May 18, 2006

Question: I am an internist. I had fibromyalgia symptoms for ten years, and interestingly, I developed Hashimotos 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 Ive been on 3 grains, Ive had hardly any pain and I now have normal energy. With the information on your website, Ive 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 Im 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 thats 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, Ive 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 reasonbeing 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, Im sure your patients will benefit immensely from your personal experience.

You mentioned that youve 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 chapters title is “Adverse Effects of Excessive and Inadequate Thyroid Hormone.” Youll find that in that chapter as in every chapter of the bookI use scientific evidence and logical discourse to show the truth of the matter. This approach, of course, differs distinctly from the endocrinology specialtys scientifically-groundless, commercially-driven ex cathedra pronouncements about TSH suppression. Our treatment team uses the TSH level only initially to help clarify a patients thyroid status. But during treatment, we completely ignore the level. The reason is that the TSH level is totally irrelevant to normalizing the patients 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 glands “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 thyroidhormone dose that properly regulates the metabolism of all body cells. The problem is that for individual patients, we dont 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 hormoneand just how much more sensitive in individual patients, we do not know!we cant 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 vigour. Hence, from an individual patients 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 commercenot 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. Theyve 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 youve 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 youll 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 youre hypothyroid in just ten minutes. You dont have to wait days, like I had to, to find out whether youre 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 thats provided by TSH tests run in medical labs.

We are currently conducting a study in which were 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 thingno 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. Weve included more patients in your study than the Quebec researchers used. Because of this, we have moreTSH 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 dont show a correlation.

What our study shows is that the TSH level is not an accurate gauge of a patients 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-replacementwith an “in range” TSH levelhas a metabolic rate thats abnormally low. Often, the patients metabolic rate is severely low, sometimes as much as 50% below normal.

For this all-to-common under treated patientwho suffers from chronic hypothyroid symptomsthe 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 patients 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 dont 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 thats largely useless is, ipso facto, largely useless.

January 16, 2004

Question: For over a year now, Ive 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 aesophagus and penetrates into my right jaw and ear. I see my doctor again tomorrow for the pain. Im really scared that something serious is going on, although my thyroid blood tests are normal. Can you tell me if theres 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 its 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 www.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 TSHlevel, 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 cant accurately predict what a patients 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 doesnt 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 wont, we’ll be happy to order the tests for you. Just phone us at 303-413-6003, or write to Tammy Lowe at [email protected]. She’ll help you make arrangements.

Another possible cause of your neck symptoms is an aesophageal spasm induced by anxiety. This is fairly common, especially in the patient left with doubts and distress from her doctors failure to find the cause of her symptoms. If the appropriate thyroid-related tests dont point to a thyroid disorder, you should ask your doctor to evaluate you for a possible aesophageal 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. Im 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 thatthis 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! Ive just changed endocrinologists. This new endo is listening and mentioned Cytomel.She says that before shell add Cytomel, she needs to check the T3 level in my blood, so shes 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 thaton averagesuppression occurs at 145 mcg (0.145 mg) of T4;[1] others have reported thaton averagesuppression occurs at 171 mcg (0.171 mg).[2]Ive 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 responseto a TSH level that the typical conventional endocrinologist adores, the glands of some patients will release enough thyroid hormone to keep metabolismnormal. In response to this same TSH level, the thyroid glands ofother patients will release too little thyroid hormone to keep metabolism normal. These patients will remain ill with symptoms of slow metabolismdespite the same TSH level that keeps other patients well.

The same applies to T3 blood levels: Patients fall into a bell curvesome enjoying normal metabolism with a particular T3 level, others suffering from symptoms of slow metabolism with the same T3 level. Whats 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 thats 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 its 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 patientsformerly kept ill by TSH-adjusted thyroid hormone dosesfully 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 Ive gotten, these practitioners only recently finished their specialty training and somehow avoided adopting the disease-causing and -sustaining practice guidelines thatconventional endocrinology has promoted for the past thirty years. You may be able to find one of these younger endocrinologists wholl treat you based on how your tissuesrather than your lab valuesare 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 whos holistically, nutritionally oriented. Many of these practitioners, when treating patients with thyroid hormone, completely ignorethe 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, youll 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 Ive read, I understand that both hormones being how 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 causedby immunoglobulin G antibodies. These antibodies result from a defective gene involved in immune system regulation. Because these antibodies stimulate the thyroid gland, theyre called “thyroid-stimulating antibodies.” Most Graves 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 glands release of TSH. The inhibited release lowers the blood’s TSH level. When a patients 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 thana 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.”

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 doesnt 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, andmy 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 its a valid measure that can be used to diagnose hypothyroidism; others say its 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, Ive 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 its highly pertinent to the practical concerns of patients such as yourselfpatients who remain ill despite thyroidhormone 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 isnt 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 doctors decisions about a patients 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 patients TSH levels, and not, as he falsely believes, on a reliable measure of the functional status of the patients thyroid gland.

Urinary T3 and T4 levels may also vary according to factors other than the effectiveness of the patients thyroid gland in producing thyroid hormone. Ill 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 through9 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 patients 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 patients urine test result. Hed 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 doctors decision about the patients 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 therapyproviding 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 responsesregardless 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 patients 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 patients dose of thyroid hormone is safe and effective, hes making an inference based on a gauge (T3 and T4 levels). What most doctors dont 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 isnt correlated with metabolic status, as I showed in The Metabolic Treatment of Fibromyalgia. Thus, most doctors use an un-calibrated gauge, and as a result, their therapeutic aimmuch 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 studythat 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 youre likely to progress to overt hypothyroidism. During those waxing and waning years, youll have low thyroid hormone levels at intervals. When your hormone levels are low, youll 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 doesnt 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 patients 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 patients optimal dosage. What’s important is the patients 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-Morreales studies make one thing clearcirculating free T3 and T4 levels don’t allow us to accurately predict T3 concentrations in the cells of most tissues. His studies show that theres simply too much variation in cell T3 concentrations in differenttissues 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. Whats 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 behaviour 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 thegraphs, we can see how the patients tissues are responding to the present dosage. We carefully consider the graphed data in view of the patient’s and our collaborative judgement 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 healthall without regard for the blood levels of the TSH, free T3, or free T4. We know from hundreds of trial runs that this systematic behavioural 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 dont carefully and systematically assess a patient’s tissue responses to any particular thyroid hormone dosage, youre not focusing on what’s most importantthe 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 approachwhich ignores blood hormone levelsprovides.”

So, to specifically answer your question: No, we don’t finally have a blood test that mattersnot unless a doctor’s goal is to treat another lab value rather than his patients.

References:
1. Escobar-Morreale, H.F., Obregn, M.J., Escobar del Rey, F., and Morreale de Escobar, G.: Replacement therapy for hypothyroidism withthyroxine 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., Obregn, 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.