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Thyroid Testing
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May
18, 2006
Question: I am an internist. I had
fibromyalgia symptoms for ten years, and interestingly, I developed
Hashimoto’s about the time my fibromyalgia symptoms came on. For that ten
years, I took the brand of T4 advertised most aggressively to physicians. My
pain and fatigue tormented me so much that I could hardly practice until I
switched to Armour Thyroid. Since I’ve been on 3 grains, I’ve had hardly
any pain and I now have normal energy. With the information on your website,
I’ve begun treating some of my fibromyalgia patients with Armour and some
with T3. For the most part, the results are just as you claim, and I’m
amazed at the positive results, although I know I have a lot to learn. I
just ordered your book The
Metabolic Treatment of Fibromyalgia so that I can gain and in depth
understanding of your approach. I have just one concern, and that’s my low
TSH, and my patients’ low TSH levels, on the Armour. Should I be concerned
about the low TSH levels?
Dr. Lowe: For years, I’ve received
emails from physicians such as you, and to my satisfaction, the number is
increasing. As I say to most of the physicians, I sincerely regret that you
suffered needlessly. Many millions of other people still suffer for the same
reason—being on T4-replacement and expecting it to work well. Of course, recent
studies show that T4-replacement is ineffective for and harmful to many
patients. But personal experience seems the best teacher. And although I
regret that you suffered so long before you switched to Armour, I’m sure
your patients will benefit immensely from your personal experience.
You mentioned that you’ve ordered The
Metabolic Treatment of Fibromyalgia. I discuss suppression of the
TSH in many parts of the book. However, to gain a thorough understanding of
how the endocrinology specialty has misled the medical profession about
TSH-suppressive doses of thyroid hormone, I refer you to Chapter 4.4, pages
859-898. The chapter’s title is "Adverse Effects of Excessive and
Inadequate Thyroid Hormone." You’ll find that in that chapter—as in
every chapter of the book—I use scientific evidence and logical discourse
to show the truth of the matter. This approach, of course, differs
distinctly from the endocrinology specialty’s scientifically-groundless,
commercially-driven ex cathedra pronouncements about TSH suppression.
Our treatment team uses the TSH level only initially to help clarify a
patient’s thyroid status. But during treatment, we completely ignore the
level. The reason is that the TSH level is totally irrelevant to
normalizing the patient’s whole body metabolism and relieving his or her
suffering. The only clinical value of the TSH level is to see the
effect of a particular dose of thyroid hormone on the pituitary gland’s
"thyrotroph" (TSH-secreting) cells.
The thyrotroph cells are vastly more sensitive to thyroid hormone than
are other body cells. Some endocrinologists argue that we know the ratio of
two sensitivities: that is, the ratio of the sensitivity of the pituitary to
a dose of thyroid hormone to the sensitivity of other tissues to that dose.
From knowledge of that ratio, they argue, we can use the TSH to gauge the
thyroid hormone dose that properly regulates the metabolism of all body
cells.
The problem is that for individual patients, we don’t know that
ratio. These endocrinologists fail to realize that statistical inferences
from large groups of patients do not tell us specifically enough what
we need to know clinically about individual patients.
Because the pituitary is far more sensitive than other tissues to thyroid
hormone—and just how much more sensitive in individual patients, we do not
know!—we can’t reliably deduce the effects of a particular dose of
thyroid hormone on most body cells from the effect of that dose on the
pituitary thyrotroph cells.
The near impossibility of this deduction being valid is made clear by
many studies in the field of thyroid hormone resistance. The studies show
that in many patients, various tissues differ in how sensitively they
respond to a particular dose of thyroid hormone. That is, not all tissues
respond to the same dose of thyroid hormone with the same vigor. Hence, from
an individual patient’s TSH level, we can reliably validly deduce nothing
about the effects of a thyroid hormone dose on tissue cells other than
the pituitary thyrotrophs.
You may find it helpful to keep in mind a clear-cut double standard of
the endocrinology specialty. Endocrinologists keep thousands of thyroid
cancer patients on TSH-suppressive doses of thyroid hormone. But these
specialists vociferously warn of grave dangers if hypothyroid patients use
the same TSH-suppressive doses. However, meta-analyses of studies show that
these doses are harmless to thyroid cancer patients, despite them staying on
the doses for decades. Rather than harming the cancer patients,
TSH-suppressive doses appear to benefit them: researchers write that the
patients report feeling better on these doses than hypothyroid patients do
on T4-replacement. (In T4-replacement, of course, the patient uses a dose of
thyroid hormone that doesn't suppress the TSH.)
The endocrinology specialty cannot reconcile this discrepancy in its
practice guidelines for the two different groups of patients. This to me is
one of many pieces of evidence that T4-replacement is driven by commerce—not
by science or an aim for therapeutic effectiveness. I provide rock-hard
evidence for this conclusion in my forthcoming book Tyranny
of the TSH.
There is a growing coterie of physicians such as you. They’ve all
enlightened themselves despite the shroud of darkness tenaciously held over
the eyes of modern medicine by the endocrinology specialty. That you have
freed yourself from so-called "fibromyalgia" is good. But that you’ve
joined that growing clique of physicians suggests that the long-overdue
liberation of millions of patients is on its way. Welcome to our side, and
thank you for the patients you’ll free from the horrors of T4-replacement.
January 1, 2005
Question: I just now read about the new ThyroTest that the FDA
recently approved. Your doctor takes two drops of blood in his clinic, adds
a solution to the blood, and he can tell if you’re hypothyroid in just ten
minutes. You don’t have to wait days, like I had to, to find out whether
you’re hypothyroid. The test will keep patients from waiting and
wondering, but do you think the test is any more useful than the TSH test
labs use?
Dr. Lowe: The intended purpose of the
new ThyroTest, as with other TSH tests, is two fold: (1) to decide whether a
patient needs thyroid hormone therapy, and (2) if she does, what dosage
works best for her. For these purposes, the ThyroTest provides the same
largely useless information that’s provided by TSH tests run in medical
labs.
We are currently conducting a study in which we’re comparing patients’
TSH levels with their resting metabolic rates. We have not found a
correlation between the two measures. A couple of years ago, researchers in
Quebec[] found the same thing—no correlation between hypothyroid patients’
TSH levels and their resting metabolic rates. However, the researchers found
a weak correlation when they used a statistical procedure called "log
transformation." Log transforming is a statistical method we use to
detect correlations too weak to otherwise show up. When the Quebec
researchers log transformed their patients’ TSH levels, the weak
correlation with metabolic rates showed up.
I reran the Quebec researchers’ statistics. If they reported their
numbers correctly, log transforming their patients’ TSH levels does indeed
reveal a weak correlation. But in our present study, log transforming the
TSH levels has failed to show even a weak correlation. We’ve included more
patients in your study than the Quebec researchers used. Because of this, we
have more TSH levels and metabolic rates to work with. That should make it
easier to find a correlation, if in fact there were one. Clearly, though,
our numbers don’t show a correlation.
What our study shows is that the TSH level is not an accurate
gauge of a patient’s metabolic rate. This finding is consistent with what
we regularly see when we
do metabolic evaluations for patients. We often find that a hypothyroid
patient on T4-replacement—with an "in range" TSH level—has a
metabolic rate that’s abnormally low. Often, the patient’s metabolic
rate is severely low, sometimes as much as 50% below normal.
For this all-to-common undertreated patient—who suffers from chronic
hypothyroid symptoms—the TSH level is simply not an accurate gauge;
that is, the TSH level fails to correctly tells us what thyroid hormone
dosage will give her a normal metabolic rate.
Typically, when the patient increases her dosage high enough to raise her
metabolic rate to normal, she then has a "suppressed" TSH level.
The endocrinology specialty, of course, will argue, or at least imply, that
her suppressed level shows that her metabolic rate is too high. But this is
proven false by our actual measurements of the patient’s metabolic rate.
Our measurements of patients’ metabolic rates, then, are objective
evidence that TSH levels do not correspond to patients' metabolic
rates. If the goal of thyroid hormone therapy is to provide a patient with a
normal metabolic rate, the TSH level is for all practical purposes useless.
In answer to your question, I don’t see whether it matters whether one
get her TSH level within a few days or, as with the ThyroTest, within ten
minutes. A test result that’s largely useless is, ipso facto,
largely useless.
January 16, 2004
Question: For over a year now, I’ve had 85% of the symptoms in
your hypothyroid symptoms list.
I have several intense symptoms. I have memory problems, and my hair and
skin are dry. My feet are extremely dry and cracked. My hands and feet are
numb, and my legs and back ache most of the time. My body temperature is low
(usually 97.3), and my hands and feet are cold. My eyes are puffy in the
morning, and my menstrual flow is heavy and prolonged.
Last month, at my request, my doctor did a TSH (1.37), T4 (0.85), and
antibody (<0.5) test. He said all the results were normal.
Three weeks ago I developed pain in the front of my neck and a choking
sensation when I lie on my back at night. The pain is on the right side of
my esophagus and penetrates into my right jaw and ear. I see my doctor again
tomorrow for the pain. I’m really scared that something serious is going
on, although my thyroid blood tests are normal. Can you tell me if there’s
any other test I should ask him to do? Should I be concerned that this could
be my thyroid? Is there anything else it could be?
I know you are very busy, so thank you for your time. By the way, I think
it’s a great service that you offer, answering questions for free,
especially since many people have lost all faith in their doctors and the
world of medicine.
Dr. Lowe:
Thanks for your kind comment
about our answering emails. This educational section of our website, of
course, is a cooperative venture between those of us at drlowe.com and
patients such as you who submit questions to us. So in turn, I extend my
thanks to all of you.
Your neck pain and choking sensation raise the possibility that your
thyroid gland is enlarged (goitrous). Swelling of the gland is usually
accompanied by an elevated TSH level. Of course, on the day your doctor
measured your TSH level, it was within the reference range. Your level,
however, may be "normal" one day, but high the next. The
endocrinology specialty, of course, discourages recognition of such
variations in the TSH level; the TSH test, implies the specialty, is as
reliable as the rising of the sun each day. But despite this, TSH levels
vary. For example, in The
Metabolic Treatment of Fibromyalgia, I describe a 1997 study by
Kraus and his colleagues. In the study, they found no correlation of
TSH levels from week to week. (The low correlation they found, r=0.17, was
not statistically significant.)[1] This
means that we can’t accurately predict what a patient’s TSH level will
be next week based on her level this week.
Because you have neck pain and a choking sensation, your doctor should
palpate your neck for thyroid gland nodules or swelling. If he suspects he
feels a nodule, he should order an ultrasound scan of the gland. If he doesn’t
feel a nodule, or if he feels a diffuse swelling, he should order a sed rate
and c-reactive protein. These are tests for inflammation; if either of the
tests is positive, your thyroid gland may be swollen from inflammation. Your
symptoms, then, might be caused by hypothyroidism due to inflammatory
thyroiditis.
You gave only one test result for antithyroid antibodies. We measure two
types of antibodies: those against thyroglobulin and thyroid peroxidase. In
some patients, the level of one type of antibody is high but not the other.
Hence, measuring only one level and finding a normal value can leave a
patient with undiagnosed autoimmune thyroiditis. I encourage you to have
your doctor measure both. If he won’t, we'll be happy to order the tests
for you. Just phone us at 303-413-6003, or
write to Tammy Lowe at Tammy@drlowe.com.
She'll help you make arrangements.
Another possible cause of your neck symptoms is an esophageal spasm
induced by anxiety. This is fairly common, especially in the patient left
with doubts and distress from her doctor’s failure to find the cause of
her symptoms. If the appropriate thyroid-related tests don’t point to a
thyroid disorder, you should ask your doctor to evaluate you for a possible
esophageal spasm.
Reference
[1] Kraus, R.P., Phoenix, E.,
Edmonds, M.W., Nicholson, I.R., Chandarana, P.C., and Tokmakejian, S.:
Exaggerated TSH responses to TRH in depressed patients with
"normal" baseline TSH. J. Clin. Psychiatry, 58(6):266-270, 1997.
January 2, 2002
Question:
In June of this year, I had a complete thyroidectomy. I’m currently taking
100 mcg of Synthroid. This dose of Synthroid has been effective in keeping
my TSH level at 0.13. My endocrinologist advises me that this is exactly
where he wants my TSH. He doesn't seem interested in the fact that I
feel absolutely miserable. I have joint pain, mood swings, cry at the drop
of a hat, feel short of breath at times, am losing hair, have interrupted
sleep, and people who know me say I've changed since the thyroid surgery. I
feel I've changed!! I just want my old self back! I’ve just changed
endocrinologists. This new endo is listening and mentioned Cytomel. She says
that before she’ll add Cytomel, she needs to check the T3 level in my
blood, so she’s sending me for blood work. The new endo was surprised that
my TSH could be so suppressed on such a low dose of Synthroid. Any thoughts?
Thanks.
Dr Lowe:
Different researchers have
reported that different doses of T4 suppress the TSH level. Some researchers
have reported that—on average—suppression occurs at 145 mcg
(0.145 mg) of T4;[1]
others have reported that—on average—suppression occurs at 171
mcg (0.171 mg).[2]
I’ve italicized the words "on average" to emphasize an
important point: that patients fall into a
bell curve regarding the amount
of T4 (or T3) that suppresses their TSH levels. Patients also fall into a
bell curve regarding how their thyroid glands respond to any particular
blood level of TSH. In response to a TSH level that the typical conventional
endocrinologist adores, the glands of some patients will release enough
thyroid hormone to keep metabolism normal. In response to this same TSH
level, the thyroid glands of other patients will release too little thyroid
hormone to keep metabolism normal. These patients will remain ill with
symptoms of slow metabolism—despite the same TSH level that keeps other
patients well.
The same applies to T3 blood levels: Patients fall into a bell curve—some
enjoying normal metabolism with a particular T3 level, others suffering from
symptoms of slow metabolism with the same T3 level.
What’s most important to realize is this: The variation in how
different patients respond to the same TSH or T3 level makes the reference
ranges (formerly called the "ranges of normal") for the T3, TSH, or
any other hormone totally without value in finding the dose of
thyroid hormone that’s safe and effective for individual patients.[1,p.1217]
In my experience, most conventional endocrinologists, seemingly unaware of the
bell-curve
phenomenon, make a trouble-causing presumption: that researchers have
scientifically established the safe and effective dose of thyroid hormone
for all human beings. That dose, they presume, is one that keeps the
TSH and thyroid hormone levels within their reference ranges. This, however,
is a false and scientifically unjustified presumption.
Many patients know the presumption is false; they know it’s false
because they, like you, become and remain ill when their doctors adjust their thyroid hormone dose according to the TSH
level. I know the presumption is false for three reasons: (1) I've studied
the research literature which shows that the presumption hasn't been
established. (2) I've objectively assessed the tissue metabolic status of
patients whose thyroid hormone doses were regulated by TSH levels and found
the tissues understimulated. And (3), I've seen hundreds of such patients—formerly
kept ill by TSH-adjusted thyroid hormone doses—fully recover their health
when my cotreating doctors and I treated them in violation of the guidelines
of the conventional endocrinology specialty.
I get the impression that a new breed of endocrinologist has recently
appeared on the health care scene. From communications I’ve gotten, these
practitioners only recently finished their specialty training and somehow avoided adopting the disease-causing and -sustaining practice
guidelines that conventional endocrinology has promoted for the past thirty
years. You may be able to find one of these younger endocrinologists who’ll
treat you based on how your tissues—rather than your lab values—are
responding to a dose of thyroid hormone. If not, I recommend that you
consult a naturopathic physician (if N.D.s have prescribing privileges in
your state) or a family physician or internist who’s holistically,
nutritionally oriented. Many of these practitioners, when treating patients
with thyroid hormone, completely ignore the guidelines of conventional
endocrinology. Their unconventional approach to thyroid hormone therapy
rescues many patients from the chronic illness that the guidelines have caused.
With the help of one of these practitioners, you’ll stand a much better
chance of getting your "old self back!"
December
30, 2001
Question:
On our thyroid-information website, I have many people come to me who
have low levels of both TSH and T4. I need clarification about what this
means. From studies I’ve read, I understand that both hormones being low
could mean a problem with the pituitary. But I also know of a lady whose
doctor wrote in her notes, "TSH blocking." I've looked this up
in a book which says, ". . . antibodies which block the TSH receptors
on the surface of the thyroid cells. If these receptors are blocked, the
TSH produced by the pituitary cannot stimulate thyroid hormone
production." Is this the "TSH blocking" the doctor referred
to? And if so, does this mean that if a doctor sees low levels of both TSH
and T4, he should think about doing antibody testing?
Dr.
Lowe:
The
doctor probably was referring to antibodies blocking TSH from binding to
TSH-receptors on the thyroid gland. But when a doctor sees both a low TSH
and low T4, testing for these antibodies is not ordinarily the proper
procedure. The reason is that when the antibodies are active in a patient,
her TSH level is likely to be low, but her T4 level is likely to be high. Let me explain.
Blocking of TSH from binding to TSH-receptors on the thyroid gland is caused
by immunoglobulin G antibodies. These antibodies result from a defective
gene involved in immune system regulation. Because these antibodies
stimulate the thyroid gland, they’re called "thyroid-stimulating
antibodies." Most Grave’s disease patients have high titers of the
antibodies.
The typical patient with a high titer of the antibodies has a low TSH level,
but her thyroid hormone level is high. The antibodies have a
longer-lived stimulating effect on the thyroid gland than does TSH. The
more prolonged stimulation usually causes the gland to enlarge. We call
the enlargement
"hyperplastic goiter."
From the enlargement, the gland produces and releases an
excess of thyroid hormone. The thyroid hormone level in the blood then
rises, exposing tissues to an excess of thyroid hormone. The excess
overstimulates the tissues, causing the syndrome we call "thyrotoxicosis."
The high level of thyroid hormone in the blood also inhibits the
pituitary gland’s release of TSH. The inhibited release lowers the
blood's
TSH level. When a patient’s thyroid gland is affected by the antibodies,
then, she usually has a low TSH level and a high T4 level. It is
this pattern (rather than a low TSH and low T4) that should prompt a
doctor to order a thyroid-stimulating antibody test.
When both TSH and T4 levels are low, my first thought is whether these
levels are reliable. To learn whether the levels are reliable, a doctor
can order the tests several times during the same day, and
possibly on different days. I recommend this because TSH and T4 levels
fluctuate during the same day and on different days. If we measure the
levels only once and find them both low, this may merely reflect a
simultaneous low point in their fluctuating daily levels. Concluding from
the low levels that the patient has impaired pituitary release of TSH might
be a diagnostic error. To confirm that a patient has impaired pituitary
release of TSH, we order a TRH-stimulation test. If
during this test, the pituitary releases less than a normal amount of TSH, the appropriate diagnosis
may be
"pituitary hypothyroidism."
Continued at
top of right column . . .
|
| Problems with T4 replacement |
|
Weight gain and the TSH (at Thyroid Science) |
Continued from
bottom of right column . . .
November
24, 2001
Question:
Thanks from Belgium for all the
information you provide on your site! Based on my symptoms, I fit perfectly
well in the pattern of hypothyroidism with fibromyalgia. However, my TSH
doesn’t say much. The level is 3.8. My serum T4 is in the middle of the
range, and my serum T3 is within the range but close to the lower limit. The
TRH stimulation test came back within range.
Here in Belgium, some doctors are measuring
the levels of T3 and T4 in 24-hour urine samples. The laboratory states that
the results of this test are based on a 13-year study of 832 people
previously diagnosed with hypothyroidism. The conclusion of the study is
that the optimal level of T3 in the urine is 1400-to-2600 pmol/24hours. And
the optimal level of T4 is 1925-to-3000 pmol/24hours. On this test, my T3
was 276 pmol/24hours, and my T4 was 1570 pmol/24hours. Obviously, my urinary
T4 is low, and my T3 is extremely low.
There is a big controversy in our country
over this test. Supporters say it’s a valid measure that can be used to
diagnose hypothyroidism; others say it’s not scientifically proved and
deny it totally. I'd like to know what you think about this test. Have you
ever heard or read about it, and can you refer to me publications on it? I
have been through 25 therapists from every possible specialization during
the last 4 years, all without success so far. I would appreciate if you had
any hint about where to move next.
Dr. Lowe:
I've never used T3 and T4 urine
levels in my clinical practice. To understand thyroid hormone physiology
better, however, I’ve studied the published literature on urinary thyroid
hormone levels. Because of this, some of my comments about the test are
academic. At the same time, though, my criticism of doctors basing their
treatment decisions on T3 and T4 levels is not academic; the
criticism is based on substantial scientific evidence and extensive clinical
experience, and it’s highly pertinent to the practical concerns of
patients such as yourself—patients who remain ill despite thyroid hormone
therapy based on hormone levels.
Despite the bravado of many lab test-obsessed
endocrinologists, all tests that measure levels of T3, T4, and TSH suffer
serious technical shortcomings. For example, a host of environmental,
physiological, and disease factors can alter the levels. The level-altering
effects of such factors often make diagnostic and treatment decisions based
on the levels dubious and debatable. When a doctor isn’t aware that such
factors have influenced hormone levels, his treatment decisions for a
patient may be wrong and harmful. This is certainly true of the TSH test,
which most endocrinologists seem to view as infallible. Kraus, for example,
found a lack of correlation between TSH levels week-to-week.[1]
If TSH levels naturally vary week-to-week, a doctor’s decisions about a
patient’s treatment may also vary, depending on the particular weeks he
chooses to measure the patients’ TSH level. His decisions may be based on
natural, rhythmical fluctuations in the patient’s TSH levels, and not, as
he falsely believes, on a reliable measure of the functional status of the
patient’s thyroid gland.
Urinary T3 and T4 levels may also vary
according to factors other than the effectiveness of the patient’s thyroid
gland in producing thyroid hormone. I’ll mention a few factors cited in
the research literature. You can find abstracts of these studies by going to
at PubMed and typing in
key words from the references I've placed below.
In a study of presumably healthy individuals,
24-hour urine samples were taken. Researchers found that urinary T4 levels
increased from 6 AM through 9 PM. The T4 level was lowest at night. The T3
level was increased in the urine only from 6PM to 9PM.[6]
In one study, physical and psychological stress increased the urinary
excretion of T3 and T4.[4]
A patient’s stress level may increase her urinary T3 and T4 levels by an
unpredictable amount. If a patient remains stressed through the day and
night, her excretion of T4 or T3 during that 24-hour time may be much higher
than otherwise. The doctor would need to consider this when interpreting the
patient’s urine test result. He’d also have to consider seasonal
variations in the ambient temperature: Researchers found that the urinary
excretion of both T3 and T4 was higher during the coldest months (January
and February) and lowest during the hottest months (May-July).[7]
Researchers have reported other potentially
complicating factors. Half or more of the thyroid hormone in urine is bound
to proteins or other substances.[2]
A patient may have a condition in which unusual substances that bind thyroid
hormone are excreted in the urine. Such binding may alter the levels of free
as opposed to bound T3 and T4 in the urine. The result might influence a
doctor’s decision about the patient’s thyroid status. Also, some factors
can alter the ability of the kidney tubules to take up T3 and T4. During
fasting, for example, the membrane of the kidney tubules takes up less T3
and T4. The inhibited uptake may result from reduced energy in the tubule
cells.[3]
Many factors, for example nutritional deficiencies and poor diet, might
alter the energy metabolism of tubule cells, and these factors might alter
the T3 and T4 urine levels.
Despite such potential problems, researchers
have found that T3 and T4 urinary levels correlated with thyroid status
based on serum testing. Researchers found that hyperthyroid patients had
high T3 and T4 urine levels, and hypothyroid patient had low levels.[5][6][8]
Shakespear, R.A. and Burke acknowledged the relationship between free T3 and
free T4 blood and urine levels. They argued, however, that for clinical
purposes, urine levels have few practical advantages over serum levels.[8]
One practical advantage of urine testing, however, will be of interest to
many patients. Taking a blood sample is invasive and painful. In contrast,
while getting a 24-hour urine sample is inconvenient for the span of a day,
it's non-invasive and painless for most patients.[9]
The merits and demerits of using urine rather
than blood levels of T3 and T4 are interesting to ponder. But another matter
is far more important to consider: the lack of relevance of blood and urine
T3 and T4 levels to the aim of effective thyroid hormone therapy—providing
the patient with health through normal tissue metabolism.
In deciding what dose of thyroid hormone is
safe and effective for a patient, urine levels of T3 and T4 are as useless
as blood levels of the TSH, T3, and T4. (Elsewhere,
I've give my view on the use of free T3 and free T4 serum levels to
adjusting thyroid hormone dosage.) The response to a particular dose of
thyroid hormone varies in different tissues in the same patient, and the
response varies in the same tissues in different patients. The typical
patient wants more than most anything else to overcome her symptoms and
recover her health. To achieve this, variable tissue responsiveness dictates
that she use a thyroid hormone dose that produces desirable tissue responses—regardless
of what the dose does to her blood or urine T3 and T4 levels.
The point in using either serum or urine T3
and T4 levels is the same: to adjust a patient’s thyroid hormone dose so
that her T3 and T4 levels conform to some ideal average or range. But this
is like trying to make the same-sized shoe fit all customers while
disregarding the different sizes of their feet. This approach is doomed to
leave many patients suffering from continuing hypothyroid symptoms.
We have only one way to accurately decide
whether a particular thyroid hormone dose is safe and effective for an
individual patient: by assessing how that dose affects different tissues in
the patient. We can not make this assessment with blood and urine
levels of T3 and T4. When a doctor decides on the basis of a blood or urine
level of T3 and T4 whether a patient’s dose of thyroid hormone is safe and
effective, he’s making an inference based on a gauge (T3 and T4 levels).
What most doctors don’t seem to know is that studies have not shown
this gauge to be correlated with tissue metabolic status. Moreover, ample
clinical and experimental evidence shows that the gauge isn’t
correlated with metabolic status, as I showed in The
Metabolic Treatment of Fibromyalgia. Thus, most doctors use an
uncalibrated gauge, and as a result, their therapeutic aim—much to their
patients’ sorrow!—remains far off target.
Based on these considerations, I can only
recommend one thing: that you consult a doctor who ignores serum and urine
T3 and T4 levels during treatment, and who bases his dosage decisions on his
patients’ tissue responses to thyroid hormone.
References
[1]
Kraus, R.P., Phoenix, E., Edmonds, M.W., Nicholson, I.R., Chandarana, P.C.,
and Tokmakejian, S.: Exaggerated TSH responses to TRH in depressed patients
with "normal" baseline TSH. J. Clin. Psychiatry,
58(6):266-270, 1997.
[2]
Burke, C.W. and Shakespear, R.A.: Triiodothyronine and thyroxine in urine.
II. Renal handling, and effect of urinary protein. J. Clin. Endocrinol.
Metab., 1976 Mar;42(3):504-513, 1976.
[3]
Rolleman, E.J., Hennemann, G., van Toor, H., Schoenmakers, C.H., Krenning,
E.P., and de Jong, M.: Changes in renal tri-iodothyronine and thyroxine
handling during fasting. Eur. J. Endocrinol., 2000
Feb;142(2):125-130.
[4]
Habermann, J., Eversmann, T., Erhardt, F., Gottsmann, M,. Ulbrecht, G., and
Scriba, P.C.: Increased urinary excretion of triiodothyronine (T3) and
thyroxine (T4) and decreased serum thyreotropic hormone (TSH) induced by
motion sickness. Aviat. Space Environ. Med., 49(1 Pt 1):58-61, 1978.
[5]
Rogowski, P. and Siersbaek-Nielsen, K.: Radioimmunoassay of thyroxine and
triiodothyronine in urine using extraction and separation of Sephadex
columns. Scand. J. Clin. Lab. Invest., 37(8):729-734, 1977.
[6]
Habermann, J., Horn, K., Ulbrecht, G., and Scriba, P.C.: Simultaneous
radioimmunassay for urinary thyroxine (T4) and triioldothyronine (T3). J.
Clin. Chem. Clin. Biochem., 14(12):595-601, 1976.
[7]
Rastogi, G.K. and Sawhney, R.C.: Thyroid function in changing weather in a
subtropical region. Metabolism, 1976 Aug;25(8):903-908, 1976.
[8]
Shakespear, R.A. and Burke, C.W.: Triiodothyronine and thyroxine in urine.
I. Measurement and application. J. Clin. Endocrinol. Metab.,
42(3):494-503, 1976.
[9]
Hassi, J., Sikkila, K., Ruokonen, A., and Leppaluoto, J.: The
pituitary-thyroid axis in healthy men living under subarctic climatological
conditions. J. Endocrinol., 169(1):195-203, 2001.
October 5, 2000
Question:
My symptoms include drowsiness, fatigue, and
occasional muscle aches. I have a "normal" TSH of 4.5 (range of
0.4 to 5.0), but my thyroid antibodies were elevated. My internist overrode
my endocrinologist's suggestion of "doing nothing." But the
internist prescribed Synthroid, the medication you say doesn't work well. My
symptoms have continued despite my using Synthroid. Should I ask the
internist to prescribe something else? Your advice would
be helpful.
Dr.
Lowe:
In an important recent study, researchers followed patients for 20 years after
their initial thyroid function testing. At follow-up, patients who initially
had TSH levels above 2.0 had a much higher incidence of overt hypothyroidism.
Many researchers, including me, have reached a conclusion from this study—that
the upper half of the "normal" reference range for the TSH is
contaminated with TSH values of patients with incipient thyroid disease. In
practical terms, this means that when a patient's TSH is over 2.0, suspecting
that she has thyroid disease is reasonable, although the disease may only be
dawning. The most common thyroid disease that results in primary hypothyroidism
is chronic autoimmune thyroiditis. Elevated thyroid antibodies show autoimmune
thyroiditis. Your elevated antibodies suggest that this disease is already
under way in your thyroid gland.
Together, your lab test results and your symptoms (which are
characteristic of hypothyroidism) suggest some degree of hypothyroidism.
Even if your thyroiditis waxes and wanes for years, ultimately you’re
likely to progress to overt hypothyroidism. During those waxing and waning
years, you’ll have low thyroid hormone levels at intervals. When your
hormone levels are low, you’ll suffer from hypothyroid symptoms. Some
clinicians will diagnose these symptoms as "fibromyalgia,"
"chronic fatigue syndrome," or one of the other "new
diseases." But you can avoid the symptoms and these pointless diagnoses
simply by using the proper form and dosage of thyroid hormone.
In view of all this, your endocrinologist's do-nothing position doesn’t
make good sense to me. I heartily agree with your internist that you should
be taking thyroid hormone. However, I emphatically qualify that you
should use an effective dosage of a proper thyroid hormone preparation! As
to proper preparations, your prospects for improving with any brand of T4
alone (including Synthroid) are far less than with two other preparations.
Treatment results are far superior when the hypothyroid patient uses either
(1) plain T3, or (2) a T4/T3 combination that has four parts T4 to one part
T3. Two excellent brands of the latter preparation are Armour Thyroid and
Thyrolar.
Regarding effective dosages, our typical patient achieves optimal
treatment results only when we adjust her dosage by the responses of
her tissues to the hormone. Results are less than optimal when the patient’s
thyroid hormone dosage is adjusted according to blood levels of hormones
(such as the TSH and the free T3 and free T4). Every patient and every
doctor should always bear in mind critical advice of Dr. Broda Barnes: Blood
levels of any thyroid-related hormone are thoroughly irrelevant to finding a
patient’s optimal dosage. What's important is the patient’s tissue
response to a particular dosage of thyroid hormone. Unless you and your
doctor follow Dr. Barnes’ sage advice (which I have echoed in The
Metabolic Treatment of Fibromyalgia), you're simply not likely to get
optimal therapeutic results.
September
7, 2000
Question:
Several
alternative doctors on the Internet are now saying that the free T3 is the
ultimate thyroid test to use in adjusting our dose of thyroid hormone. Do
we finally have a blood test that matters?
Dr.
Lowe: Mary Shomon publishes the
online newsletter titled Sticking Out Our Necks: The Thyroid
Disease News Report. In this newsletter, Mary reports news related
to thyroid disease and provides insightful commentary. At the top of each issue, she writes, "We're
patients, NOT Lab Values!!" The alternative doctors you refer to should
heed Mary's assertion. As usual, the doctors can learn from her instead of
the other way around. Her assertion applies as much to dependence on the
free T3 and free T4 as it does to the TSH.
One of the alternative doctors you mentioned (whose name
we deleted), who touts the superiority of the free T3 and free T4,
recently wrote to me: "I believe my approach is the best in the world:
Tell me why it's not and why yours is better!" I replied:
|
"I don't believe
that measuring the free T4, free T3, or any other circulating
hormone level, is the most effective approach to adjusting patients’
thyroid hormone dosages. My belief is based partly on the studies of
Escobar-Morreale and colleagues in Spain.[1][2] Those who advocate
the use of free T3 and free T4 levels to adjust patients' dosages
imply that these levels reliably predict T3 concentrations in cells.
However, Escobar-Morreale’s studies make one thing clear—circulating
free T3 and T4 levels don't allow us to accurately predict T3
concentrations in the cells of most tissues. His studies show that
there’s simply too much variation in cell T3 concentrations in
different tissues in the same patient. Moreover, there's too much
variation between the tissues of different patients. This makes
predicting the physiological and clinical effects of different
dosages, and of different circulating free T3 and T4 blood levels,
unreliable. Again, there's simply too much variation between
patients to allow accurate predictions from blood hormone levels.
"Dr. Broda Barnes was right
when, long ago, he wrote that circulating levels of hormones don't
measure what's most important. What’s most important is (1) how
the patient's tissues are responding to a dosage of thyroid hormone,
and (2) the physiological and clinical effects on the patient of
that dosage.
"Our model of assessment (within
metabolic rehabilitation) is taken from behavior modification, in
which I was trained in the early 1970s. Using this model, we make
multiple measures of how tissues are responding to a particular
dosage. We repeat the measures at short intervals and post the
results to several line graphs. By inspecting the graphs, we can see
how the patient’s tissues are responding to the present dosage. We
carefully consider the graphed data in view of the patient's and our
collaborative judgment of how he or she is responding to the
treatment. We can then intelligently adjust the hormone dosage (and
any other features of the patient's treatment regimen) until he or
she achieves optimal metabolic health—all without regard for the
blood levels of the TSH, free T3, or free T4. We know from hundreds
of trial runs that this systematic behavioral approach enables us to
control the metabolic status of patients more precisely than with
any other method.
"I concede that you can do some
fairly
good tweaking of a patient's clinical status by adjusting dosage
according to free T3 blood levels. This is so because the free T3
blood level appears to better correlate with the metabolic status of
tissues than does the TSH level. Despite this, if you don’t
carefully and systematically assess a patient's tissue responses to
any particular thyroid hormone dosage, you’re not focusing on
what's most important—the patient's physiological and clinical
responses to the hormone. These responses are the pure essence of
what patients seek, and it's what our systematic approach—which
ignores blood hormone levels—provides." |
So, to specifically answer your question: No,
we don't finally have a blood test that matters—not unless a doctor's goal
is to treat another lab value rather than his patients.
References
1. Escobar-Morreale,
H.F., Obregón, M.J., Escobar del Rey, F., and Morreale de Escobar, G.:
Replacement therapy for hypothyroidism with thyroxine alone does not
ensure euthyroidism in all tissues, as studied in thyroidectomized rats.
J. Clin. Invest., 96:2828-2838, 1995.
2.
Escobar-Morreale,
H.F., del Rey, F.E., Obregón, M.J., and de Escobar, G.M.: Only the
combined treatment with thyroxine and triiodothyronine ensures
euthyroidism in all tissues of the thyroidectomized rat. Endocrinology,
137(6): 2490-2502, 1996.
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