The Medical Definition of Hyperthyroidism is flawed
The Medical Definition of Hyperthyroidism is flawed
John V. Billings ARNP
5/28/2010
Hyperthyroidism, by
medical definition, is when the Thyroid
Stimulating Hormone (TSH) level less than 0.40 (uIU/mL), if the
pituitary is working correctly. A Thyroxine (T4) level is often added
to establish that the pituitary is working properly. Triiodothyronine
(T3) is the third, and most important thyroid hormone. It is the only
hormone that actively regulates the Basal Metabolism Rate (BMR). Only
when T3 is too high is the person actually hyperthyroid. However, T3
is consistently left out of the equation. Hyperthyroidism may be
treated by using medications to stop T4 and/or T3 production, or by
surgery to remove the thyroid gland.
Hypothyroidism, by medical definition, is when the TSH level is above
5.0, but it is generally not treated until the level is above 10.0. T4
is included only as a marker to rule out an abnormal pituitary
response. Again, T3 is left out of the picture. However, when free T3
levels drop below a certain level the individual will begin to
experience symptoms of hypothyroidism. This can occur when the TSH and
T4 levels are within the normal reference range. It is generally
assumed that if the TSH and T4 levels are normal, then the T3 is also
normal, which is an assumption that cannot be substantiated.
Hypothyroidism is treated with medication containing T4. In the
treatment of hypothyroidism it is stressed that the TSH should never be
lowered below 0.40, and absolutely never decreased to zero. To do so
would put the patient in a state of hyperthyroidism (by definition).
There is no part of routine medical treatment of hypothyroidism that
involves measurement of T3. In fact, the routine measurement of T3 is
highly discouraged.
TSH has no direct effect on the BMR. It's only function is to
stimulate the thyroid gland to make T4. T4 is biologically inert as
far as the BMR is concerned, and only provides a reservoir so that the
tissues can make T3.
If you want to know definitively if there is hyperthyroidism you must
examine the T3 level and corresponding symptoms. The T3 level in and
of itself does not determine if a person is hyperthyroid because the
optimum T3 level can be vastly different from person to person.
At best, TSH is an indirect measurement of the combination of both T4
and T3, with T3 having four times the effect on TSH than T4.
Therefore, if the T3 is low the T4 will be elevated to compensate.
There is no correlation between TSH and T3. You cannot determine the
T3 level by measuring the TSH, nor can you determine the TSH level by
measuring the T3.
Since T3 is the more important of the three thyroid hormones (TSH, T4,
and T3), why even bother measuring TSH? TSH is a screening tool and as
such is useful only in primary care to rule out a thyroid problem when
symptoms suggest a thyroid condition. It's use is driven only by the
fact that Medical standards have made it the Gold Standard, and it is
relatively inexpensive. In fact, routine measurement of TSH in primary
care is discouraged because it rarely elucidates a thyroid condition
where there are no symptoms.
Clinically, a TSH level less than 0.40 may generally indicate
hyperthyroidism, only if the individual is not on any thyroid hormone
replacement therapy (THRT). However, a person not on THRT can have a
normal TSH and a low T3. In my clinical practice, most of the patients
I have seen for over the past 12 years (about 500) have had normal TSH
levels below 5.0, and yet their T3 levels have been too low.
Clinically, When I have had a patient whose T3 levels are low and I
have added THRT, even though they are euthyroid (normal thyroid),
dropping the TSH level below 0.40 rarely indicates hyperthyroidism
(high T3) and almost always has initially indicated a worsening
hypothyroidism (low T3). Any addition of levothyroxine will initially
increase the T4 level. Increasing the T4 will also increase the T3.
As a result the TSH will drop and the thyroid will decrease it's
contribution of T4 to the mix, ultimately lowering the T4 and T3
levels. If the loss of the thyroid contribution of T4 is greater than
the addition of T4 with levothyroxin, the net result is a lowering of
the T4 and thus a lowering of the T3.
The signs and symptoms of cardiac arrhythmia and bone loss, that have
been attributed to over-treatment of hypothyroidism, and have been
erroneously assumed to be caused by hyperthyroidism, are in fact
symptoms of hypothyroidism. In the original studies done that
established cardiac arrhythmia and bone loss as the outcome of
over-treatment, the only measurement done was a TSH. And the medical
Gold Standard defining hyperthyroidism erroneously attributed these
symptoms to hyerthyroid, not hypothyroid. There was no correlation
done between the TSH and T3 levels.
In addition, I have found no subsequent research that has established
that the initial lowereing of TSH below 0.40 when treating
hypothyroidism is actually an elevated T3 level. What I did find
curious was a statement in a very thorough article on the medical
standard of treating hypothyroidism, where it was admitted that only
one third to one half of all those treated for hypothyroidism report
feeling any relief from the symptoms of hypothyroidism. That
observation in itself should indicate further research as to why
treating hypothyroidism has such low treatment success of alleviating
the symptoms.
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