The Thyroid Gland
The thyroid gland is an important endocrine gland regulating metabolism
in every cell of your body.
Until 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.
Since 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.
A large 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.
Most estimates 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.
The enzyme 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.
A better 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.
The Thyroid Gland
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 up.
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 iodine.
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
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 administration 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
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
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 susceptibility.
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 thyroid function.
Hyperthyroidism
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
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 microorganisms 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 in iodine.
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 of iodine.
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 gland.
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 reuses 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 reenters 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 system.
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
- Used to make thyroid hormone in the thyroid gland.
- Main body surveillance mechanism for abnormal cells in the body.
- Triggers apoptosis (programmed death of cells) in normal cells and
abnormal cells.
- Detoxifies chemicals.
- Reacts with tyrosine and histidine to inactivate enzymes and denature
proteins.
- Antiseptic to bacteria, algae, fungi viruses and protozoa.
- Detoxifies biological toxins food poisoning, snake venoms etc.
- Anti allergic process. Makes external proteins non-allergic.
- Anti-autoimmune mechanism by making intracellular proteins spilled
into blood non-allergic.
- Protection of double bonds in lipids for delivery to cardiovascular
system and synaptic membranes in brain and retina.
- Fetal source of apoptotic mechanisms during development in fetus and
breast-fed children.
- Protection from apoptotic diseases such as leukemia.
- Possible initial source of thyroxine in early fetal development.
- Antiseptic activity in stomach against helicobacter pylori.
Other Challenges
Many factors influence thyroid function. Commonly unrecognized causes
of thyroid underproduction have been attributed to excessive consumption
of soybean products. Mercury binds to the sulfur 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 thyroid gland.
Mercury Toxicity
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 and
infertility.
In pregnant women who suffer from hypothyroidism, there is a four-time
greater risk for miscarriage during the second trimester than in those
who don't. 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 cofactor in activating key enzymes in the adrenal
cortex. The adrenal cortex is able to synthesize cholesterol and to also
take it up from circulation. All steroid hormones produced by the adrenal
glands are derived from cholesterol through a series of enzymatic actions,
which are all stimulated initially by ACTH. Steroid biosynthesis involves
the conversion of cholesterol to pregnenolone, which is then enzymatically
transformed into the major biologically active corticosteroids. Camp is
produced from adenosine triphosphate (ATP) by the action of adenylate
cyclase. Adenylate cyclase activity in the brain is inhibited by micromolar
concentrations of lead, mercury, and cadmium. One of the key biochemical
steps in the conversion of adrenal pregnenolone to cortisol and aldosterone
involves an enzyme identified as 21-hydroxylase.
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 foreign substances.
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.
Suicide
Part of the reason for depression is related to mercury's effect
of reducing the development of posterior pituitary hormone (oxytocin).
Low levels of pituitary function are associated with depression and suicidal
thoughts, and appear to be a major factor in suicide of teenagers and
other vulnerable groups. As a profession, dentists rank highest in suicide.
Autopsy studies in Sweden showed that the pituitary glands of dentists
held 800 times more mercury than people who were not in dentistry. Suicidal
thoughts are not limited to dental personnel though. Suicide is close
to the number-one cause of death in teenagers. Braces increase the electrical
and toxic load people are carrying if they have amalgam in their mouths.
Amalgam can create suicidal tendencies by itself, but the addition of
braces, nickel crowns, or even gold crowns evidently increases the exit
rate of mercury, and the glands react--or actually stop reacting. Suicidal
tendencies tend to disappear within a few days of supplemental oxytocin
extract, along with dental metal removal. Menstrual cycle problems, also
normalize and fertility increases and endometriosis symptoms subside.
Frequent Urination
The center that controls the need to get up several times each night
to urinate is the posterior pituitary gland. There is a certain amount
of solid material that must be disposed of daily in the urine. If the
concentration of these solids is high (yield a specific gravity of 1.022
to 1.025) then the proper volume of urine will be excreted in a day. Should
the concentration be half that, or yielding a specific gravity of 1.012
for instance, then it will take double the amount of urine to rid yourself
of the same amount of solid. In other words, the solids remain the same.
If the concentration of the urine is reduced, the total volume of urine
is increased substantially. This ability of the kidney is controlled by
the posterior pituitary.
Adrenal Glands
Mercury accumulates in the adrenal glands and disrupts adrenal gland
function. During stress, the adrenal glands increase in size as a normal
reaction in order to produce more steroids (hormones). Both physical and
physiological stress will stimulate the adrenal glands. 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 sense.
Perchlorates
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 US Environmental
Protection Agency currently 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 US 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.
Nutritional Considerations
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 well.
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.
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