Most people are probably familiar
with the classic symptoms of low thyroid hormone such as fatigue, cold
intolerance, cold extremities, and weight gain or difficulty losing weight. There
are, however, a myriad of other symptoms, mainly because thyroid hormone
affects the metabolism of every single organ system in the body. So, symptoms
of low thyroid can include depression, brain fog, panic attacks, muscle and
joint aches, muscle cramping, irregular periods, PMS, dry and brittle hair,
diffuse hair loss, low body temperature, constipation, irritability, weakness, sluggishness,
lack of libido, slow heart rate and high cholesterol. Often people experience
many of these symptoms but are told their thyroid labs are normal. This usually
means a TSH (thyroid stimulating hormone) level has been checked and maybe a
free T4 and/or free T3 level have been checked.
To continue this discussion, it
is necessary for the reader to understand some terms and definitions, as well
as some basic physiology. Under normal conditions (at least in theory) the pituitary
gland sends TSH to the thyroid gland as a message to make thyroid hormone. The
thyroid mainly makes thyroxin which is abbreviated T4 for the number of iodine
atoms attached to the molecule. T4 then circulates in the bloodstream and is available
for uptake into the cells of all the different organ systems via receptors on
the cells. Once inside the cells T4 is converted to triiodothyronine,
abbreviated T3, again for the number of iodine atoms attached to the molecule
(plus it’s just easier to say and spell).
This is important because T3 is much more powerful than T4 and is a
major player in terms of how much energy the cell has, how well it metabolizes and
how well it does its job. (The thyroid gland also makes some T3.) The pituitary
gland receives feedback about how much thyroid hormone is in the bloodstream so
it can adjust the amount of TSH it is sending out and therefore regulate the
amount of circulating thyroid hormone. This
is why doctors look at the TSH level—it should be high if there is too little
thyroid hormone and it should be low if there is too much thyroid hormone.
The problem with this is, under many
conditions, including obesity, weight gain, diabetes, insulin/leptin
resistance, depression, illness, autoimmune disorders, chronic fatigue
syndrome, fibromyalgia, chronic pain, opioid use, physical or emotional stress,
dieting, excessive exercise, menopause, heart disease, injury, chronic
infection, cancer or iron deficiency, the TSH level has been shown to be a very
poor marker for hypothyroidism and does not reflect the often severe levels of
hypothyroidism present inside the cells.
Likewise, measuring levels of T4 and T3 in the bloodstream does not give
us any information about what is taking place inside the cells. It has been demonstrated that even small
decreases in serum T3 levels reflect a severe intracellular deficit. When serum T3 levels decrease by 30% they may
still be within the normal range, but T3 levels in peripheral tissues may be
decreased by 70-80% resulting in severe tissue hypothyroidism with normal lab
values. This is bad news because I challenge you to find a single adult human
who does not have at least one of those conditions, even if it is only dieting
or weight gain. Even the range of normal lab values has been challenged as this
normal range is based on the general population, and it is estimated that much
of the general population has undiagnosed hypothyroidism.
The reasons behind this
discrepancy between what is happening inside cells and what the pituitary is
doing are complex and varied. Here are
some of them: under the conditions listed above there is less uptake of T4 and
T3 into the cells (less thyroid hormone gets taken into the cells), there is
less conversion of T4 to T3 and, most importantly, there is increased
conversion of T4 to reverse T3, abbreviated rT3. Reverse T3 occupies the same
receptors that T3 would, but is metabolically inactive. This means the rT3 uses T4 as a substrate,
blocks the entry of T4 and T3 into the cell and blocks the action of T3 inside
the cell.
All the conversions of T4 to T3
or rT3 are under the control of a group of enzymes called deiodinases (D1, D2
and D3 for short). In addition to the
reactions to stress listed above, the pituitary behaves completely differently
in its reaction to stress. The pituitary continues to take up T4 and T3,
continues to convert T4 to T3 and does not convert any T4 to rT3. Therefore, the pituitary never “sees” the
lack of T3 and continues to release TSH as if everything were normal.
This condition has been called
Wilson’s thyroid syndrome or Wilson’s temperature syndrome after one of the
first physicians to recognize and describe it, Dr. Denis Wilson. We could also call it a T4/T3 transport
problem and/or a T4 to T3 conversion problem or intracellular hypothyroidism or
low cellular thyroid levels. This syndrome is more common in women for several
reasons. Women have more prolonged,
sustained elevations of stress hormones under conditions of stress, which
drives the changes listed above. Also,
women have lower levels of D1 (the T4 to T3 enzyme) to begin with.
What this means to physicians is
they must listen to the patient. When
the patient has some or all the symptoms of hypothyroidism, other signs and
labs should be checked. It is important
to check TSH, free T4, free T3 and reverse T3; but also, the antibodies
associated with Hashimoto’s thyroiditis to rule out an autoimmune cause of
hypothyroidism. The free T3 to reverse
T3 ratio will be very low when intracellular hypothyroidism is present. Sex hormone binding globulin (abbreviated
SHBG) is often low. Another cardinal
sign is low body temperature—any temperature below 98.6° F is a sign of
abnormally low metabolism. A person with
normal metabolism will have a normal temperature, period. The basal metabolic rate can also be checked,
which will be low in the presence of intracellular hypothyroidism. Tendon reflexes should be checked as in
certain locations there will often be a delayed relaxation phase in the
presence of intracellular hypothyroidism.
It should be obvious that if this
syndrome is present, replacement of deficient thyroid hormone with a T4
preparation will not be sufficient. (Remember there is a problem with
converting T4 to the more powerful, more active, more useful T3.) A T3 or combination T4/T3 preparation will be
needed to successfully replace thyroid hormone.
There is a well-studied, well-documented protocol using sustained
release T3 that can correct this syndrome, called, of course, Wilson’s T3
Protocol after its developer, Dr. Denis Wilson. Why and how this works is the
subject of another essay.
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