Thyroidal Dysfunction versus Non-Thyroidal Dysfunction
(a work in progress)
Hypothyroid
and hyperthyroid are not the same thing as hypothyroidism and
hyperthyroidism. The condition of being hypothyroid, hyperthyroid, or
euthyroid (or normal thyroid) is defined primarily by the serum level of
Thyroid Stimulating Hormone (TSH). Generally speaking, a TSH between
0.4 and 5.0 is considered to be euthyroid. Whereas a TSH below 0.4 is
hyperthyroid and a TSH above 5.0 is hypothyroid. The other hormone that
is often measured in conjunction with the TSH is Thyroxin or T4, which
is the primary hormone produced by the thyroid gland. The serum level
of these two hormones, the TSH and T4, are the only measures that are
needed to determine if an individual is euthyroid, hypothyroid, or
hyperthyroid.
Hypothyroidism
and hyperthyroidism are actually non-thyroidal conditions. These are
two serious health conditions that have specific symptoms that indicate
the level of dysfunction. The only hormone that can create the symptoms
of hypothyroidism and hyperthyroidism is triiodothyronie or T3. The
thyroid gland releases about 10 to 20 percent of the circulating serum
T3, and the liver contributes about 80 percent of the circulating T3,
but the main source of T3 is the conversion of T4 to T3 at the cellular
level. It is an oft quoted fact that T3 levels give little useful
information about thyroid function. However, the converse is also true,
that TSH and T4 levels give little useful information about the
performance of T3 at the cellular level.
A
person can live without a thyroid gland. There is controversy about
the role of TSH, but there are data that support the concept that a
person can live without TSH (which will be examined later). T4 is a
pro-hormone and has no direct effect on the metabolism rate. Whether a
person can live without T4 is not known, and it may have regulatory
function that we may or may not be able to live without. However, we
cannot exist without T3. This should set a priority for which of these
three hormones are important. And yet the Gold standard,
that was established in the 1960’s, for determining if a person has
hypothyroidism or hyperthyroidism is not the symptoms of these
disorders, nor the level of T3, but rather serum TSH levels.
The
medical standard is so strict that nearly all of the thousands of
studies done involving the thyroid, over the past 50 years, are rigidly
conducted within the limits of the euthyroid state. To purposely allow
the TSH to elevate too high, or to suppress the TSH below the normal
reference limit is hardly ever allowed in research design. Furthermore,
research done on the effects of sub-clinical hyperthyroidism, and the
effects of TSH suppression with L-thyroxin have mostly been examined
without looking at non-thyroidal dysfunction. Additionally,
measurement of the T3 levels in medical clinical practice has rarely
been done, and is highly discouraged. Without examination of
non-thyroidal dysfunction in conjunction with TSH levels invalidates any
conclusions made concerning the relationship between thyroidal and
non-thyroidal dysfunction.
T4
is the main source of T3 and without T4 the body cannot produce T3.
Therefore, T4 is a vital hormone. As stated previously, it has no
direct effect on the regulation of metabolism. T4 is also the source of
Reverse T3 (RT3). RT3 is an unavoidable byproduct of the conversion of
T4 to T3 and the regulatory function of RT3 (if any) has not been
elucidated.
T3
regulates the constant production of the mitochondrial Adenosine
Triphosphate (ATP). ATP is the ultimate product of metabolism and an
organism cannot live without it. If T3 levels decrease, the constant
production of ATP decreases. ATP cannot be stored and it is used as
fast as it is made, therefore production must be continuous.
T3
and RT3 compete at the receptor site that regulates the mitochondrial
production of Adenosine Triphosphate (ATP). There are many research
articles that document the inverse relationship between T3 and RT3. As
RT3 levels rise, T3 levels decline. As a result the dwindling T3 levels
spend less time in the receptors regulating ATP. A small decrease in
the levels of the T3 that is free of protein, or free T3 (fT3), can
cause significant decrease in the constant level of energy.
As
the ATP production decreases the person experiences increased fatigue
and lethargy. They complain of being too cold and have little appetite.
And even though they are not eating very much they are unable to loose
weight or are gaining weight. These individuals also become depressed,
and treatment with antidepressants are usually inadequate.
The
symptoms of hypothyroidism occur when the cellular levels of T3
decrease and/or when RT3 levels increase too high. Clinical
observations have found that elevated fT4 levels in a euthyroid state,
frequently indicate a low or declining fT3 level, and are accompanied by
increasing symptoms of hypothyroidism. Since the Gold standard
for assessing hypothyroidism is nearly exclusively based on the TSH and
T4 levels, and rarely correlated with fT3 or the symptoms of
hypothyroidism, a person with hypothyroidism as a result of elevated RT3
is considered normal and the symptoms are attributed to other
processes. In several articles expounding the medical standard for
evaluating and treating hypothyroidism, there have been statements made
that indicated that most of the people treated for hypothyroidism in the
past 50 years have not felt any better after treatment.
T3
is not the only hormone that effects the production of ATP.
Adrenaline, or Epinephrine increases the production of ATP and is the
source of the energy needed for the fight or flight response.
Adrenaline, however, is not consistent and the levels fluctuate
depending on the emergent energy needs of the individual. Adrenaline,
in concert with Cortisol, provide protection from environmental
stressors, but can also be quite harmful to the overall health of the
individual.
The
increase dependence on adrenaline, which can occur when T3 levels are
low, can lead to chronic anxiety and panic attacks, mood swings,
insomnia, high blood pressure, hot flashes, night sweats, and excessive
sweating upon exertion.. The elevated levels of cortisol will cause
elevated levels of glucose which increase the production of insulin and
heavily tax the insulin producing cells in the pancreas. The
combination of increased glucose and insulin cause the liver to increase
the conversion of glucose to lipids, which increases the cholesterol,
triglyceride, and LDL levels. The elevated cortisol levels, as well as
the lowered T3 levels, also decrease estrogen and testosterone.
Cortisol interferes with the conversion of T4 to T3 and therefore
elevated Cortisol levels will also cause the decrease of T3 and the
increase of RT3. Cortisol also suppresses the immune and inflammatory
systems making the individual more susceptible to infection and
increased healing time, and can cause anemia.
Treating
the thyroid dysfunction of being hypothyroid only adequately treats
half or less of those suffering from hypothyroidism caused by thyroid
dysfunction. The other half of those inadequately treated for
hypothyroidism, after correcting a thyroidal dysfunction, and all of
those who are euthyroid but suffer from non-thyroidal hypothyroidism,
represent a significant population of individuals whose health problems
and psychiatric problems caused by low T3, could be inexpensively
treated with thyroid replacement therapy by measuring the non-thyroidal
dysfunction through assessing symptoms and monitoring not only TSH and
T4, but fT4 and fT3 as well. There is an article, supported with good
documentation, that the very best measure of cellular hypothyroidism is
the ration of fT3/rT3.
The Gold standard
of TSH is held inviolate with research results that are 50 years old,
and because little research has been done that push the TSH out of the
normal reference range, the original results have been perpetuated. The
conclusions of those early studies showed that decreasing the TSH below
the lower limit of normal, can result in increased cardiac arrhythmias
and bone loss. These serious health conditions are attributed to over
treatment with thyroid replacement therapy causing hyperthyroidism.
This is actually a misnomer. Over treatment with thyroid replacement
initially causes a hyperthyroid state, but the individual is actually in
a state of hypothyroidism, and the specific arrhythmia that is caused
is atrial fibrillation as a result of too little T3. The bone loss also
is caused by hypothyroidism, which decreases the process of bone
formation and throws the balance towards bone re-absorption. Bone loss
and cardiac arrhythmia also occur with hyperthyroidism, which confuses
the situation, but the initial hyperthyroid state caused by TSH
suppression is a long way away from hyperthyroidism.
After reviewing all of the articles
The
cardiac muscle is dependent on T3 and when T3 levels decrease, cardiac
output decreases. This decrease causes poor perfusion in the
extremities and is partially responsible for the parathesia, neuropathy,
cold extremities, and edema in the extremities. As T3 levels increase
the heart rate can actually decrease, blood pressure can decrease and at
the same time pulse pressure will increase. As cardiac output
increases, the venous pressure decreases and allows for better venous
return. This decreases peripheral edema and may improve varicose veins.
Extremities become warm, and in fact one clinical case of Reynaud’s
has been in remission for almost two years since increasing the fT3
levels. Increased perfusion of the brain, along with increased
metabolic activity by increased T3 in cranial tissue can, and has
improved cognitive functioning.
Most
of the claims of health improvement made in this article come from
clinical observations and have not been submitted to the rigors of the
scientific method. However, the distinction between thyroidal function
and non-thyroidal function is defensible with current research articles
and the consistent and increasing clinical data. The unyielding dogma
of the medical standard for assessing and treating non-thyroidal illness
by only assessing and treating thyroidal function is dangerous and
needs to be challenged and reevaluated in the crucible of the scientific
method. Evidence based medicine is only as good as the evidence
collected. If the evidence behind treatment of hypothyroidism is based
only on thyroidal function at the exclusion of non-thyroidal function
then the treatment will continue to be myopic and ineffective in
reducing and resolving symptoms of hypothyroidism.#Article #Practice