1) The Thyroid Gland
2) Estrogen Dominance and Thyroid
6) From Childhood On
9) Iodine and the Thyroid Gland
10) Iodine Functions in the Body
11) Iodine and Apoptosis
12) Iodine Excretion in the Urine
13) Iodine and Lipids
14) Iodine and Pregnancy
15) Functions of Iodine in the Human Body
16) Other Challenges
17) Mercury Toxicity
18) Thyroid and Mercury
19) Posterior Pituitary Gland
21) Frequent Urination
24) Health Risks of PCBE's
25) Just One Does may be Harmful
26) Nutritional Considerations
27) Basal Temperature Test
a little more than one hundred years ago, the single controlling force
for all of the complex processes that go on in the human body was thought
to be the nervous system. But there were too many phenomena that, when
carefully analyzed, seemed to have no relationship to the nervous system,
too many differences in people--in size and energy, for example--that
could not be accounted for satisfactorily in terms of nervous activity
alone. The explanation was to be found in certain glands, the endocrines,
of which the thyroid is one and, in fact, one of the first to be discovered.
Because commonly used tests for thyroid function are not accurate particularly
when it comes to mild and even some moderate forms of hypothyroidism,
and many if not most of those with low thyroid function remain undiscovered.
the hormones of the thyroid gland regulate metabolism in every cell
of the body, a deficiency of thyroid hormones can affect virtually all
bodily functions. The degree of severity of symptoms in the adult range
from mild deficiency states which are not detectable with standard blood
tests (subclinical hypothyroidism) to severe deficiency states which
can be life-threatening (myxedema). There is an old medical saying that
just a few grains of thyroid hormone can make the difference between
an idiot and an Einstein. It aptly characterizes the thyroid as a quickener
of the tempo of life. All of the endocrine glands play remarkable roles
in the body's economy. Unlike the many millions of other glands such
as the sweat glands in the skin, the salivary glands in the mouth, the
tear glands in the eyes, which perform only local functions, the endocrine
glands pour their hormone secretions into the bloodstream which carries
them to all parts of the body. From the pea-sized pituitary gland at
the base of the brain come hormones that influence growth, sexual development,
uterine contraction in childbirth, and milk release afterward. The adrenals,
rising like mushrooms from atop the kidneys, pour out more than a score
of hormones, including hydrocortisone and adrenaline needed for the
body's response to stress and injury. Also in the endocrine system are
the sex glands—ovaries and testes; the pineal gland in the brain whose
hormones play a role in nerve and brain functioning; the thymus behind
the breastbone which appears to be involved in establishing the body's
immunity function; and areas in the pancreas, the islets of Langerhans,
which secrete insulin.
majority of the thyroid hormone secreted from the thyroid gland is T4,
but T3 is the considerably more active hormone. Although some T3 is
also secreted, the bulk of the T3 is derived by deiodination of T4 in
peripheral tissues, by the enzyme thyroid peroxidase especially liver
and kidney. Deiodination of T4 also yields reverse T3, a molecule with
no known metabolic activity. Deficiency of thyroid hormone may be due
to lack of stimulation by the pituitary gland, defective hormone synthesis
or impaired cellular conversion of T4 to T3 (often caused by mercury
toxicity). The pituitary gland regulates thyroid activity through the
secretion of thyroid-stimulating hormone (TSH). The combination of low
thyroid hormone and elevated TSH blood levels usually indicates defective
thyroid hormone synthesis, which is defined as primary hypothyroidism.
When TSH and thyroid hormone levels are both low, the pituitary gland
is responsible for the low thyroid function, a situation termed secondary
hypothyroidism. Normal blood thyroid hormone and TSH blood levels combined
with low functional thyroid activity (as defined by a low basal metabolic
rate) suggest cellular hypothyroidism.
on the rate of hypothyroidism are based on the levels of thyroid hormones
in the blood. This may result in a large number of people with mild
hypothyroidism going undetected. Before the use of blood measurements,
it was common to diagnose hypothyroidism based on basal body temperature
(the temperature of the body at rest) and Achilles reflex time (reflexes
are slowed in hypothyroidism). With the advent of sophisticated laboratory
measurement of thyroid hormones in the blood, these "functional" tests
of thyroid function fell by the wayside. However, it is known that the
routine blood tests may not be sensitive enough to diagnose milder forms
of hypothyroidism. The diagnosis of hypothyroidism by laboratory methods
is primarily based on the results of total T4, free T4, T3, and TSH
levels. The typical blood tests measure thyroxine (T4), which accounts
for 90% of the hormone secretion by the thyroid. However, the form that
affects the cells the most is T3 (triiodothyronine) which cells make
from T4. If the cells are not able to convert T4 to the four-times more
active T3, a person can have normal levels of thyroid hormone in the
blood, yet be thyroid-deficient.
thyroid peroxidase, converts T4 to T3 and is blocked by mercury in the
body, primarily from dental mercury amalgam fillings and thimerosol,
a mercury preservative found in vaccinations and other medicines. Genistein
and daidzein from soy also inactivate thyroid peroxidase enzyme. In
the case of T4 and T3, more than 99% is normally protein-bound in the
blood. Less than 1% is free. Only the free hormone exerts biologic activity.
The protein-bound hormone is inactive. The saliva test is a more accurate
and sensitive way to assess thyroid function because new technology
allows for direct measurement of the free thyroid hormones.
way of assessing thyroid function is to measure its effects on the body.
This is done by measuring a person's resting metabolic rate, which is
controlled by the thyroid gland. Dr. Broda Barnes found that measuring
basal body temperature (description follows) was a good way of assessing
basal metabolic rate (BMR) and thus the body's response to thyroid hormones,
regardless of their blood levels. As mild hypothyroidism is the most
common form of hypothyroidism, many people with hypothyroidism are going
undiagnosed. The basal body temperature is the most sensitive functional
test of thyroid function. Nonetheless, using blood levels of thyroid
hormones as the criteria, it is estimated that between 1 and 4% of the
adult population have moderate to severe hypothyroidism, and another
10-12% have mild hypothyroidism. The rate of hypothyroidism increases
steadily with advancing age. Using only blood tests, thyroid function
is commonly low in older adults. When using medical history, physical
examination, and basal body temperatures along with the blood thyroid
levels as the diagnostic criteria, estimated rates of hypothyroidism
approach 90% or more of the adult population.
It is the thyroid gland, lying in front of the throat below the Adam's
apple and just above the breastbone, which regulates the rate at which
the body utilizes oxygen and controls the rate at which various organs
function and the speed with which the body utilizes food. Thyroid secretion
is essential for the operation of the cells and, in effect, determines
how hot the fire gets in the cell and the speed of activity in the cell.
The influence of thyroid secretion on body processes and other organs
is incredibly widespread and important. When the thyroid gland is removed
from an otherwise normal animal, all metabolic activity is reduced.
After removal of the thyroid gland, excess amounts of water, salts,
and protein are retained within the body. Blood cholesterol also goes
The thyroid, the body's thermostat, secretes two hormones that regulate
body temperature, energy usage, and calorie burning. The thyroid has
many effects on all the cells in the body, including the synthesis of
RNA protein and consumption of oxygen by cells, affecting overall bodily
metabolism. Thyroid function influences and is influenced by the pituitary,
adrenals, parathyroid, and sex glands, all of which work together. The
pituitary produces TSH (thyroid-stimulating hormone), which helps regulate
thyroid hormone production. Thyroid malfunctioning is also influenced
by abnormal immune responses and the adrenals. People with type-O blood
are said to be genetically prone to hypothyroidism and low levels of
iodine. Approximately 46% of people are blood Type-O.
The thyroid plays an important role in growth processes. In the human,
growth and maturation fail to take place normally when the thyroid is
absent or functioning far below normal. Children lacking normal thyroid
function may remain small; their stature can be improved considerably
by thyroid supplementation and detoxification started at an early age.
Growth of the skin, hair, and nails may be retarded in thyroid deficiency
and accelerated again by thyroid treatment. Healing of bone is delayed
in thyroid deficiency. A rather severe anemia may develop in severe
hypothyroidism. Thyroid hormone is essential for normal nervous system
functioning and reaction time, and hypothyroidism may produce slow reactions
and mental sluggishness. Muscle health too is dependent on thyroid secretion
and with marked thyroid deficiency the muscles may become sluggish and
infiltrated with fat. There are interrelationships between the thyroid
and the other endocrine glands. When, for example, thyroid deficiency
is marked, the effect on the sex glands is shown by subnormal sexual
development and function and impairment of libido. In hypothyroid women,
menstrual disturbances are present frequently.
Estrogen Dominance and Thyroid
Estrogen, progesterone, and thyroid hormones are interrelated. The thyroid
is the hormone that regulates metabolic rate. Low thyroid tends to cause
low energy levels, cold intolerance, and weight gain. Excess thyroid
causes higher energy levels, feeling too warm, and weight loss. The
thyroid gland makes two versions of thyroid hormone from tyrosine and
Both versions are then enveloped in a relatively large glycoprotein
complex called thyroglobulin and stored in the thyroid gland. To be
released into the bloodstream for circulation throughout the body, the
hormones are separated from thyroglobulin and bound to a much smaller
globulin thyroxin-binding globulin or albumin. However, only 0.5% of
thyroid hormone is "free" to be biologically active. Thyroid's action
in the cell is to increase the biosynthesis of enzymes, resulting in
heat production, oxygen consumption, and elevated metabolic rate. Thyroid
stimulates the oxidation of fatty acids, and reduces cholesterol by
oxidizing it into bile acids. Thyroid also stimulates enzymes for protein
synthesis and, when present in excessive amounts, can catabolize (destroy)
muscle protein. Estrogen causes food calories to be stored as fat. Thyroid
hormone causes fat calories to be turned into usable energy. Thyroid
hormone and estrogen have opposing actions. Estrogen inhibits thyroid
action in the cells, interfering with the binding of thyroid to its
receptor. Both hormones have phenol rings at a corner of their molecule.
The respiratory enzymes of cells are thyroid-dependent. When thyroid
function is low, cellular oxygen is low (cellular hypoxia). Thus, estrogen-induced
thyroid interference contributes to less-than-optimal brain function.
Excess estrogen may compete with thyroid hormone at the site of its
receptor. In so doing, the thyroid hormone may never complete its mission,
creating hypothyroid symptoms despite normal serum levels of thyroid
hormone. Progesterone, on the other hand, increases the sensitivity
of estrogen receptors for estrogen and yet, at the proper level, inhibits
many of estrogen's side effects. GABA (gamma-aminobutyric acid) is an
amino acid that acts as a neurotransmitter-inhibitor and tends to have
a calming effect. When estrogen interferes with thyroid production and
slows the metabolism of brain cells, it indirectly decreases GABA production
and increases brain cell excitability, a factor in epilepsy.
Hypothyroidism occurs at all ages. Hypothyroidism has been estimated
to affect as many as 90% of people in the United States, 90% of which
are women. In children, mild deficiency may be the cause of behavior
problems, or of a mild degree of mental slowness, which often is not
abnormal enough to be given much consideration. In children of this
type startling results occasionally follow the administration of small
doses of thyroid extract. At puberty and in the early teens diminished
endurance and a tendency to anemia, nervous disorders, problems with
menstrual cycles or digestive disturbances often are explained by a
mild degree of hypothyroidism. Extreme physical and nervous exhaustion
in young adults, the depressions of middle life, and aggravated symptoms
of menopause may be partially explained on the basis of low thyroid.
Late symptoms which simulate senile changes frequently are distinctly
improved by the administraion of thyroid extract or iodine supplementation.
Undiagnosed thyroid problems can be behind many unidentified symptoms
of fatigue, many recurring illnesses, and non-responsive health problems.
The body systems affected by this disorder are quite variable. A lack
of thyroid hormones leads to a general decrease in the rate of utilization
of fat, protein, and carbohydrate. Moderate weight gain combined with
sensitivity to cold weather (cold hands and feet) is a common finding.
Cholesterol and triglyceride levels are increase in even the mildest
forms of hypothyroidism. This elevation greatly increases the risk of
serious cardiovascular disease. Studies have shown an increased rate
of heart disease due to atherosclerosis in individuals with hypothyroidism.
Hypothyroidism also leads to increases in capillary permeability and
slow lymphatic drainage. Often this will result in swelling of tissues
(edema). Circulation symptoms are referred chiefly to the heart and
are caused by myocardial degeneration. Hypothyroidism predisposes to
premature arteriosclerosis. Hypothyroidism can also cause hypertension,
reduce the function of the heart and reduce heart rate. Nervous disorders,
such as headaches, neurasthenia, mild psychic disturbances, especially
affective disorders (depression), fears, anxieties, poor memory, and
difficult concentration are frequently seen. Gastrointestinal symptoms
are extremely common, including anorexia, distress after eating, belching
of gas, vomiting, obstinate constipation, and occasional diarrhea.
A variety of hormonal symptoms can exist in hypothyroidism. Perhaps
the most common is a loss of libido (sexual drive) in men and menstrual
abnormalities in women. Women with mild hypothyroidism have prolonged
and heavy menstrual bleeding, with a shorter menstrual cycle. Every
type of disturbance may be seen from amenorrhea (no period), to profuse
menorrhagia (heavy bleeding), especially at menopause. Infertility may
also be a problem. If the hypothyroid woman does become pregnant, miscarriages,
premature deliveries, and stillbirths are common. Rarely does a pregnancy
terminate in normal labor and delivery in the overtly hypothyroid woman.
Muscle weakness and joint stiffness are predominate features of hypothyroidism.
Some individuals with hypothyroidism may also experience muscle and
joint pain, and tenderness. Dry, rough skin covered with fine superficial
scales is seen in most hypothyroid individuals while the hair is course,
dry, and brittle. Hair loss can be quite severe. The nails become thin
and brittle and typically show transverse grooves. The brain appears
to be quite sensitive to low levels of thyroid hormone. Depression along
with weakness and fatigue are usually the first symptoms of hypothyroidism.
Later, the hypothyroid individual will have difficulty concentrating
and be extremely forgetful.
Frequently, blood tests of hormone levels are normal, but basal body
temperature is abnormally low. Shortness of breath, constipation, and
impaired kidney function are some of the other common features of hypothyroidism.
This condition is often associated with Wilson's syndrome, physical
and emotional stress, and Hashimoto's disease. Fortunately, cretinism
and myxedema, the extreme forms of hypothyroidism, are relatively rare.
Occipital-cervical aching with radiation to the shoulders or intrascapular
area is common. Also rheumatoid pains may occur in various joints and
parts of the body without evidence of inflammation. Blood cholesterol
is often elevated. If the cholesterol is elevated, it is a presumptive
diagnosis of hypothyroidism. All of these symptoms have been treated
with thyroid extract and iodine supplementation successfully. The only
reliable diagnostic tests worth doing are the basal metabolic rate,
saliva test, and serum cholesterol.
Cretinism is a condition found in infants and children resulting from
a deficiency of thyroid hormone during fetal or early life. The thyroid
gland may be entirely absent or greatly reduced in size. In a cretin
child, the skin is thick, dry, wrinkled, and sallow; the tongue is enlarged;
the lips thickened; the mouth open and drooling; the face broad; the
nose flat; the feet and hands puffy. The child is dull and apathetic.
Although a cretin child may be unusually large at birth, development
is defective and, if the child is untreated, he becomes small for his
age in childhood and a dwarf in adulthood, suffering mental retardation
along with growth failure. With early and adequate thyroid treatment
for cretinism, growth may become normal and mental status may improve.
Myxedema is the reaction in adulthood to lack of thyroid hormone, either
because the thyroid gland wastes away or has to be removed, or because
of failure of the pituitary gland to stimulate thyroid activity. Myxedema
brings with it gradual personality changes along with marked physical
changes. They include a general, progressive slowing of mental and physical
activity, an increase in weight, and a decrease in appetite. Facial
changes occur and may progress steadily to produce a mask-like appearance,
as the skin becomes thick and somewhat rigid, interfering with expression.
The skin also becomes dry, cold, rough, and scaly; it appears waterlogged
and swollen. Characteristically, the upper eyelids become waterlogged
or edematous and the eyebrows may be elevated because of efforts to
keep the eyes open. The hair becomes coarse, brittle, and falls out;
the nails become brittle and grow slowly; there is sensitivity to cold
with feelings of being chilly in rooms of normal temperature; and perspiration
is decreased or absent even during hot weather.
Many myxedematous patients are troubled by joint pains and stiffness.
Resistance to infection is decreased, wounds heal slowly, and ulcers
may be persistent. The tongue and lips become large and thick and, because
of this and also because of retarded mental reaction and decreased muscular
coordination, the speech becomes slow, thick, and clumsy and may resemble
that of a slightly intoxicated person. A myxedema victim generally appears
slow, drowsy, and placid. Normal mental effort cannot be maintained.
A tendency to drop off to sleep during the day may be present. Anemia
is usually present in some form; constipation is nearly always present;
depression is common as is decline in libido and sexual function. Yet,
all of these manifestations are dramatically controllable when thyroid
treatment is administered in suitable form. Virtually no system of the
body may escape the effects of severe lack or complete absence of thyroid
hormone secretions. Yet, even in extreme forms of hypothyroidism, there
are variations in manifestations, some being more overt and troublesome
than others. Hypothyroidism of milder degree can be far more subtle.
It, too, may affect many systems of the body but not all to the same
degree. One patient may have manifestations that another does not. There
are variations among individuals in organs and systems which are most
susceptible to thyroid deficiency. Such varying susceptibility is well
known in allergy. In the allergic person, a food, pollen, or other material
to which there is sensitivity may produce varying symptoms depending
upon the "target" organs affected--the organs with greater allergic
From Childhood On
Relatively mild thyroid deficiency in a newborn may not be readily apparent.
Such a child may be quieter than others and may sleep more. Sometimes,
the face may be broader than normal and may rarely change expression,
breathing may be somewhat noisy, and the baby may appear to have a cold
much or all of the time. Preschool children with low thyroid function
may have a somewhat dull and apathetic appearance and be less active
than normal youngsters. Yet, paradoxically, a few will be very nervous,
hyperactive, and unusually aggressive. Emotional problems are frequent.
A low thyroid child may cry for no apparent reason and object vigorously
to any restrictions. Temper tantrums are common, probably related to
undue fatigue. The child may sleep longer than other youngsters of his
or her age, be a slow starter in the morning, have a short attention
span, and flit from one activity to another. And infections are common.
Once a low-thyroid child starts to school, other problems may arise.
With low energy endowment, the child may lack self-confidence and have
difficulties in associating successfully with other children. He may
be unable to sit quietly and study and his progress in school may be
slow. His susceptibility to respiratory infections from other youngsters
has increased and with his resistance weakened by low thyroid function
he acquires far more than his fair share. Removal of tonsils may end
repeated resistance to other respiratory infections, sore throats, earaches,
and the like. With puberty, other problems may develop. Sports may further
deplete low energy endowment; so may any part-time jobs; and school
failure may occur. Girls beginning the menstrual cycle may develop low-grade
anemia as the result of periodic blood loss, and this further depletes
their energy. Although in childhood growth may be stunted by a marked
thyroid deficiency, there may be a seemingly paradoxical effect of a
minor deficiency at puberty. The individual may become unusually tall.
Growth stops with the closing of the growth centers at the end of each
long bone. Thyroid hormone plays a part in causing these centers to
close normally. With thyroid deficiency, growth may continue for some
time. In adulthood, many of the effects of low thyroid function experienced
in childhood may be carried over and new ones may emerge. The "problem"
child--who was experiencing the effects of low thyroid function--may
become an adult who all too easily may be mislabeled a -"neurotic-"
or "hypochondriac" because of persistent or even accentuated fatigue,
headaches, circulatory disturbances, and other manifestations of low
In a person with normal thyroid function, when there is a need for more
thyroid secretion, a signal is received by the pituitary gland which
then releases a substance to stimulate thyroid function. As soon as
the needed amount of thyroid secretion has then been released into the
bloodstream, the pituitary gland gets the message, stops releasing its
thyroid-stimulating substance, and less thyroid hormone is produced.
Through this sensitive "feedback" mechanism, the amount of thyroid hormone
in the bloodstream is maintained in an effective, narrow range. When
thyroid function is deficient, the gland cannot respond adequately to
the stimulus from the pituitary. If the pituitary gland is toxic from
mercury or other heavy metals, it can lose its sensitivity to thyroid
hormone in the blood and the body's precise control of thyroid level
in the bloodstream is thwarted; and it is possible that the patient
may even have too much hormone in the blood and may develop some or
many of the symptoms of hyperthyroidism. Symptoms of overproduction
of thyroid hormone include: weight loss, fatigue, nervousness, anxiety,
rapid heartbeat, tremors, difficulty sleeping, moist skin, excessive
sweating, sensitivity to heat, elevated temperature, bulging eyes, goiter,
diarrhea, other gastrointestinal disturbances, and chest pain. This
condition is often called Graves' disease.
Iodine-containing compounds are found in ashes of burnt seaweed, salty
oil-well brines and Chilean saltpeter, which is sodium iodate (NaIO3).
Iodine is extracted in huge amounts by Japanese seaweed farming. Originally,
during the formation of the earth, iodine dispersed throughout rock
formations. Much later ocean water, plants and animals also contained
iodine in low amounts. It was abundant, however, in seaweeds. Detoxified
Iodine can be supplemented by placing a few drops in water daily to
provide adequate amounts to the body.
Iodine is widely dispersed in rocks but the concentration is extremely
low and even the leeching of iodine from soil over ages did not raise
the ocean's concentration significantly. Early development of single
celled organisms such as bacteria, fungi, viruses, and protozoa arose
without iodine. Because of iodine's low concentrations everywhere on
the planet, almost without exception single celled micro-organisms did
not use iodine for any purpose. Erosion of the rocks by rain, glaciers,
ice age, and later melting, leeched these small amounts of iodine out
of the soil and rocks and washed them into the oceans where concentrations
of sea salt is so low it does not prevent goiter in humans. The earliest
signs of iodine use are in diatoms (algae), but significant iodine concentration
occurred in seaweeds.
Because rains containing iodine from the ocean, older soils seen in
New Mexico, contain more iodine than younger soils. Also, soil areas
stripped of topsoil by glaciers, such as the North American Great Lakes
regions, became endemic goiter areas. Dogs, humans, fish and likely
other animals were iodine deficient and had goiters (enlargement of
thyroid gland) . In humans, goiter incidence fell below 1% because of
iodine salt supplementation, but fish of the great lakes still show
goiter formation. Iodine replacement of soil depleted by rain is a slow
process. Soils depleted of iodine by the last ice age are still deficient
The most significant evolutionary event for eukaryotes (nucleated celled
organisms), including humans, occurred when seaweeds concentrated iodine.
From this process came multicellular organisms, vertebrates and humans.
Because iodine was not available in significant concentrations for much
of evolution, single-celled organisms reproduced themselves with structural
membrane proteins having the amino acids tyrosine or histidine exposed
to the surrounding medium or extra-cellular fluids. Iodine kills single
celled organisms by combining with these same two amino acids. All single
celled organisms showing tyrosine (tyrosyl) linkages exposed in the
membrane proteins are killed by this simple chemical reaction that denatures
proteins and destroys enzymes, killing the cells.
Seaweed was the first to start capturing iodine from ocean water by
a membrane transport mechanism that today still concentrates iodine
to 20,000 times the ocean's concentration. What is not generally appreciated,
and perhaps not thought of in this light, was that the high concentrations
of iodine in seaweed, whether the seaweed was dead or alive, gave birth
to a brand new environment chemically different from the rest of the
planet up to that time. This was the world of high iodine. Never before
had such an environment been created. For the first time there were
no bacteria, fungi, viruses, or protozoa present. Archea are a different
form of bacteria capable of growing in harsh environments and might
have been the type of organism to colonize this niche. However, any
new microorganism trying to grow here would be under the influence of
iodine and thyroxine. As iodination of proteins is a simple easy and
predictable chemical reaction, which automatically produces thyoxine
within the protein, so intracellular iodination of proteins likely was
an original source of thryoxine to these early developing cells. These
cells did not need to have an outside source of thyroxine.
Soon, in evolutionary time, the precursor of the thyroid, the endostyle
or thyroid-hormone-making site in the pre-vertebrate animals arrived.
This organ, in the back of the pharynx of primitive pre-vertebrates,
excreted protein bound thyroxine into the gut and there it was hydrolyzed,
absorbed and delivered all over the body. Later, in early vertebrates,
at a site close by to where the endostyle was, the first thyroid gland
follicles can be discerned. By then thyroid hormone was being secreted
internally into the blood. At this point, there was no brain, pituitary
or hypothalamus control mechanisms to influence the thyroid function.
Thyroid hormone is the first endocrine hormone to arrive in evolution
and it is the first to arrive during fetal life. But almost simultaneously
with the development of the thyroid gland, the central nervous system
started to develop since the nerve cells were assured of a constant
supply of thyroxine and this in turn depended upon a constant supply
Thyroxine controls all endocrine organs which is what we would expect
if the thyroid controls the genome and also was the first to arrive
in evolution and in fetal development. Later the brain evolved into
our present system of the hypothalamic-pituitary-thyroid system giving
the hypothalamus overall control of the output of the thyroid gland.
It appears that the most important event in the life of the pituitary/thyroid
system occurs at birth. Because the hypothalamus and the thyroid hormone
controls the body temperature at birth there is a surge in TSH (thyroid
stimulating hormone) which greatly increases the thyroid hormone excreted
into the blood at birth. This relates to metamorphic changes in the
lungs and other systems as the baby switches over to air breathing.
After birth, the thyroid starts putting out a fairly constant supply
of thyroid hormone for the rest of the human's life. The reserve of
the thyroid gland to stress and its ability to respond appear related
to adequate iodine intake before the age of puberty, which is the first
real test of the thyroid's reserve abilities. Stress on the thyroid
can be detected and the size of the thyroid gland measured accurately
by ultrasound. The thyroid enlargement from physiological stress found
in areas of borderline low iodine intake, occur during adolescence,
pregnancies and menopause. These enlargements are good indicators of
borderline iodine supplementation indicating a degree of iodine deficiency,
but at the same time this illustrates the increased needs for thyroid
hormone during period of physiological stress during life.
Disturbance of the thyroid system relates to disease. A low output of
thyroid hormone will not provide the cellular DNA with adequate thyroid
hormone for proper maintenance. Also as each tissue controls its own
thyroid metabolism, the same levels of thyroid in the blood may not
be adequate for the tissue adaptation mechanisms in another. There is
no feedback system from individual tissues to tell the thyroid TSH system
to rise higher because one tissue is not getting enough. The brain seems
to have the highest priority for maintenance of thyroid hormone levels.
For example, if the patient has a thyroid gland that by lab tests is
normal, but the patient has a low thyroid dependent depression, the
depression will continue until somehow the level of thyroid hormone
is raised above its current levels. Although cretinism and related goiters
have been noted throughout all ages, it wasn't until the discovery of
iodine that some progress was made in the understanding of the thyroid
But clinically the most historic document on thyroid occurred in 1888.
This committee described a variable syndrome in persons whose thyroid
had been removed or were suffering from a completely failed thyroid.
To this was given the name myxedema to stand for the presence of a peculiar
type of mucin that gathered in almost all the connective tissues of
the body. One of the characteristics of extreme low thyroid is to find
this mucin in virtually every organ of the body. With the realization
that there are receptors for thyroid hormones in the cell membrane,
the cytosol (intracellular fluid), the mitochondria and the nucleus,
we begin to understand how important this thyroid control system is.
Iodine and the Thyroid Gland
The thyroid gland is a factory. To produce its secretions it must have
raw material. If it lacks adequate raw materials, its production slumps.
When this happens, when the slump is great enough, there may be signals
from elsewhere in the body that amount to exhortations for the gland
to increase its output. Trying to oblige, the gland may increase in
size in a kind of blind effort to add to its output even though it cannot
increase production for lack of raw material. The gland may enlarge
until a noticeable lump may appear in the throat. And the swelling,
or goiter, may become large enough to interfere with breathing or swallowing.
The cause of goiter is lack of sufficient iodine in the soil and drinking
water, or from inability to utilize iodine because of mercury toxicity
from amalgam dental fillings and from mercury in immunizations.
The thyroid gland is the principle user of iodine in the body. Two-thirds
of the body's store of iodine is located in the thyroid gland. In a
normal person, dietary iodine is absorbed from the gut into the blood
and then, in the thyroid, it is removed from the blood, "trapped" in
the gland, and incorporated there into compounds, which in turn are
assembled into thyroid hormone secretions. The average iodine intake
of a normal adult on an ordinary diet in a non-goiter region is about
0.03 milligrams, a day. This tiny amount is only about one-seventh of
what is needed for daily thyroid hormone production, but the body practices
great economy and re-uses much of its iodine store repeatedly in producing
hormone secretions. In goiter regions, not even the 0.03 milligram per
day is available in the food and water. Goiter regions are to be found
all over the world. No continent is free of them. Generally they are
the mountainous and inland areas of the globe. A high incidence of goiter
is found in the Himalayas in Asia, in the regions of the Alps and the
Carpathian and Pyrenees mountains in Europe, and in the high plateaus
of the Andes in South America. In North America, the goiter zone is
the Great Lakes basin and the area of the St. Lawrence River, extending
westward through Minnesota, the Dakotas, and the neighboring Canadian
territory as far as the northwest and including Oregon, Washington,
and British Columbia. This great belt extends an arm southward in the
rocky Mountain area and another in the Appalachian area.
It is in such high and inland areas that, through the ages, the soil
has yielded most or all of its soluble iodine content to water on the
way to the sea. In areas close to the sea, the soil as well as drinking
water is usually rich in iodine. Fruits and vegetables grown in such
soil contain iodine in abundance and this is equally true of sea food
and sea vegetables. The incidence of goiter in high and inland areas
in the past was extremely great. In some Alpine areas, for example,
the incidence approached 100%. The most important discovery in relation
to goiter was that the disorder could be prevented by administration
of iodine. The iodine could be added to community water supplies in
goiter regions, or it could be administered in the form of tablets or
drops, or it could be taken in the form of iodized salt. Today, the
use of iodized salt is the most widely accepted method of goiter prevention.
But even though goiter is now far less of a problem, it is not so with
hypothyroidism. For low thyroid function can be--and commonly is--present
in the absence of goiter, especially with the "fear of salt" introduced
by the medical establishment.
The basic unit of the thyroid gland is the follicle. The thyroid gland
captures dietary iodine, synthesizes thyroid hormone from it, and stores
thyroid hormone until it is needed. Colloid, the material in the center
of the follicles, stores thyroid hormone in a large protein called thyroglobulin.
Hydrolysis (digestion) of thyroglobulin releases thyroid hormone into
the circulation in the form of thyroxine (T4) and triiodothyronine (T3).
Iodination of almost any large protein results in the formation of thyroxine
(T4). Iodide, which is ingested in food and water, is actively concentrated
by the thyroid gland, converted to organic iodine by thyroid peroxidase,
and incorporated into tyrosine in thyroglobulin within the thyroid follicular
cell. The tyrosines are iodinated at one (monoiodotyrosine) or two (diiodotyrosine)
sites and then coupled to form the active hormones (diiodotyrosine +
diiodotyrosine = tetraiodothyronine (thyroxine, T4); diiodotyrosine
+ monoiodotyrosine = triiodothyronine (T3).
Radioactive tracing of iodine shows that much of the iodine goes to
the thyroid gland, nasal secretions, gut, breast, stomach, bone and
in the extracellular fluids and connective tissue of almost all organs.
Iodine can be found everywhere, for example, iodine appears in the cervical
mucus within two minutes after injection. In evolution the gut served
as the source of iodine before the thyroid gland appeared and now the
gut serves as a reservoir of iodine for immediate needs of the body.
Iodine Functions in the Body
The main function of the iodine is synthesis, storage and secretion
of thyroid hormone. What iodine is left over is taken up in other tissues
especially extracellular fluids and excreted in the urine. From extracellular
fluids iodine travels in the lymphatics and re-enters the blood stream
via the main lymphatic channel, the thoracic duct. In the 1960s it was
established that if the daily dose of iodine was increased to over 2-3
mgs of iodine per day, within two weeks, the thyroid became saturated
and no longer took up iodine in significant amounts. So a normal person
who raised their daily dose of iodine above, say 3 mgs, within two weeks
their thyroid was almost completely stop taking up iodine as it became
saturated, but more important to the body, all of the dietary iodine
now went to perform other body functions.
Iodine and Apoptosis
In areas of the body, where many cells die, (apoptosis) there is always
an endless source of iodine. All the sites in the body of high apoptosis
(natural death of cells on a regular and predictable schedule) find
iodine in plentiful supply. The secretions into the nasal passages and
lumen of the stomach, for instance, have both a high death rate and
an endless supply of iodine. Not only is iodine an antiseptic against
bacteria, it also is an anticancer agent.
Iodine Excretion in the Urine
Iodine has an unusual excretion pattern in the urine. There are no reabsorption
mechanisms or preservation mechanisms in the urinary tract to keep this
element from excretion in the urine and hence loss from the body. Iodine
is the trigger mechanism for apoptosis and it is imperative that a constant
source of iodine in the urine be available. If the body was capable,
and it is not, of holding the iodine inside and therefore allowing urine
with no iodine to flow through the renal system, then the renal system
would be deprived of iodine. This would immediately lead to abnormal
cells and cancer. The Western diet contains nowhere near the levels
of iodine needed to saturate the thyroid. An increase of at least 10
times would be helpful, but more effective would be levels that are
comparable to the Japanese, having the highest daily intake of iodine
and the lowest rates of cancer in the world.
Iodine and Lipids
One of the ways to measure the number of double bonds in fat is to measure
the amount of iodine 100 grams of fat will take up. This is called the
iodine number or value. The most unsaturated fat has the highest iodine
value. Dietary fat removes iodine from the diet. Iodine protects double
bonds while they are being transported to the sites where they are needed
such as blood vessels and synaptic membranes of the central nervous
Iodine and Pregnancy
During pregnancy the placenta captures iodine to the point of raising
the levels in the fetal circulation to five times the mother's level.
As there are a huge number of cells dying by apoptosis during fetal
growth, so iodine is of importance to the fetal development. The brain
has more apoptosis going on during development than most other organs,
so it follows that low iodine can cause abnormal brain development.
Early fetal development is partly under the guidance of maternal thyroid
hormones that have crossed the placenta, but it is theorized that the
primitive cells at the beginning of fetal development still have the
ability to make thyroid hormone themselves for their own use as in the
early evolution of eukaryotes.
In 1912 it was shown that thyroid hormones would change a tadpole into
a frog. This metamorphosis is complex at all levels. The tails dissolve
away, legs are developed on the side, the lungs are changed over to
air breathing, and the liver, without any detectable change in the DNA
or cellular morphology, changes over biochemical mechanisms from an
ocean water animal to a land animal. Although the effects of thyroid
hormone appear to be systemic in the tadpole, in fact, thyroid hormone
is affecting each cell individually. But more importantly, if the thyroid
gland is removed and iodine is given in any form--injection, orally
or in the bathing solution--metamorphosis will carry along at the same
rate as if thyroid hormone was present. This suggests that the ability
of tadpoles to synthesize thyroid hormone from iodine alone is retained
inside every cell. If these phenomena of intracellular synthesis of
thyroxine have been carried over from the first days of eukaryote genesis,
it is likely that human fetal development, also in its early stages,
is dependent on thyroxine manufactured from iodine within the cells.
The only factor which completely eliminates cretinism, hypothyroidism
in the fetus, and mental retardation is iodine, given by any means,
as long as it is adequate--before conception.
Japanese women, who consume the highest amounts of dietary iodine per
woman in the world, have the lowest rate of stillbirth and perinatal
and infant mortality in the world. Among the folklore of Japanese mothers
is the interesting concept that seaweed will prevent cancer.
Functions of Iodine in the Human Body
to make thyroid hormone in the thyroid gland.
body surveillance mechanism for abnormal cells in the body.
apoptosis (programmed death of cells) in normal cells and abnormal
with tyrosine and histidine to inactivate enzymes and denature proteins.
to bacteria, algae, fungi viruses and protozoa.
biological toxins food poisoning, snake venoms etc.
allergic process. Makes external proteins non-allergic.
mechanism by making intracellular proteins spilled into blood non-allergic.
of double bonds in lipids for delivery to cardiovascular system and
synaptic membranes in brain and retina.
source of apoptotic mechanisms during development in fetus and breast-fed
from apoptotic diseases such as leukemia.
initial source of thyroxine in early fetal development.
activity in stomach against helicobacter pylori.
Many factors influence thyroid function. Commonly unrecognized causes
of thyroid underproduction have been attributed to excessive consumption
of soybean products. Mercury binds to the sulphur in thyroglobulin and
renders it unavailable for the production of thyroid hormones. Fluoride
in tap water and toothpastes as well as chlorine in tap water both block
iodine receptors in the thyroid gland that result in lowered thyroid
hormone production. Sulfa and antihistamine drugs aggravate iodine uptake
by the thyroid. Synthroid and other synthetic thyroid drugs can cause
as much as a 13% loss of bone mass, according to a study done at the
University of Massachusetts. Underactive thyroid conditions respond
best when supplemented with detoxified iodine, kelp and dulse, essential
fatty acids, thyroid glandulars and other nutrients that nourish the
The affinity of mercury for the pituitary gland was first identified
by Stock in 1940. Autopsy studies in 1975 revealed that, contrary to
accepted belief that the kidney was the prime accumulator of inorganic
mercury, the thyroid and pituitary retain and accumulate more inorganic
mercury than the kidneys. It has been well documented that mercury is
an endocrine system disrupting chemical in animals and people, disrupting
function of the pituitary gland, thyroid gland, enzyme production processes,
and many hormonal functions at low levels of exposure. People with high
mercury levels in their bodies have more hormonal disturbances, immune
disturbances, recurring fungal infections, hair loss and allergies.
Hormones that are most often affected by mercury are thyroid, insulin,
estrogen, testosterone, both anterior and posterior pituitary, and adrenaline.
Almost all hormones have binding sights capable of connecting to metabolic
cofactors, but mercury can bind here, too. Mercury frequently has a
stronger affinity for these binding sites than the normal activators;
even though the hormone is present in the bloodstream, it may not be
able to act as it is supposed to act.
Mercury (especially mercury vapor 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. Mercury, through
its affects on the endocrine system, is documented to cause other reproductive
problems including infertility, low sperm counts, abnormal sperm, endometritis,
PMS, adverse effects on reproductive organs, etc. In general, immune
activation from toxins such as heavy metals, resulting in cytokine release
and abnormalities of the hypothalamus-pituitary-adrenal axis, can cause
changes in the brain, fatigue, and severe psychological symptoms such
as depression, profound fatigue, muscular-skeletal pain, sleep disturbances,
gastrointestinal and neurological problems as are seen in CFS, fibromyalgia,
and autoimmune thyroiditis. Symptoms usually improve significantly after
amalgam removal. A direct mechanism involving mercury's inhibition of
hormones and cellular enzymatic processes by binding with the hydroxyl
radical (SH) in amino acids, appears to be a major part of the connection
to allergic/immune reactive/autoimmune conditions such as autism/ADHD,
schizophrenia, lupus, scleroderma, eczema, psoriasis and allergies.
Mercury inhibits the activity of dipeptyl peptidase (DPP IV) which is
required in the digestion of the milk protein casein as well as xanthine
oxidase. Studies involving a large sample of autistic and schizophrenic
patients found that over 90% of those tested had high levels of the
neurotoxic milk protein beta-casomorphine-7 in their blood and urine
and defective enzymatic processes for digesting milk protein. Elimination
of milk products from the diet improves the condition. ADHD populations
have high levels of mercury and recover after mercury detoxification.
As mercury levels are reduced, the protein binding is reduced and improvement
in the enzymatic process occurs. Additional cellular level enzymatic
effects of mercury binding with proteins include blockage of sulfur
oxidation processes, enzymatic processes involving vitamins B6 and B12,
effects on cytochrome-C energy processes, along with mercury's adverse
effects on mineral levels of calcium, magnesium, zinc, and lithium.
Thyroid and Mercury
Organic mercury causes severe damage to both the endocrine and neural
systems. Studies have documented that mercury causes hypothyroidism,
damage of thyroid RNA, autoimmune thyroiditis (inflammation of the thyroid),
and impairment of conversion of thyroid T4 hormone to the active T3
form. Large percentages of women have elevated levels of antithyroglobulin
(anti-TG) or antithyroid peroxidase antibody (anti-TP). Slight imbalances
of thyroid hormones in expectant mothers can cause permanent neuropsychiatric
damage in the developing fetus. Hypothyroidism is a well-documented
cause of mental retardation. Maternal hypothyroidism appears to play
a role in at least 15% of children whose IQs are more than 1 standard
deviation below the mean, millions of children. Studies have also established
a clear association between the presence of thyroid antibodies and spontaneous
abortions. Hypothyroidism is a risk factor in spontaneous abortions
In pregnant women who suffer from hypothyroidism, there is a four-time
greater risk for miscarriage during the second trimester than in those
who don't. Women with untreated thyroid deficiency are four-times more
likely to have a child with a developmental disability and lower I.Q.
Mercury blocks thyroid hormone production by occupying iodine-binding
sites and inhibiting hormone action even when the measured thyroid levels
appears to be in the proper range. There are several aspects of iodine
deficiency and hypothyroidism-related effects on fetal and perinatal
brain development that can be aggravated or otherwise affected by the
presence of mercury. Mercury has the ability to reduce cerebellar brain
weight through significant reductions in total cell population of the
cerebellum. Reductions of total body weight at birth are related to
maternal exposure to mercury. Lead and mercury also have a direct effect
on neuronal development leading to learning deficits. These are the
same type of birth defects produced by maternal iodine deficiency and
hypothyroidism. Mercury can have a negative effect on both iodine and
thyroid status. A pregnant woman with a mouthful of mercury amalgam
fillings has a much greater chance of experiencing some degree of hypothyroidism
and/or iodine deficiency during pregnancy than one without amalgam fillings.
Both the pituitary and the thyroid display an affinity for accumulating
mercury. The enzymatic effects of mercury intoxication can be overcome
by the administration of the thyroid hormone thyroxine. Through a feedback
loop, the pituitary releases thyrotropin-releasing hormone, which in
effect tells the thyroid how much thyroxine hormone to release into
the blood. Mercury first stimulates and then suppresses the thyroid
function. Chronic intake of mercury for more than ninety days results
in signs of mercury poisoning, together with decreased uptake of iodine
and depression of thyroid hormonal secretion. The thyroid and hypothalamus
regulate body temperature and many metabolic processes including enzymatic
processes that, when inhibited, result in higher dental decay. Mercury
damage thus commonly results in poor body temperature control, in addition
to many problems caused by hormonal imbalances such as depression. Such
hormonal secretions are affected at levels of mercury exposure much
lower than the acute toxicity effects normally tested. Mercury also
damages the blood brain barrier and facilitates penetration of the brain
by other toxic metals and substances. Hypothyroidism is also a major
factor in cardiovascular disease.
The thyroid gland has four binding sites for iodine. When mercury attaches
to one of these sites, the hormone activity is altered. There is a relationship
between thyroid function and the nutritional status of folate, vitamin
B12, and methionine. There is also a strong association between lowered
zinc intake, lowered basal metabolic rate, lowered thyroid hormones
and lowered protein utilization. Mercury affects the nutritional status
of folate, vitamin B12, methionine, and zinc, as well as protein. The
thyroid is one of the important glands influencing dental decay.
There is a fluid flow from the pulp chamber, through the dentin, through
the enamel and into the mouth in people who have no dental decay. Thyroid
is part of the endocrine function that controls the direction of this
fluid flow. Low thyroid hormone production allows this fluid flow to
run in the opposite direction--from the mouth, into the enamel, dentin,
and pulp chamber. This fluid brings bacteria and debris from the mouth
with it, leading to dental decay. When the teeth are susceptible to
decay, the whole body is susceptible to degenerative disease. The thyroid
is involved with maintenance of proper body temperature. Most mercury
toxic patients have lower than optimum body temperatures. The most toxic
persons may have temperatures as low as 96.2. When the amalgam fillings
are removed, there is a trend for the temperature to approach 98.6,
sometimes within 24 hours of removing all of the amalgams. The thyroid
gland is controlled by the pituitary gland. When the thyroid is influenced
by mercury, there is a high incidence of unexplained depression and
anxiety. A person may have adequate levels of T3 and T4 hormones, but
if the hormones are contaminated, the person is functionally thyroid
deficient. Thyroid imbalances cause chronic conditions such as clogged
arteries and chronic heart failure. People who test hypothyroid usually
have significantly higher homocysteine and cholesterol--documented risk
factors in heart disease.
Fifty percent of those also have high levels of homocysteine, and 90%
are either hyperhomocystemic or hypercholesterolemic. The major regulator
of adrenocortical growth and secretion activity is the pituitary hormone
ACTH (adreno-cortico-tropic hormone). ACTH attaches to receptors on
the surface of the adrenal cortical cell and activates an enzymatic
action that ultimately produces cyclic adenosine monophosphate (cAMP).
cAMP, in turn, serves as a co-factor in activating key enzymes in the
adrenal cortex. The adrenal cortex is able to synthesize cholesterol
and to also take it up from circulation. All steroid hormones produced
by the adrenal glands are derived from cholesterol through a series
of enzymatic actions, which are all stimulated initially by ACTH. Steroid
biosynthesis involves the conversion of cholesterol to pregnenolone,
which is then enzymatically transformed into the major biologically
active corticosteroids. cAMP is produced from adenosine triphosphate
(ATP) by the action of adenylate cyclase. Adenylate cyclase activity
in the brain is inhibited by micromolar concentrations of lead, mercury,
and cadmium. One of the key biochemical steps in the conversion of adrenal
pregnenolone to cortisol and aldosterone involves an enzyme identified
Mercury causes a defect in adrenal steroid biosynthesis by inhibiting
the activity of 21a-hydroxylase. The consequences of this inhibition
include lowered plasma levels of corticosterone and elevated concentrations
of progesterone and dehydroepiandrosterone (DHEA). DHEA is an adrenal
male hormone. Because patients with 21-hydroxylase deficiencies are
incapable of synthesizing cortisol with normal efficiency, there's a
compensatory rise in ACTH leading to adrenal hyperplasia and excessive
excretion of 17a-hydroxyprogesterone, which, without the enzyme 21-hydroxylase,
cannot be converted to cortisol. The inhibition of the 21-hydroxylase
system may be the mechanism behind the mercury-induced adrenal hyperplasia.
Adrenal hyperplasia can stress the adrenal glands by their accelerated
activity to produce steroids to the point that production begins to
diminish and the glands will atrophy. The result is a subnormal production
of corticosteroids. Both lead and mercury can precipitate pathophysiological
changes along the hypothalamus-pituitary-adrenal and gonadal axis that
may seriously affect reproductive function, organs, and tissues. Leukocyte
production, distribution, and function are markedly altered by glucocorticosteroid
administration. In Addison's disease (hypofunction of adrenal glands),
neutrophilia occurs 4-6 hours after administration of a single dose
of hydrocortisone, prednisone, or dexamethasone. Neutrophilia is an
increase in the number of neutrophils in the blood. Neutrophils are
also called polymorphonuclear leukocytes (PMNs). Mercury not only causes
a suppression of adrenocorticosteroids that would normally have stimulated
an increase of PMNs, but at the same time also affect the ability of
existing PMNs to perform immunity by inhibiting a reaction that destroys
Posterior Pituitary Gland
The pituitary gland controls many of the body's endocrine system functions
and secretes hormones that control most bodily processes, including
the immune system and reproductive systems. One study found mercury
levels in the pituitary gland ranged from 6.3 to 77 ppb, while another
found the mean levels to be 30 ppb, levels found to be neurotoxic (toxic
to nerves) and cytotoxic (kills cells). Amalgam fillings, nickel and
gold crowns are major factors in reducing pituitary function. The posterior
pituitary hormone joins forces with the thyroid in influencing emotions.
Posterior pituitary hormone is really two hormones, oxytocin and vasopressin.
High blood pressure is related to the function of the posterior pituitary
hormone vasopressin. It is a short trip for mercury vapor to leave a
filling, and travel into the sinus, and then travel an inch through
very porous, spongy tissues to the pituitary gland. Mercury is detected
in the pituitary gland in less than a minute after placing amalgam in
teeth of test animals.
Part of the reason for depression is related to mercury's effect of
reducing the development of posterior pituitary hormone (oxytocin).
Low levels of pituitary function are associated with depression and
suicidal thoughts, and appear to be a major factor in suicide of teenagers
and other vulnerable groups. As a profession, dentists rank highest
in suicide. Autopsy studies in Sweden showed that the pituitary glands
of dentists held 800 times more mercury than people who were not in
dentistry. Suicidal thoughts are not limited to dental personnel though.
Suicide is close to the number-one cause of death in teenagers. Braces
increase the electrical and toxic load people are carrying if they have
amalgam in their mouths. Amalgam can create suicidal tendencies by itself,
but the addition of braces, nickel crowns, or even gold crowns evidently
increases the exit rate of mercury, and the glands react--or actually
stop reacting. Suicidal tendencies tend to disappear within a few days
of supplemental oxytocin extract, along with dental metal removal. Menstrual
cycle problems, also normalize and fertility increases and endometriosis
The center that controls the need to get up several times each night
to urinate is the posterior pituitary gland. There is a certain amount
of solid material that must be disposed of daily in the urine. If the
concentration of these solids is high (yield a specific gravity of 1.022
to 1.025) then the proper volume of urine will be excreted in a day.
Should the concentration be half that, or yielding a specific gravity
of 1.012 for instance, then it will take double the amount of urine
to rid yourself of the same amount of solid. In other words, the solids
remain the same. If the concentration of the urine is reduced, the total
volume of urine is increased substantially. This ability of the kidney
is controlled by the posterior pituitary.
Mercury accumulates in the adrenal glands and disrupts adrenal gland
function. During stress, the adrenal glands increase in size as a normal
reaction in order to produce more steroids (hormones). Both physical
and physiological stress will stimulate the adrenal glands. The outer
shell of the adrenal gland is called the cortex, and the inner core
of the gland is called the medulla. The cortex produces three types
of steroids called glucocorticoids. Cortisone is a corticoid essential
to life and functions to maintain stress reactions. Mineral corticoids,
such as aldosterone, regulate the balance of blood electrolytes and
also cause the kidneys to retain sodium and excrete potassium and hydrogen.
Mineral corticoids are also involved in gluconeogenesis, which is the
process whereby your body converts glycogen to glucose (blood sugar).
Small amounts of corticoid sex hormones, both male and female, are also
produced by the adrenal cortex. Two primary nutrients for the adrenal
glands are pantothenic acid and vitamin C. A deficiency of pantothenic
acid can lead to adrenal exhaustion (chronic fatigue) and ultimately
to destruction of the adrenal glands. A deficiency of pantothenic acid
also causes a progressive fall in the level of adrenal hormones produced.
One of the largest tissue stores of vitamin C is the adrenals; it is
exceeded only by the level of vitamin C in the pituitary.
Physical and mental stress increase the excretion of adrenocorticotropic
hormone (ACTH) from the pituitary, which is the hormone that tells the
adrenals to increase their activity. The increased adrenal activity,
in turn, depletes both vitamin C and pantothenic acid from the glands.
Humans cannot produce vitamin C. They therefore attempt to replenish
the needs of the adrenals by taking the vitamin from other storage locations
in the body. If your overall ascorbate status is low, there may be an
insufficient amount available to satisfy the needs of the adrenals.
Under this condition, normal adrenal hormone response may become inadequate,
leading to an inadequate immune function.
Mercury builds up in the pituitary gland and depletes the adrenals of
both pantothenic acid and vitamin C. Stress and the presence of mercury
will have a very negative effect on the adrenal production of critical
steroids. The ability of the adrenal gland to produce steroids is called
steroidogenesis and is dependent upon reactions mediated by the enzyme
cytochrome P-450. Cytochrome P-450 reacts with cholesterol to produce
pregnenolone, which is then converted to progesterone. Cytochrome P-450
can then convert progesterone to deoxycorticosterone which is then converted
to corticosterone or aldosterone by other enzymes in the adrenals. These
adrenal functions are also affected by metal ions. Still today, the
ADA and other governmental agencies tell us that the mercury in your
mouth, or from vaccinations, is perfectly safe. Scientists say this
is a ridiculous statement that is in violation of science and common
Perchlorate, the explosive main ingredient of rocket and missile fuel,
contaminates drinking water supplies, groundwater or soil in hundreds
of locations in at least 43 states, according to Environmental Working
Group 's updated analysis of government data. EWG's analysis of the
latest scientific studies, which show harmful health effects from minute
doses, argues that a national standard for perchlorate in drinking water
should be no higher than one-tenth the level the U.S. Environmental
Protection Agency currrently recommends as safe. Perchlorate is a powerful
thyroid toxin that can affect the thyroid 's ability to take up the
essential nutrient iodide and make thyroid hormones. Small disruptions
in thyroid hormone levels during pregnancy can cause lowered IQ and
larger disruptions cause mental retardation, loss of hearing and speech,
or deficits in motor skills for infants and children.
Health Risks of PBDEs
As highly flammable synthetic materials have replaced less-combustible
natural materials in consumer products, chemical fire retardants have
become ubiquitous in consumer products. Of the many different kinds
of fire retardants, one of the most common is a class of bromine-based
chemicals known as polybrominated diphenyl ethers, or PBDEs. A growing
body of research in laboratory animals has linked PBDE exposure to an
array of adverse health effects including thyroid hormone disruption,
permanent learning and memory impairment, behavioral changes, hearing
deficits, delayed puberty onset, fetal malformations and possibly cancer.
Research also shows that exposure to brominated flame retardants in
utero or infancy leads to much more significant harm than adult exposure,
and at much lower levels. Today PBDEs are in thousands of products,
in which they typically comprise 5 to 30 percent of product weight.
During manufacturing, PBDEs are simply mixed in to the plastic or foam
product, rather than chemically binding to the material as some other
retardants do, making PBDEs more likely to leach out. PBDEs are the
chemical cousins of PCBs, another family of persistent and bioaccumulative
toxins that came to the attention of regulators only after millions
of pounds had been released into the environment. Used primarily as
electrical insulators, PCBs were found to be rapidly building up in
people and animals before they were banned in 1977.
Many of the known health effects of PBDEs are thought to stem from their
ability to disrupt the body's thyroid hormone balance, by depressing
levels of the T3 and T4 hormones important to metabolism. In adults,
hypothyroidism can cause fatigue, depression, anxiety, unexplained weight
gain, hair loss and low libido. This can lead to more serious problems
if left untreated, but the consequences of depressed thyroid hormone
levels on developing fetuses and infants can be devastating. One study,
for instance, found that women whose levels of T4 measured in the lowest
10 percent of the population during the first trimester of pregnancy
were more than 2.5 times as likely to have a child with an IQ of less
than 85 (in the lowest 20 percent of the range of IQs) and five times
as likely to have a child with an IQ of less than 70, meeting the diagnosis
of "mild retardation." Even short-term exposures to commercial PBDE
mixes or individual congeners can alter thyroid hormone levels in animals,
and the effects are more profound in fetuses and offspring than in adults.
These results aren't surprising, but are ominous as data in humans indicate
that pregnancy itself stresses the thyroid, and developing fetuses and
infants don't have the thyroid hormone reserves adults do to help buffer
insults to the system.
Most studies on thyroid hormone disruption by PBDEs have been very short--with
exposures of 14 days or less. The real question is how low doses over
the long term affect the body's thyroid hormone balance. The answer
is important, because the entire U.S. population is exposed daily to
low levels of PBDEs, and studies of other thyroid hormone disrupters
have found that long-term exposures can cause more serious harm at lower
levels of exposure. Although no direct link could be made, one study
found higher rates of hypothyroidism among workers exposed to brominated
flame retardants on the job.
Just One Dose May Be Harmful
Experiments have shown that just one dose of PBDEs at a critical point
in brain development can cause lasting harm. In two different studies
a small dose--as little as 0.8 milligrams per kilogram of bodyweight
per day (mg/kg-day)--given to 10-day-old mice caused "deranged spontaneous
behavior," significant deficits in learning and memory and reduced ability
to adapt to new environments, with these problems often becoming more
pronounced with age. The few studies that have looked at changes in
organ structure have found that semi-chronic PBDE exposure can cause
thyroid hyperplasia and enlarged livers at relatively low doses (10
mg/kg-day) and other adverse effects such as hyaline degeneration, focal
necrosis and deformation in the kidney, hyperplastic nodules in the
liver, decreased hemoglobin and red blood cell counts at higher doses.
Only one PBDE congener has been tested for causing cancer, in a single
study more than 15 years ago. High doses of deca-BDE given to rats and
mice caused liver, thyroid and pancreas tumors.
Zinc, vitamin E and vitamin A function together in many body processes
including the manufacture of thyroid hormone. In addition to iodine,
a deficiency of any of these nutrients would result in lower levels
of active thyroid hormone being produced. Low zinc levels are common
in the elderly, as is hypothyroidism. The B vitamins riboflavin (B2),
niacin (B3), and pydidoxine (B6), and vitamin C are also necessary for
normal thyroid hormone manufacture. The trace minerals zinc, copper,
and selenium are the required cofactors for iodothyroinine iodinase,
the enzyme which converts T4 to the far more active T3. There are several
different forms of this enzyme, each requiring a different trace mineral.
Supplementation with zinc (the second most common mineral deficiency)
has been shown to re-establish normal thyroid function in hypothyroid
patients who were zinc-deficient, even though they had normal serum
T4 levels. Dental mercury removal and heavy metal detoxification will
restore many vitamin, mineral and trace elements to normal levels as
Similarly, selenium supplementation may be important, as those living
in areas of the world where selenium is deficient have a greater incidence
of thyroid disease. Of particular significance is the fact that while
a selenium deficiency does not decrease the conversion of T4 to T3 in
the thyroid or the pituitary, it does result in a great decrease in
this conversion in the other cells of the body. People with a deficiency
of selenium have elevated levels of T4 and TSH.
Supplementation with selenium results in a decrease in T4 and TSH and
normalization of thyroid activity. Selenium is deficient in about 50%
of people's diets, which, along with the high incidence of mercury toxicity,
may account for the large number of people with low thyroid activity.
Research demonstrates that a selenium deficiency results in low thyroid
activity in the cells even though hormone levels are normal or even
elevated,and provides some support for Barnes' contentions.
Basal Temperature Test
The Barnes test or basal temperature test is a simple measurement of
oral temperature--"at rest"--taken with an ordinary oral thermometer.
The basal temperature test is a better index of hypothyroidism and need
for thyroid therapy than the basal metabolic rate test. It costs nothing.
Any patient can self-administer the test at home in ten minutes. It
is done upon waking in the morning while the body is completely at rest,
before engaging in any activity or eating anything, before getting out
of bed, even to urinate. The thermometer should already have been shaken
down the night before so as not to create heat from the muscle activity
of shaking the thermometer. The thermometer is placed in the mouth for
ten minutes by the clock while resting quietly. Body heat depends upon
the amount of foodstuffs burned. Thyroid hormone is essential for the
oxidation or burning of fuel in the body, and in the thyroid-deficient
person body temperature falls below normal because of inadequate oxidation.
The normal range of basal temperature is between 97.8 and 98.2 degrees
Fahrenheit, if there is no sinus or throat infection present. A reading
below this normal range suggests low thyroid function. If it is above
the normal range, one must be suspicious of some infection or an overactive
thyroid gland. In women of menstruating years, because temperature can
be elevated with ovulation, basal temperature is best measured on the
second and third days of the period after flow starts. Before the menarche
or after the menopause, the basal temperature may be taken on any day.
When symptoms of thyroid deficiency are present, the basal temperature
may be one, two, or even three degrees below normal. With thyroid therapy,
the temperature will start to rise toward normal.