There are two problems in the general area of the diagnosis and
treatment of the symptoms of hypothyroidism, language and science.
The language surrounding "hypothyroidism" is not clear. The root of
this is the dual meaning of "hypothyroidism." It can either mean the
"clinical consquences of deficient secretion by the thyroid gland," or the
"clinical consequences of inadequate levels of thyroid hormones in the
body." Medical science, begun by Refetoff and Braverman, found bodily
functions between the thyroid gland and the symptom producing cells. The
first of these post thyroid functions is the peripheral metabolism of the
relatively inactive hormone thyroxine (T4) to the active hormone
triiodothyronine (T3). The second is the reception by the peripheral
cells of the T3 for use by the cells' nuclei. As Dr. Ridgway noted -- the
action is not T4 in the serum but T3 in the nuclei.
Consequently, the two definitions of hypothyroidism are markedly
different. Since the medical community does not follow its own standards
of care for medical practice guidelines by stipulating the definition,
confusion reigns. If the definition were stipulated, and logical
consistency maintained, there would be no problem.
However, the definition is not stipulated and logical consistency is
not maintained. Consider the medical practice guideline for
hypothyroidism by the British Thyroid Association. They use the broad
definition of hypothyroidism (hormone levels in the body) but then focus
on the thyroid gland only. This focus can be seen in the tests which go
to the thyroid gland's input (TSH), output (fT4), and internal behavior
and can be seen in the levothyroxine-only therapy, which is soley oriented
to replace thyroid gland secretion deficiency. There is no logical
consistency here. Just the confusion suggesting that the symptoms of
hypothyroidism can be managed with levothyroxine sodium only.
The supporting studies for levothyroxine-only did not use post
thyroid deficient subjects, they ignored the small percentages of positive
responses for T3 therapies, used insignificant doses of T3, and certainly
intimated a broad interpretation of their efforts. Consequently, these
studies are not broadly applicable. They are really only applicable to
primary hypothyroidism.
The recent statement/guideline by the Royal College of Physicians is
supposed to be soley about primary hypothyroidism. However, in the
concluson section, their recommendations extend beyond primary
hypothyroidism and into the realm of post thyroid deficiencies --
deficient peripheral metabolism and deficient peripheral cellular hormone
reception. Both of these can produce symptoms in spite of "normal"
thyroid function tests -- predominately because the thyroid functions
tests do not address post thyroid activity.
The lack of success of the endocrinology establishment and their
demand for a levothyroxine-only therapy can be seen in their 13% failure
rate (Saravanan, et al.) and their proscription of the very therapies that
have been proven to properly care for their failures (Baisier, et al.)
Medical ethics require keeping abrest of medical science. The
science of the post thryoid functions was begun in the 1960's and is now
quite established -- apparently except in the minds of the endocrinolgy
establishment. The American Thyroid Association claims that T3 is not
needed ("Wilson's Syndrome") because the peripheral metabolism is "highly
regulated." This unsubstantiated statement effectively makes the claim
that a bodily function never fails in any person for all time.
Medical ethics require placing the patient's well-being first and
foremost. This is not done either. Rather the endocrinolgy establishment
prefers to make excuses for itself with "nonspecific symptoms" or blame
the patient with "functional somatoform disorders" Neither of these
diagnoses can be made until all physicial etiologies have been excluded
per differential diagnostic protocol. But is made anyway and contributes
to the 13% error rate.
If the practice of medicine were competitive, a 13% error rate would
spell professional death -- as it should considering the virtual torture
that the victims of post thyroid deficiencies must endure daily.
Competing interests:
The return to health of those suffering from post thyroid deficiencies which mimic deficient thyroid gland secretion, primary hypothyroidism
Rapid Response:
Ignored Science
There are two problems in the general area of the diagnosis and treatment of the symptoms of hypothyroidism, language and science.
The language surrounding "hypothyroidism" is not clear. The root of this is the dual meaning of "hypothyroidism." It can either mean the "clinical consquences of deficient secretion by the thyroid gland," or the "clinical consequences of inadequate levels of thyroid hormones in the body." Medical science, begun by Refetoff and Braverman, found bodily functions between the thyroid gland and the symptom producing cells. The first of these post thyroid functions is the peripheral metabolism of the relatively inactive hormone thyroxine (T4) to the active hormone triiodothyronine (T3). The second is the reception by the peripheral cells of the T3 for use by the cells' nuclei. As Dr. Ridgway noted -- the action is not T4 in the serum but T3 in the nuclei.
Consequently, the two definitions of hypothyroidism are markedly different. Since the medical community does not follow its own standards of care for medical practice guidelines by stipulating the definition, confusion reigns. If the definition were stipulated, and logical consistency maintained, there would be no problem.
However, the definition is not stipulated and logical consistency is not maintained. Consider the medical practice guideline for hypothyroidism by the British Thyroid Association. They use the broad definition of hypothyroidism (hormone levels in the body) but then focus on the thyroid gland only. This focus can be seen in the tests which go to the thyroid gland's input (TSH), output (fT4), and internal behavior and can be seen in the levothyroxine-only therapy, which is soley oriented to replace thyroid gland secretion deficiency. There is no logical consistency here. Just the confusion suggesting that the symptoms of hypothyroidism can be managed with levothyroxine sodium only.
The supporting studies for levothyroxine-only did not use post thyroid deficient subjects, they ignored the small percentages of positive responses for T3 therapies, used insignificant doses of T3, and certainly intimated a broad interpretation of their efforts. Consequently, these studies are not broadly applicable. They are really only applicable to primary hypothyroidism.
The recent statement/guideline by the Royal College of Physicians is supposed to be soley about primary hypothyroidism. However, in the concluson section, their recommendations extend beyond primary hypothyroidism and into the realm of post thyroid deficiencies -- deficient peripheral metabolism and deficient peripheral cellular hormone reception. Both of these can produce symptoms in spite of "normal" thyroid function tests -- predominately because the thyroid functions tests do not address post thyroid activity.
The lack of success of the endocrinology establishment and their demand for a levothyroxine-only therapy can be seen in their 13% failure rate (Saravanan, et al.) and their proscription of the very therapies that have been proven to properly care for their failures (Baisier, et al.)
Medical ethics require keeping abrest of medical science. The science of the post thryoid functions was begun in the 1960's and is now quite established -- apparently except in the minds of the endocrinolgy establishment. The American Thyroid Association claims that T3 is not needed ("Wilson's Syndrome") because the peripheral metabolism is "highly regulated." This unsubstantiated statement effectively makes the claim that a bodily function never fails in any person for all time.
Medical ethics require placing the patient's well-being first and foremost. This is not done either. Rather the endocrinolgy establishment prefers to make excuses for itself with "nonspecific symptoms" or blame the patient with "functional somatoform disorders" Neither of these diagnoses can be made until all physicial etiologies have been excluded per differential diagnostic protocol. But is made anyway and contributes to the 13% error rate.
If the practice of medicine were competitive, a 13% error rate would spell professional death -- as it should considering the virtual torture that the victims of post thyroid deficiencies must endure daily.
Competing interests: The return to health of those suffering from post thyroid deficiencies which mimic deficient thyroid gland secretion, primary hypothyroidism
Competing interests: