
relieve insomnia. Increases production of the
neurotransmitter serotonin. Suggested Dosage(566):
Start with a low dose, 50 mg two to three times a day; after two weeks,
increase the dose to 100 mg three times a day. Risks: Mild nausea or diarrhea.
Before starting, get off antidepressants (under a doctor’s supervision); the
combination can produce an overload of serotonin. Tyrosine is another amino acid found to often
be useful in overcoming depression.
Essential fatty acids (EPA/DHA) benefits are among the best documented. The reason they’re so
effective is EFAs are part of every cell membrane, and if those membranes
aren’t functioning well, then neither is your brain. Suggested Dosage(566):
For depression, take at least 2,000 to 4,000 mg of fish oil a day. Should be
purified or distilled so it’s free of heavy metals. Risks: Very safe, albeit
unstable. Since it can oxidize in your body, take it along with other
antioxidants, like vitamin E (400 IUs a day).
DHEA is a hormone marketed in Europe specifically for postmenopausal
depression, though it may be helpful for other forms as well. It has been used
in conjunction with estrogen to treat hot flashes. Not clear why it helps boost
mood and energy. Suggested Dosage(566): 10 to 200 mg a
day. Risks: Any hormonal supplement has the potential to increase cancer risk.
Rhodiola rosea is considered an adaptogen, which means it can
increase your resistance to a variety of stressors. It may be good for mild to
moderately depressed patients. Suggested Dosage(566):
Take 100 to 200 mg three times a day, standardized to 3 percent rosavin. Risks: More than 1,500 mg a day can cause
irritability or insomnia.
Other nutrients found to cause depression when low or
to usually be low in depression or to be effective additions in treating
depression include ginkgo biloba, DHEA, natural
progesterone, pregnenolone, DMAE, L-Carnitine, NADH, Phenylalanine, Folic Acid, Vit B12 (cobalamine), B6, other B
vitamins, choline,
vit D, vit C,
potassium, testosterone in men over 40 (580,582,565,566). A product that contains several of these
nutrients is Happiness 1-2-3 (vit B complex,
magnesium, St.Johns Wort,
L-Theanine, 5-HTP, magnolia) (583). Other companies referenced here have similar combinations(580,582).
Lower levels of fish
oil (EPA) has been found to be significantly related to depression.
Elderly people have been found to be of special risk regarding depression.
Studies have found higher levels of EPA to be associated with lower likelihood
of depression or dementia (580b) in the elderly. Theoflavins
from black or green tea and curcumin (turmeric) have
also been found to be significantly effective against inflammation, which is a
major factor in depression(580). Poor digestion results in poor mineral and
nutrient absorption and is a factor in many chronic conditions. Digestive
problems often increase with aging, due to reductions in digestive enzyme
production and availability as well as increased proliferation of pathogenic
organisms. Supplementation with digestive enzymes and probiotics
often significantly improves digestion and improves digestive related conditions(580).
VII.
Anxiety
Disorders include Panic Disorder, OCD, PTSD, Phobias, and General Anxiety
Disorder.
(584) As previously noted, anxiety or panic
disorder can be related to not acknowledging or burying feelings(583). Panic disorder is characterized by repeated
episodes of intense fear. Affects 3 to 6 million. Obsessive-Compulsive Disorder
(OCD) is characterized by anxious thoughts and uncontrollable ritualistic
behavior. Affects 2%
of the population. Some studies have
suggested OCD patients usually have high glutamate levels, which overexcites
areas of the brain (581). Post-Traumatic Stress Disorder(PTSD)
is a debilitating illness resulting from a traumatic event or events. It
affects a large number of people. Phobias are irrational fears of things or
situations. Affects
over 10% of the population.
Generalized
Anxiety Disorder
(GAD) is chronic, daily worrying about health, finances, work, family,
etc. Stress is a psychological and
physical response to the demands of daily life that exceed the person’s ability
to cope successfully. Stress can have physical effects prolonged stress can
have debilitating effects. Two conventional non-pharmaceutical treatments for
anxiety are behavioral therapy(breathing techniques,
exposure therapy, etc.) and cognitive therapy(modification of thinking patterns).
As
previously note, environmental toxins can be a factor in causing nutritional
deficiencies, imbalances, and inflammation related to anxiety disorders and
reductions in exposures have been found to be beneficial. Hypoglycemia may be a factor in some anxiety disorders- eat more frequent small
quantities including protein, nuts, etc. Many are adversely affected by
stimulants such as caffeine. Irregular or insufficient sleep patterns can be a
significant factor. Regular exercise is
generally beneficial in anxiety disorders.
Massage therapy, including aromatherapy is often helpful, along with
meditation and deep breathing exercises.
Music,
yoga, muscle relaxation techniques, biofeedback, etc. are also often helpful.
Deficiency of B vitamins and
magnesium have
been found to be common factors in anxiety disorders. (583). Adapton (fish
oil) is commonly used helpful treatment for anxiety in Europe. (580) Very successful for fatigue, etc. Theanine (green tea
extract) -
calming and lowers blood pressure. (580,582,583)
Ginseng
has been found effective for many post-menapausal
women’s anxiety, fatigue, depression. Reishi has helped
some and Ashwagunda (Indian Ginseng). (580) A product with several of these nutrients is Calming Balance
(vit B complex, magnesium, L-Theanine,
Magnolia extract). (583). The other sources
referenced here have similar products (580,582).
References
(5) Consensus
paper of the WFSBP Task Force on Biological Markers:
Biological
Markers in Depression, R. MOSSNER, O. MIKOVA,, E. KOUTSILIERI, M. SAOUD,A-C
EHLIS1, N. MULLER5, A. J. FALLGATTER1 & P. RIEDERER
The World Journal of Biological Psychiatry, 2007; 8(3): 141_174; http://wfsbp-verband.globit.com/fileadmin/pdf/guides/WFSBP_Consensus_Paper_Biological_Markers_in_Depression.pdf
(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
(10) Science News, Vol 158, Oct 14, 2000
(13)S.Hussain et al, “Mercuric chloride‑induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci Health B 1997 May;32(3):395‑409; & S.Tan et al, “Oxidative stress induces programmed cell death in neuronal cells”, J Neurochem, 1998, 71(1):95-105. & J.S. Bains et al, “Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death”, Brain Res Rev, 199, 25(3):335-58; & P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36; & Pocernich CB, Cardin AL, Racine CL, Lauderback CM, Allan Butterfield D. Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: relevance to brain lipid peroxidation in neurodegenerative disease. Neurochem Int 2001 Aug;39(2):141-9;
(15) Insulsin Resistance: the Surprising Cause Behind This Highly Destructive Process, Vitamin Research News, Vol 22, No. 6, June 2008; & Houstis N, Rosen ED, Lander ES, Reactive oxygen species have a causal role in multiple forms of insulin resistance, Nature, 2006, Apr 13; 440(7086): 944-8; & Meigs JB, Larson MG, et al, Association of oxidative stress, insulin resistance, and diabetes risk phenotypes: the Framingham Offspring Study, Diabetes Are. 2007, Oct;30(10):2539-35.
(30) Irving Kirsch and Guy Sapirstein, Prevention & Treatment, 1998 & Listening to Prozac but Hearing Placebo. 2002; & The Emperor's New Drugs: Exploding the Anti-depressant Myth. 2010
(31) The Journal of the American Medical Association (JAMA)
January 6, 2010; 303(1):47-53
(33)B. Windham, Multiple Sclerosis(MS): the mercury connection; www.flcv.com/ms.html
(34) Patrick Störtebecker, Associate Professor of Neurology, Karolinska Institute , Stockholm. Mercury Poisoning from Dental amalgam‑ a hazard to the human brain, Bio-Probe, Inc. ISBN: 0-941011001-1
(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, http://www.hugnet.com
(43) B.Rajanna et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”, J Biol Chem. 1997 Dec 19;272(51):32411-8., &
(50) (a)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)
(61) 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; & G.Drasch et al, “Mercury Burden of Human Fetal and Infant Tissues”, Eur J Pediatr 153:607-610,1994;
(66) B.Windham, Alzheimer’s Disease: the mercury connection, www.flcv.com/alzhg.html ;
(over 150 peer-reviewed medical studies)
(72) D.L.Smith,"Mental effects of mercury poisoning",South Med J 71:904-5,1978.
(74) A.C.Bittner et al, “Behavior effects of low level mercury exposure among dental professionals”, Neurotoxicology & Teratology, 1998, 20(4):429-39.
(88) Activation of methionine
synthase by insulin-like growth factor-1 and
dopamine: a target for neurodevelopmental toxins and
thimerosal, Waly M,
Olteanu H, Deth RC et al, Mol Psychiatry. 2004 Apr;9(4):358-70
(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.
(94)F.Berglund, Case reports spanning 150 years on the adverse effects of dental amalgam, Bio- Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured)
(95) Lichtenberg, HJ "Elimination of symptoms by removal of dental amalgam from mercury poisoned patients", J Orthomol Med 8:145-148, 1993; & Lichtenberg H, "Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals", Journal of Orthomolecular Medicine,1996, 11(4): 195-203. (119 cases)
(98) B.Windham, Parkinson’s Disease: the mercury connection; www.flcv.com/parkins.html
(over 100 peer-reviewed medical studies)
(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
(108)M.Henningsson et al,"Defensive characteristics in individuals with amalgam illness", Acta Odont Scand 54(3): 176-181,1996.
(109) Y.X. Liang et al,"Psychological effects of low exposure to mercury vapor",Environmental Med
Research, 60(2): 320-327, 1993; & T.Kampe et al,
"Personality traits of adolescents with intact and repaired dentitions",Acta
Odont Scand,44:95-,1986; & R.Kishi
et al, 1994, Residual neurobehavioral effects of chronic exposure to mercury vapor”, Occupat. Envir.
Med., 1:35-41.
(114) 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; & T.V. O’Halloran, “Transition metals in control
Of gene expression”, Science, 1993, 261(5122):715-25; & 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; Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct 1995; 20(3): 233-8; & Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system.. Biol Signals 1994, 3:181-7.
(115)G.Hall,
V-TOX, Mercury levels excreted after Vit C IV as chelator‑ by number of fillings Int Symposium
"Status Quo and Perspectives of Amalgam and Other Dental Materials"
European Academy, Ostzenhausen/Germany.
April 29 ‑ May 1, 1994; & Heavy Metal Bulletin, Apr
1996,Vol.3,Issue 1, p6-8 (200
cured or significantly improved)
(119) (a) L.Ronnback et al, "Chronic encephalopaties
induced by low doses of mercury or lead",
Br J Ind Med 49: 233-240, 1992; &(b) H.Langauer‑Lewowicka,” Changes in the nervous system
due to occupational metallic mercury poisoning” Neurol
Neurochir Pol 1997 Sep‑Oct;31(5):905‑13;
&(c) Langauer-Lewowicka H. [Chronic toxic encephalopathies] [Polish]
Med Pr. 1982;33(1-3):113-7; & (d)[Pneuropsychological
disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)] Rev Neurol. 2000 Oct
16-31;31(8):712-6. Tirado V, Garcia MA et al; & (f) Neurobehavioral
effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999;6(4):193-200, Haut
MW, Morrow LA et al.
& (g) Personality
traits in miners with past occupational elemental mercury exposure.
Environ Health Perspect. 2006 Feb;114(2):290-6; Kobal Grum D, Kobal AB et al
(122) B.Ono
et al, “Reduced tyrosine uptake in strains sensitive to inorganic mercury”,
Genet, 1987,11(5):399-
(140) R.L.Siblerud, "Health Effects After Dental Amalgam Removal", J Orthomolecular Med 5(2): 95-106.
(141)R.L.Siblerud et al, "Evidence that mercury from dental fillings may be an etiological factor in smoking",Toxicol Lett,v68,n3,1993,p307- & v69(3):305.
(142) Ariza ME; Bijur GN; Williams MV. Lead and mercury mutagenesis: role of H2O2, superoxide dismustase, and xanthine oxidase. Environ Mol
Mutagen 1998;31(4):352‑61
(175) Soderstrom S, Fredriksson A, Dencker L, Ebendal T, “The effect of mercury vapor on cholinergic neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995, 85:96-108; & Toxicol Lett 1995; 75(1-3): 133-44.
(181)P.W. Mathieson, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30;
(196) Gowdy & Demes, 1978, in B. Wolfe and P. Wolfe, “Fillings, Mercury, and You”, Mothering magazine, Summer, 1987.
(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; & (b)Dr.I.Gerhard, Dr. E.Roller, et al, Tubingen Univ. Gynecological Clinic,Heidelberg,1996
(207) Pendergrass JC, Haley BE, Univ. Of Kentucky Dept. Of Chemistry “ The Toxic Effects of Mercury on CNS Proteins: Similarity to Observations in Alzheimer’s’s Disease”, IAOMT Symposium paper, March 1997 & “Mercury Vapor Inhalation Inhibits Binding of GTP ...-Similarity to Lesions in Alzheimer’s Diseased Brains”, Neurotoxicology 1997, 18(2)::315-24; & Met Ions Biol Syst, 1997, 34:461-
(212) Ziff, M.F., “Documented clinical side effects to dental amalgams”, ADV Dent. Res.,1992; 1(6):131-134; & Ziff, S.,Dentistry without Mercury, 8th Edition, 1996, Bio-Probe, Inc.,ISBN 0-941011-04-6; & Dental MercuryDetox, Bio-Probe, Inc. www.bioprobe.com. (cases:FDA Patient Adverse Reaction Reports- 762,Dr.M.Hanson-Swedish patients-519,Dr. H. Lichtenberg-100 Danish patients,Dr. P.Larose- 80 Canadian patients, Dr. R.Siblerud, 86 Colorado patients, Dr. A.V.Zamm, 22 patients)
(222) M. Daunderer, “Improvement of Nerve and Immunological Damages after
Amalgam Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991
(229) M.Davis,editor, Defense Against Mystery Syndromes”, Chek Printing Co.,
March, 1994(case histories documented)
(230) Sherry A. Rogers, M.D., Depression--Cured at Last! (1997), SK Publishing, P. O. Box 40101, Sarasota, FL 34242.
(233)Sven Langworth et al,”Amalgamnews and Amalgamkadefonden, 1997 and Svenska Dogbladet,1997 (286 cases); & F.Berglund,Bjerner/Helm,Klock,Ripa,Lindforss,Mornstad,Ostlin), “Improved Health after Removal of dental amalgam fillings”, Swedish Assoc. Of Dental Mercury Patients, 1998. (www.tf.nu) (over 1000 cases) (Sweden has decided to phase out amalgam fillings & Gov’t maintains health records on all citizens)
(251)(c)Omura, Yoshiaki; Abnormal Deposits of Al, Pb, and Hg in the Brain, Particularly in the Hippocampus, as One of the Main Causes of Decreased Cerebral Acetylcholine, Electromagnetic Field Hypersensitivity, Pre-Alzheimer's Disease, and Autism in Children; Acupuncture & Electro-Therapeutics Research, 2000, Vol. 25 Issue 3/4, p230, 3p
(252) B.J.Shenker et al, Dept. of Pathology, Univ. of Pennsylvania, “Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cellular glutathione content”, Immunopharmacol Immunotoxicol 1993, 15(2-3):273-90.
(254) al-Saleh I, Shinwari N. Urinary mercury levels in females: influence of dental amalgam fillings. Biometals 1997; 10(4): 315-23;
(257) I. Smith et al, “Pteridines and mono-amines: relevance to neurological damage”, Postgrad Med J, 62(724): 113-123, 1986; & A.D.Kay et al, “Cerebrospinal fluid biopterin is decreased in Alzheimer’s’s disease”, Arch Neurol, 43(10): 996-9, Oct 1986; & T.Yamiguchi et al, “Effects of tyrosine administration on serum bipterin In patients with Parkinson’s Disease and normal controls”, Science, 219(4580):75-77, Jan 1983; & T.Nagatsu et al, “Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s”, Neurol, 1984, 40: 467-73.
(258)Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incicdence?, Bull Environ Contam Toxicol,
2001, 67: 800-6; & Clinical Management of Poisoning, 3rd Ed.,(p753) Haddad, Shannon, and Winchester, W.B. Sounders and Company, Philadelphis, 1998;
(259) C.K.Mittal et al, “Interaction of heavy metals with the nitric oxide synthase”, Mol Cell Biochem,149-150:263-5, Aug 1995; & J.P.Bolanos et al, “Nitric Oxide mediated mitochondrial damage in the brain”, ??
(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
(280) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., “Lithium treatment protects neurons in CNS from glutamate induced excitibility and calcium influx”, Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998.
(281) T.W. Clarkson et al, “Transport of elemental mercury into fetal tissues”, Biol. Neonate. 21:239-244, 1972; & M.R.Greenwood et al, “Transfer of metallic mercury into the fetus”, Experientia, 28:1455-1456, 1972
(285)R.C.Perlingeiro
et al, “Polymorphonuclear phagentosis
in workers exposed to
mercuryvapor”,
Int J Immounopharmacology”, 16(12):1011-7,1994; ; & Mathieson
PW. 1995. Mercury:
god of Th2 cells? Clin Exp Immunol 102:229_230; &(b)
Hum Exp Toxicol 1995, 14(3):281-6; & M.L. Queiroz et al, Pharmacol Toxicol, 1994, 74(2):72-5; & (b) J.W.Albers et al, “Neurological abnormalities associated with remote occupational elemental mercury exposure”,Ann Neurol 1988, 24(5):651-9 .; &(c) Effects of low exposure to inorganic mercury on psychological performance. Br J Ind Med. 1990 Feb;47(2):105-9. Soleo L, Urbano ML, Petrera V, Ambrosi L. & (e)M.S.Hua et al, “Chronic elemental mercury intoxication”, Brain Inj, 1996, 10(5):377-84; & (f) Gunther W, et al, Repeated neurobehavioral investigations in workers ..., Neurotoxicology 1996; 17(3-4):605-14;
(288)Rajanna B, Hobson M, Harris L, Ware L, Chetty CS. Effects of cadmium and mercury on Na(+)-K(+)ATPase and uptake of 3H-dopamine in rat brain synaptosomes. Arch Int Physiol Biochem 1990, 98(5):291-6; & M.Hobson & B.Rajanna, “Influence of mercury on uptake of dopamine and norepinephrine”, Toxicol Letters, Dep 1985, 27:2-3:7-14; & McKay SJ, Reynolds JN, Racz WJ. Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatial slices. Can J Physiol Pharmacol 1986, 64(12):1507-14; & Scheuhammer AM; Cherian MG. Effects of heavy metal cations, sulfhydryl reagents and other chemical agents on striatal D2 dopamine receptors. Biochem Pharmacol 1985 Oct 1;34(19):3405‑13 ; 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; & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308.
(290) D. Echeverria et al, Neurobehavioral effects from exposure to dental amalgam” FASEB J, Aug 1998, 12(11):971-980.
(294) “Do amalgam fillings influence manic depression?”,Journal of Orthomol.. Medicine, 1998, www.depression.com/news/news_981116.htm
(295) Cecil Textbook of Medicine, 20th Ed., Bennett & Plum, W.B. Saunders and Company, Philadelphia, 1996, p 69; & Comprehensive Psychiatry, Vol 18(6), 1977, pp595-598, & poisoning & Toxicology Compendium, Leikin and Palouchek, Lexi-Comp., Cleveland, 1998..
(296) Harrison’s Principles Of Internal Medicine, 14th Ed., McGraw-Hill, N.y., 1998.
(300) C.Hock et al, “Increased blood mercury levels in patients with Alzheimer’s’s disease”, J. Neural Transm, 1998, 105(1):59-68.
(304) R.F. Kidd, Results of Dental Amalgam Removal and Mercury Detoxification, Alternative Therapies, July 2000, Vol 6, No. 4, p49-55.
(305)
Soderstrom S, Fredriksson A, Dencker L, Ebendal T, “The effect of mercury vapor on cholinergic
neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995,
85:96-108;
& Leong CC, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 2001 Mar 26;12(4):733-7
(313) V.D.M.Stejskal et al, “Mercury-specific Lymphocytes: an indication of mercury allergy in man”, J. Of Clinical Immunology, 1996, Vol 16(1);31-40.
(317) S.Zinecker, “Amalgam: Quecksilberdamfe bis ins Gehirn”, der Kassenarzt, 1992, 32(4):23; “Praxiproblem Amalgam”, Der Allgermeinarzt, 1995,17(11):1215-1221.(1800 patients)
(320) U.F.Malt et al, “Physical and mental problems attributed to dental amalgam fillings”, Psychosomatic medicine, 1997, 59:32-41. (99 cured)
(322) P.Engel, “Beobachtungen uber die gesundheit vor und nach amalgamentfernug”,Separatdruck aus Schweiz. Monatsschr Zahnm. 1998, vol 108(8).(75 cases amalgam removal) http://soho.globalpoint.ch/paul‑engel
(330) B. Windham, ALS: the mercury connection,
www.flcv.com/als.html; over 100
peer-reviewed medical study references.
(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 arthritis”, Ann Rheum Dis,
1992, 51:3,318-20; & P.Emory et al, Br J Rheumotol,
1992, 31:7,449-51; & Steventon GB, et al; Xenobiotic
metabolism in motor neuron disease, Neurology 1990, 40:1095-98.
(333) A.J.Freitas
et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain”, Brain Research, 1996, 738(2):
257-64; & 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; & E.Chavez et al,
“Mitochondrial calcium release by Hg+2",J Biol
Chem, 1988, 263:8, 3582-; A. Szucs et al,
Cell Mol Neurobiol, 1997,17(3): 273-8; & 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; & Rossi AD, et al, Modifications of Ca2+
signaling by inorganic mercury
in PC12 cells. FASEB J 1993, 7:1507-14.
(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;
(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; & Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. www.melisa.org
(372) 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;
& 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; &Brouwer M et al, Functional changes induced by heavy metal
ions. Biochemistry, 1982, 21(20):
2529-38.
(374) Benkelfat C et al, Mood lowering effect of tryptophan depletion. Arch Gen Psychiatry, 1994, 51(9): 687- 97; & Young SN et al, Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology, 1985, 87(2):173-77; & Smith KA et al, Relapse of depression after depletion of tryptophan, Lancet 1997, 349(9056):915-19; & Delgado PL et al, Serotonin function, depletion of plasma tryptophan, and the mechanism of antidepressant action. Arch Gen Psychiatry 1990, 47(5):411-18.
(375) Stejskal VDM, Danersund A, Lindvall A. Metal-specific memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters 1999; & 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
(376) Melchart D, Wuhr E, Weidenhammer W, Kremers L. A multicenter survey of amalgam fillings and subjective complaints in non-selected patients in the dental practice. Eur J Oral Sci 1998; 106:770-77 (6,744 patients in 34 clinics)
(382) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60; &(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)
(390) 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; &(b) Barregard L, Lindstedt G, Schutz A, Sallsten G - "Endocrine function in mercury exposed chloralkali workers" Occup Environ Med 51(8):536-40 (1994)
(391) Subclinical hypothyroidism: psychiatric
disorders and symptoms. Almeida C, Brasil MA, Costa AJ, Vaisman M. Rev Bras Psiquiatr.
2007 Jun;29(2):157-9, & Screening for
depression disorders in patients with chronic somatic illness. Filipcić I, Popović-Grle S, Hajnaek S, Aganović I. Coll Antropol.
2007 Mar;31(1):139-43; & Neuropsychiatric
aspects of hypothyroidism and treatment reversibility. . Davis JD, Tremont G. Minerva Endocrinol.
2007 Mar;32(1):49-65, etc.
(404) M. E. Godfrey, Candida, Dysbiosis and Amalgam. J. Adv. Med. vol 9 no 2 (1996); & Romani L, Immunity to Candida Albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol 1999, 2(4):363- 7; & Alfred V. Zamm. CANDIDA ALBICANS THERAPY: Dental mercury removal, an effective adjunct. J. Orthmol. Med. v1#4 pp261-5 (1986)
(405) Neurological Effects of Dysbiosis Involving Gluten and Casein, the Mercury Connection, Review, B Windham (Ed), 2009. www.flcv.com/autismgc.html & www.flcv.com/leakyghg.html
(407) Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J prosthet Dent 1990; 63(5):593-6; & Yonk LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341- 5; & Jaffe JS, Strober W, Sneller MC, Functional abnormalites of CD8+ T cells define a unique subset of patients with common variable immunodeficiency. Blood 1993, 82(1): 192-20.
(408) Yonk LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341-5; & Jaffe JS, Strober W, Sneller MC, Functional abnormalities of CD8+ T cells define a unique subset of patients with common variable immunodeficiency. Blood 1993, 82(1): 192-20.
(409) 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 : & Yazbak FE(MD,FAAP) Autism 99 : A National Emergency, www.garynull.com/documents/autism_99.htm
(410) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999.
(411) 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; & Kar NC, Pearson CM. Dipeptyl Peptidases in human muscle disease. Clin Chim Acta 1978; 82(1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174,etc.
(412) (a) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism. Invest Clin 1996,37(2):113-28;& Carlsson ML. Is infantile autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105(4-5): 525-35. & (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;
(413) Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers; & http://www.edelsoncenter.com; & Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; & Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998. 3(3):187-98
(416) Kim P, Choi BH. “Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes”, Yonsei Med J 1995; 36(3): 299-305; & Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56; & Albrecht J, Matyja E. Glutamate: a potential mediator of inorganic mercury toxicity. Metab Brain Dis 1996; 11:175-84; & Tirosh O, Sen CK, Roy S, Packer L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death Neuroscience. 2000;97(3):531-41
(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.; & Spivey-Fox MR. Nutritional influences on metal toxicity. Environ Health Perspect 1979; 29: 95-104; & (b) McCarty MF. High-dose pyridoxine as an ‘anti-stress’ strategy. Med Hypotheses. 2000 May;54(5):803-7.
(424) Munch G; Gerlach M; Sian J; Wong A; Riederer P. Advanced glycation end products in neurodegeneration: more than early markers of oxidative stress? Ann Neurol 1998 Sep;44(3 Suppl 1):S85‑8.
(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; & M.Burk et al, Magnesium, 4(5-
6): 325-332, 1985
(438) Stefanovic V. et al, Kidney ectopeptidases
in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8(5): 278-84
(451) Miszta H; Dabrowski Z. Effect of mercury and combined effect of mercury on the activity of acetylcholinesterase of rat lymphocytes during in vitro incubation. Folia Haematol Int Mag Klin Morphol Blutforsch 1989;116(1):151‑5; & Bear, David; Rosenbaum, Jerrold; Norman, Robert. Aggression in cat and human precipitated by a cholinesterase inhibitor. The journal Psychosomatics, July 1986, vol. 27, #7, pgs. 535‑536; & Devinsky, Orrin; Kernan, Jennifer: Bear, David. Aggressive Behavior Following Exposure to Cholinesterase Inhibitors. Journal of Neuropsychiatry, vol. 4, #2, Spring 1992, pgs. 189‑199.
(460) Edwards AE, Depression
and Candida, JAMA, 1985, 253(23):
3400; & Crook WG, Depression associated with Candida albicans
infections, JAMA, 1984, 251:22; &
Crook, W. G. 1997. The Yeast Connection Handbook. Professional Books, Inc., Jackson, Tenessee; & Genova Diagnostic Lab, www.gdx.net.
(465) Walsh WJ, Health Research Institute, Biochemical Treatment of Mental Illness and Behavior Disorders, Minnesota Brain Bio Assoc, Nov 17, 1997; http://www.hriptc.org/Minnesota.htm; & William J. Walsh, Laura B. Glab, and Mary L. Haakenson; Pfieffer Treatment Center, Biochemical Therapy and Behavior Outcomes; 2000, http://www.hriptc.org/btbres.htm
(480) Salzer HM, Relative hypoglycemia as a cause of neuropsychiatric illness, J National Med Assoc, 1996,
58(1): 12-17; & Heninger GR et al, Depressive symptoms, glucose tolerance, and insulin tolerance, J Nervous and Mental Dis, 1975; 161(6):421-32; & Winokur A et al, Insulin resistance in patients with major depression, Am J Psychiatry, 1988, 145(3): 325-30.
(481) Virkkunen M, Huttunen MO; Evidence for abnormal glucose tolerance among violent offenders, Neuropsychiobilogy, 1982, 8:30-40; &(b) Markku I, Virkkunen L; Aggression, suicidality, and serotonin, J Clinical Psy 1992, 53(10): 46-51; & (c) Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers. Bosn J Basic Med Sci. 2002 Dec;2(1-2):29-34. Pranjic N, Sinanovic O, et al.
(482) Linnoila M et al, Low serotonin metabolite differentieates impulsive from nonimpulsive violent behavior, Life Sciences, 1983, 33(26): 2609-2614; & Lopez-Ibor JJ , Serotonin and psychiatric disorders,
Int Clinical Psychopharm, 1992, 7(2): 5-11.
(483) Thomas DE et al, Tryptophan and nutritional status in patients with senile dementia, Psychological Med 1986, 16:297-305; & Yaryura-Tobias JA et al, Changes in serum tryptophan and glucose in psychotics and neurotics,
Nutrition, No.4557, p1132; Carney MWP, Brit Med J, 1967, 4:512-516.
(484) Urberg M, Zemel MB; Evidence for synergism between chromium and nicotinic acid in the control of glucose tolrerance in elderly humans, Metabolism, 1987, 36(9): 896-899; & J Family Practice, 1988, 27(6): 603-606;
& Anderson RA et al, Effects of supplemental chromium on patients with reactive hypoglycemia, Metabolism,
1987, 36(4): 351-355; & Metabolism, 1983, 32(9): 894-99.
(487) Haut MW; Morrow LA; Pool D; Callahan TS; Haut JS; Franzen MD. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol 1999;6(4):193‑200.
(490) Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S‑adenosyl‑L‑methionine. Psychiatry Res 1995 Apr 28;56(3):295‑7; & Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS. The antidepressant potential of oral S‑adenosyl‑l‑methionine. Acta Psychiatr Scand 1990 May;81(5):432‑6
(491) Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol 1997 May;7(2):147‑55; & Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive‑compulsive disorder: a double‑blind cross‑over study. Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive‑compulsive disorder: a double‑blind cross‑over study. Int J Neuropsychopharmcol 1999 Sep;2(3):193‑195; & Palatnik A, Frolov K, Fux M, Benjamin J. Double‑blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder. J Clin Psychopharmacol 2001 Jun;21(3):335‑9; & Chengappa KN, Levine J, Kupfer DJ. Inositol as an add‑on treatment for bipolar depression. Bipolar Disord 2000 Mar;2(1):47‑55
(496) Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy.
Pharmacol Ther 1999 Mar;81(3):163‑221
(521)
Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine
synthesis and tyrosine nitration induced by peroxynitrite
are differentially prevented by antioxidants. Mol
Pharmacol 2001 Oct;60(4):838-46; & Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation
and antioxidant enzyme activity in different organs of mice exposed to low
level of mercury. J Environ Sci Health B. 2001 Sep;36(5):687-97.
(522) Nutrition Supplements Found Effective for Metal Disorders, Dr. Julia Rucklidge et al, University of Canterbury, Journal of Attention Disorders , January 2010 (EMPowerPlus, TrueHope)
(524)
Torreilles F, Salman-Tabcheh
S, Guerin M, Torreilles
J. Neurodegenerative disorders: the role of peroxynitrite.Brain
Res Brain Res Rev 1999 Aug;30(2):153-63;
& (b)Aoyama K, Matsubara K, Kobayashi S.
Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated
oxidative stress in neurodegenerative diseases. Ann
Neurol 2000 Apr;47(4):524-7;
&(c ) Guermonprez L, Ducrocq
C, Gaudry-Talarmain YM. Inhibition of acetylcholine
synthesis and tyrosine nitration induced by peroxynitrite
are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46
(530) 5-HTP
Archives, Dr. G. Valentine and W. Block, Life-Enhancement, www.life-enhancement.com; & (b) Birdsall TC. 5-Hydroxytryptophan: a
clinically-effective serotonin precursor. Altern Med
Rev. 1998 Aug;3(4):271-80.
(534) Tirado V, Garcia MA, Franco A., Pneuropsychological disorders after occupational exposure to mercury vapors, Rev Neurol 2000 Oct 16-31;31(8):712-6; & Powell TJ. Chronic neurobehavioural effects of mercury poisoning on a group of chemical workers. Brain Inj 2000 Sep;14(9):797-814
(543) U.S. Centers
for Disease Control, National Center for Health Statistics, NHANES III
study(thousands of
people’s health monitored), www.flcv.com/NHanes3.html
; &
www.mercola.com/article/mercury/no_mercury.htm & Review: cancer related to mercury
exposure, B. Windham (Ed) www.flcv.com/cancerhg.html ; & (b) Laks,
Dan R. Assessment
of chronic mercury
exposure within the U.S. population, National Health and Nutrition
Examination Survey,
1999–2006. Biometals. August 2009; & Laks, D.R. et
al, Mercury has
an affinity for
pituitary hormones, Medical Hypotheses, Dec 2009; & (c) An Investigation of
Factors Related to Levels of Mercury in Human Hair, Environmental
Quality Institute,
October 01, 2005,
www.greenpeace.org/raw/content/usa/press/reports/mercury-report.pdf
www.greenpeace.org/usa/assets/binaries/addendum-to-mercury-report
(551) B. Windham, Children’s neurological conditons: the toxic exposure connection, 2001,
www.flcv.com/indexk.html (over 150 peer-reviewed studies referenced)
(552) B. Windham, Toxic effects of pesticides, 2001, www.flcv.com/pesticid.html
(560) Great Smokies Diagnostic Lab, (search news & (by condition: depression) www.gsdl.com.
(561) Maes M, Vandoolaeghe E, Neels H, Demedts P, Wauters A, Meltzer HY, Altamura C, Desnyder R. Lower serum zinc in major depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry 1997;42(5):349‑358.
(562) Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med 1989;19(1):57‑63.
(563) Naylor GJ, Smith AH, Bryce‑Smith D, Ward NI. Elevated vanadium content of hair and mania. Biol Psychiatry1984;19(5):759‑764.
(564) McIntyre IM, Judd FK, Marriott PM, et al. Plasma melatonin levels in affective states. Int J Clin Pharmacol Res. 1989;9(2):159-64; & Riemann D, Klein T, Rodenbeck A, et al. Nocturnal cortisol and melatonin secretion in primary insomnia. Psychiatry Res. 2002 Dec 15;113(1-2):17-27; & Wade AG, Ford I, Crawford G, McMahon AD, Nir T, Laudon M, Zisapel N. Efficacy of prolonged release melatonin in insomnia patients aged 55-80 years: quality of sleep and next-day alertness outcomes. Curr Med Res Opin. 2007 Oct;23(10):2597-605.
(565) Dr. Andrew Weil, www.drweilselfhealing.com
; &
www.drweil.com/drw/u/ART00696/depression-treatment
http://www.drweil.com/drw/u/QAA400692/Tyrosine-Good-Supplement-for-Depression.html
www.healthyplace.com/depression/alternative-treatments/natural-remedies-for-depression/menu-id-68/
(566) Depression Diet Dr. Mark Hyman, Editor- Alternative
Therapies in Health & Medicine and Alternative Medicine, and author of many
books on overcoming depression and other mental health issues, http://www.drhyman.com/ & http://www.naturalsolutionsmag.com/article-display/8697/subTopicID/181/Brain-Food-The-Natural-Cure-for-Depression
(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; & 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/ ; & (c) Volz HP. Controlled clinical trials of hypericum extracts in depressed patients--an overview. Pharmacopsychiatry. 1997 Sep;30 Suppl 2:72-6; & Melzer J, Brignoli R, Keck ME, et al. A hypericum extract in the treatment of depressive symptoms in outpatients: an open study. Forsch Komplementmed. 2010;17(1):7-14;
(581) 1H magnetic resonance spectroscopy
study in adults with obsessive compulsive disorder: relationship between
metabolite concentrations and symptom severity, Starck G, Carlsson ML, et al, J Neural Transm. 2008 Jul;115(7):1051-62. Epub 2008 Jun 5; & On the role of
prefrontal cortex glutamate for the antithetical phenomenology of obsessive
compulsive disorder and attention deficit hyperactivity disorder, Carlsson ML, Biol
Psychiatry. 2001 Jan;25(1):5-26
(582) Vitamin Research News, weekly journal (several editions), 2003-2009, www.vrp.com
& (b) Chikani V, Reding D, Gunderson P, et al. Wisconsin rural women’s health study psychological factors and blood cholesterol level: difference between normal and overweight rural women. Clin Med Res. 2004 Feb;2(1):47-53; & Räikkönen K, Matthews KA, Kuller LH. Trajectory of psychological risk and incident hypertension in middle-aged women. Hypertension. 2001 Oct;38(4):798-802; & Matthews KA, Owens JF, Kuller LH, et al. Are hostility and anxiety associated with carotid atherosclerosis in healthy postmenopausal women? Psychosom Med. 1998 Sep-Oct;60(5):633-8; & Horsten M, Ericson M, Perski A, et al. Psychosocial factors and heart rate variability in healthy women. Psychosom Med. 1999 Jan-Feb;61(1):49-57; & (c ) Vlastelica M. Emotional stress as a trigger in sudden cardiac death. Psychiatr Danub. 2008 Sep;20(3):411-4.
(583) Dr. J. Teitelbaum, Health & Wellness Update, Issue 198, Jan 2009; & (b)László KD, Janszky I, Ahnve S. Anger expression and prognosis after a coronary event in women. Int J Cardiol. 2010 Apr 1;140(1):60-5; & Olson MB, Krantz DS, Kelsey SF, et al. Hostility scores are associated with increased risk of cardiovascular events in women undergoing coronary angiography: a report from the NHLBI-Sponsored WISE Study. Psychosom Med. 2005 Jul-Aug;67(4):546-52.
(584) An Invitation to Health: 2009-2010 Edition, Dianne Hales, 2009.
(585) Pesticide poisoning and depressive symptoms among farm residents. Stallones L, Beseler C. Ann Epidemiol. 2002 Aug;12(6):389-94; & Depression among victims of south Mississippi's methyl parathion disaster. Rehner TA, Kolbo JR, Trump R, Smith C, Reid D. Health Soc Work. 2000 Feb;25(1):33-40.
(586) Environmental and
occupational medicine, William N. Rom, Steven B.
Markowitz, Review, 2007; & Neurobehavioural evaluation of Venezuelan
workers exposed to inorganic lead. N.A. Maizlish, GParra, O Feo, Occup Environ Med 1995;52:408-414
& (b)Major depressive disorder and panic disorder related to lead exposure, Dr. M.F. Bouchard & Dr. van Wijngaarden, Arch Gen Psychiatry. 2009;66:1313-1319
(590) Fava M, Giannelli A, Rapisarda V, Patralia A, Guaraldi GP. Rapidity of onset of the antidepressant effect of parenteral S‑adenosyl‑L‑methionine. Psychiatry Res 1995 Apr 28;56(3):295‑7; & Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS. The antidepressant potential of oral S‑adenosyl‑l‑methionine. Acta Psychiatr Scand 1990 May;81(5):432‑6
(591) Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol 1997 May;7(2):147‑55; & Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive‑compulsive disorder: a double‑blind cross‑over study. Inositol versus placebo augmentation of serotonin reuptake inhibitors in the treatment of obsessive‑compulsive disorder: a double‑blind cross‑over study. Int J Neuropsychopharmcol 1999 Sep;2(3):193‑195; & Palatnik A, Frolov K, Fux M, Benjamin J. Double‑blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder. J Clin Psychopharmacol 2001 Jun;21(3):335‑9; & Chengappa KN, Levine J, Kupfer DJ. Inositol as an add‑on treatment for bipolar depression. Bipolar Disord 2000 Mar;2(1):47‑55
(594) How I Beat Depression through Diet: http://www.squidoo.com/i_beat_depression/
& The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat by Loren Cordain
(598) Overcoming Depression, Dr. Russell Blaylock, The Blaylock Wellness Report, Vol 5, No. 3, March 2008, & Food Additives, What you eat can kill you, Vol 4, No. 10, http://www.blaylockreport.com/
(600) B.Windham, Health Effects of Mercury/Amalgam and Results after Replacement of Amalgam Fillings. (contains over 3000 medical study references and approx. 60,000 cases of amalgam replacement documenting recovery from 40 chronic health conditions, as documented by the treating doctor or dentist. www.flcv.com/amalg6.html
(601) B. Windham, Autism, PDD- the mercury connection, www.flcv.com/kidshg.html
(602) Mercury exposure levels from dental amalgam- review, B Windham(Ed), www.flcv.com/damspr1.html
(603) Effects of prenatal and neonatal mercury exposures on the fetus and infants, B Windham(Ed) , www.flcv.com/fetaln.html
(604) Neurological effects of toxic metal exposures, B Windham (Ed), www.flcv.com/tmlbn.html
(605) Health Effects of Root-Canal Teeth and Cavitations: Review www.flcv.com/damspr11.html & www.flcv.com/RChealth.html
NOTE: all references not included here can be found in (600)
You can find abstracts of the medical studies at the National Library of Medicine,
National Institute of Health (Medline) and obtain the papers there. (http://www.nlm.nih.gov/)
%%%%%%%%%%%%%%%%%%%%%%%%%%%%%
Mercury impairs alfa‑1‑adrenergic receptors, astrocytic dopamine uptake, and serotonergic 5‑HT2 receptor. The last one is stimulated by cocaine and LSD, so at least those drugs may be abused more due to mercury. We can remember
that PhD Alfred Stock, leading early century mercury/chelator chemist stated that only cocaine was able to reverse his mental impairments form mercury, which as a chemist was easily available, and it was also legal at the time yet, in the early century.
%%%%%%%%%%%%%%%%%%%%%%
Psychometric Evidence that Dental
Amalgam Mercury may be an Etiological
Factor in Manic Depression.
Siblerud, Motl and Kienholz.
J. Orthmol
Med. vol 13 no 1 p 31 ff (1998).
MMPI-2 scores for 11 subjects with
amalgams removed vs 9 with amalgams in.
&&&&&&&&&&&&&&&&&&&&&&&&
> Many of my patients reported
the lifting of depression, anxiety, moodiness
> within
a very short time of the total mercury
decontamination of their mouths.
I do not know the mechanism for that, and I am reporting this point so that
those able to study the link between
psychiatric illness and mercury would tell me one day what the mechanism is. The question here is that mercury, though out
of the mouth, is not out of the brain in such a short time (two wks.) so, could these psychiatric
illnesses be caused by the galvanic
currents alone? I do not know.
Virtually
100% of the dozens of patients I’ve had suffering depression improve within 2
wks. One patient, who was depressed before amalgam removal, told me today that shw now has a positive attitude to life that she did not
have before, and that she feels like a child!
Kindest regards. Hesham. DDS
Hesham El-Essawy [pop@EL-ESSAWY.COM]
*******
(This
was was mostly snipped from a much larger paper(600)
with over 3000 medical study references regarding common toxic exposures to
mercury that are affecting large numbers of people with neurological effects)