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Dr. Lowe How to Prepare Patient-to-Patient Fibromyalgia Research Foundation
The Metabolic Treatment
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February 26, 2007:
High Antibodies but
"Normal" TSH, T4, and T3 Levels: January 17, 2005 Dr. Lowe: I regret to say that you're embarking on what’s likely to prove a frustrating experience—one in which your quality of life may progressive worsen over time. I say this based on long clinical experience and the available scientific evidence. Many clinicians believe that when a patient has high thyroid antibodies, he or she should begin thyroid hormone therapy. I am among them. The patient should begin therapy to prevent troubling hypothyroid symptoms from developing. If your antibodies remain high, they’ll most likely damage your thyroid gland. Eventually, the damage may be so severe that the gland can no longer produce enough thyroid hormone to keep your metabolism normal. When you become deficient of thyroid hormone, your fatigue is likely to worsen, and you’ll develop other hypothyroid symptoms. For example, on T4-replacement therapy, which your doctor has prescribed, you’ll most likely gain weight you can’t lose. The problem I see for you is the T4-replacement. Late last year, we published two critiques of T4-replacement on drlowe.com. If you’ll read them, you'll see that there’s ample justification for my first paragraph in this email. Links to the critiques are below: http://www.drlowe.com/frf/t4replacement/intro.htm For your long-range welfare, I encourage you to print and read the critiques. I also recommend that you share them with your doctor. Hopefully she'll be responsive to logic and science, the bases of the critiques, and not subject you to the possible adverse effects of T4-replacement—a therapeutic approach based more on financial venture than science. My hope is that your doctor will switch you to a T4/T3 product and adjust your dosage by your symptoms rather than your TSH level. If she does, you stand a good chance of overcoming your fatigue and preventing other troubling hypothyroid symptoms from ever developing. October 12, 2004 Dr. Lowe: Your current symptoms don’t contradict our theory that hypothyroidism underlies most patients’ fibromyalgia symptoms. If you meet the criteria for fibromyalgia, then you've most likely been hypothyroid all along. The usual lab tests (TSH, T4, and T3) doctors order to rule out or diagnose hypothyroidism often fail to show that a patient is hypothyroid. This is especially true of the patient who has a marginal thyroid hormone deficiency due to autoimmune thyroiditis. You didn’t mention whether any of your doctors have ordered thyroid antibodies. If not, it’s possible that all along, you’ve had undiagnosed autoimmune thyroiditis with high thyroid antibodies. If so, it’s likely that you’ve been marginally hypothyroid despite your "normal" TSH, T3, and T4 levels. If this is the case, then your "fibromyalgia" symptoms are most likely misdiagnosed symptoms of hypothyroidism due to autoimmune thyroiditis. This mechanism is actually compatible with your current symptoms, which are characteristic of thyroid hormone overstimulation or "thyrotoxicosis." Many patients with autoimmune thyroiditis go through one or more phases of thyrotoxicosis. This happens when the autoimmune process damages the follicles of the thyroid gland enough for them to rupture. The follicles contain thyroid hormone, and when they rupture, the hormone leaks into the blood. The leakage can be so great that the patient’s tissues are exposed to too much thyroid hormone, and this causes thyrotoxicosis. Fortunately, the leakage is time-limited, and because of that, the thyrotoxicosis is transient. If your symptoms are those of transient thyrotoxicosis, Xanax is not the proper treatment. Instead, your doctor should prescribe a beta-blocker, such as propranolol. Propranolol will control the symptoms until you pass through the thyrotoxic phase. Afterward, your former hypothyroid ("fibromyalgia") symptoms will resume. It is possible, however, that the symptoms will be worse than before. They’ll be worse if you’ve lost so many thyroid follicles that your gland cannot produce as much thyroid hormone as before. If your thyroid gland follicles are releasing large amounts of thyroid hormone into your blood, your free T3 and free T4 should now be high and your TSH low. Your doctor should order these testes. It is more important, however, that he order thyroid peroxidase and thyroglobulin antibody levels to learn whether you have autoimmune thyroiditis. He should include in the order an thyroid-stimulating antibody level, just in case you’ve developed Graves’ disease. If your test results point to autoimmune thyroiditis and not Graves’, then after your thyrotoxicosis has subsided, your doctor should start you on thyroid hormone therapy. You should insist on a product that contains both T4 and T3. If your doctor refuses to order thyroid antibody levels, we’ll be happy to order them for you long distance. Read our webpage on long-distance lab orders and then phone us at 303-413-6003. My assistant will answer any questions you have and arrange a phone consultation so that we’re sure to order the right tests. If your doctor does cooperate, however, and orders the tests, I hope you’ll let me know the outcome. Meanwhile, I wish you the very best. November 13, 2003 Three months ago, I started having more hypothyroid symptoms. I’m always tired, extremely cold, constipated, fatigue, my ankles feel swollen, and I have aches and pains throughout my body. Because of these symptoms, my doctor referred me to an endocrinologist. The endocrinologist ordered a TSH level and antithyroid antibody levels. My TSH level was 3.29, which he said was normal. My thyroglobulin antibodies were high 32, and my thyroid peroxidase antibodies were high at 70. When I questioned the endocrinologist about the elevated antibodies, he told me to do nothing but stay on the same dose of Synthroid. I asked why the two antibodies were high. His explanation was that it’s normal for the levels to be high in people taking Synthroid, or it could be that high antibodies are simply normal for me. That doesn't make any sense to me! I still have the same hypothyroid symptoms I mentioned above, and my spirits are down. Do you mind giving me your opinion? Dr. Lowe: I’m sorry your spirits are down, but I certainly understand why. Many patients feel let down when the opinion of a specialist doesn’t seem to make sense. Patients should find it uplifting, however, that through the Internet, they can usually find answers that do make sense. Some patients with hypothyroid symptoms due to autoimmune thyroiditis do well on 0.88 mg of Synthroid. However, those are extremely rare patients. For most such patients, that dosage constitutes grossly inadequate treatment. It’s plausible that your symptoms have recently worsened because your Synthroid dose of 0.88 mg is too low to suppress the antithyroid antibody attack on your thyroid gland. In other words, your low dose of thyroid hormone may be allowing your autoimmune thyroiditis to progress and worsen your hypothyroidism. If your endocrinologist said your TSH of 3.29 is normal, his judgement conflicts with the current lab standard. According to the American Association of Clinical Endocrinologists, the new target TSH level is 3.0 to 3.04. Obviously, your TSH was above this target level. Some patients’ antithyroid antibodies remain high despite thyroid hormone therapy. Typically, though, the levels decline.[1][2] In my experience, effective thyroid hormone therapy decreases the levels to into the reference range or close to it. And despite your endocrinologist’s opinion, it’s highly improbable that a high antithyroid antibody level is normal for anyone who has your classic hypothyroid symptoms. A high antibody level means the person has autoimmune thyroiditis, and that’s clearly abnormal. To understand the relation of antithyroid antibodies to hypothyroid symptoms and proper thyroid hormone therapy, I strongly recommend my extensive chapter on hypothyroidism in The Metabolic Treatment of Fibromyalgia. References May 25, 2003 Dr. Lowe: Your doctor is wrong. Antibodies are often high despite "normal" TSH and thyroid hormone levels. Thyroid function tests (TSH and measures of thyroid hormone levels) often miss thyroid disease and hypothyroidism. Two Scandinavian researchers, Aarflot and Bruusgaard, found this in their study of 737 men and 771 women.[1] They found that those with chronic widespread musculoskeletal pain (often diagnosed as fibromyalgia) had a higher incidence of thyroid antibodies than those without pain. But thyroid function test results did not differ between the two groups. This means that the antibody test showed thyroid disease while the TSH and thyroid hormone levels failed to show it. The study raises a possibility that all patients with hypothyroid-like symptoms and their doctors should note: Patients may be suffering from hypothyroid symptoms due to autoimmune thyroid disease, and while thyroid function test results may be "normal," high antibody levels will reveal the disease. In fact, thyroid function test results may be "normal" for years despite patients having autoimmune thyroiditis the whole time.[2] I recently evaluated a patient whose case illustrates the importance of not depending solely on thyroid function tests. She had long suffered from hypothyroid symptoms when her family doctor found a nodule on the left side of her thyroid gland. A needle biopsy suggested that the nodule was benign. The patient suspected, however, that the nodule meant she was hypothyroid. To find out, she asked her doctor to refer her to an endocrinologist. She ended up seeing two different endocrinologists. The first ordered thyroid function tests and told her the results were normal. Based on this result, he pronounced that her symptoms could not possibly be caused by hypothyroidism. The patient wanted another opinion and asked her doctor to refer her to an endocrinologist at a Mayo Clinic. She hoped that the endocrinologist being on staff at a Mayo clinic meant he was more competent than the first. Like the first endocrinologist, he ordered thyroid function tests and said the results were normal. And again like the first endocrinologist, he confidently assured her that her symptoms couldn’t possibly be caused by hypothyroidism. While seeing the second endocrinologist, the patients consulted with a surgeon about her thyroid nodule. The surgeon told her that his wife had recently had the same type of benign nodule. She had chosen to have it surgically removed because she didn’t want to chance it becoming malignant. The patient saw the sense in the surgeon’s wife’s decision, and she decided to have him remove the part of her thyroid gland that contained the nodule. The surgeon removed the left lobe of her thyroid gland and sent the tissue to a lab for study. The lab report came back saying the patient’s thyroid tissue had destruction characteristic of Hashimoto’s thyroiditis. After reading this report, the patient’s family doctor ordered thyroid antibodies. They turned out to be extremely high. He then diagnosed the Hashimoto’s thyroiditis that the two endocrinologists had missed. This finding made it likely that the patient’s hypothyroid-like symptoms were indeed most likely hypothyroid symptoms. When the patient’s family doctor ordered the thyroid antibody test, her anti-microsomal (peroxidase) antibodies were 673. Anything above 2 was considered abnormal. The doctor prescribed T4, but she—like many hypothyroid patients—found T4-replacement ineffective. But when she began taking 2 grains of Armour and 50 μg of Cytomel, her antibody level plunged to 70. When her Cytomel dose was 75 mcg., her symptoms began to distinctly improve—pretty strong evidence that the two endocrinologists had misdiagnosed her symptoms as unrelated to hypothyroidism. She’s presently undergoing metabolic rehab. Based on her similarity to other hypothyroid Hashimoto’s patients who’ve undergone our program, I’m confident that she’ll soon fully recover from her hypothyroid symptoms. This patient’s story should make one thing clear: You should not let your doctor—even if he or she is an endocrinologist—deny you thyroid testing you believe you should have. For your own health and well-fare, you, like other patients, must face a tragic fact: Most conventional doctors are incompetent at identifying patients who need thyroid hormone therapy—even when the evidence for the need is obvious or even overwhelming. And as this patient’s case shows, endocrinologists are well represented among inept conventional doctors. You asked whether there’s anything else you can do to find out if you’re hypothyroid. There is: Demand full and proper testing, and don’t take no for an answer! If your current doctor won’t order the proper tests, fire him or her and find one who will. You may have to "go outside your insurance" to find one, but isn’t that worth getting well when conventional doctors forsake you? If it is worth it to you, you can get an accurate diagnosis and proper treatment; so-called "alternative thyroid doctors" have made them readily available for patients whom conventional doctors have failed. I wish you the best in your pursuit of a competent doctor, proper testing, and effective treatment should it turn out that you need it. References November
20, 2002 Dr. Lowe: Keep in mind that T4 alone is the least effective thyroid hormone preparation, and 50 mcg is an extremely small amount. I seriously doubt that 50 mcg is benefiting you in any way. It may, however, be harming you. T4 is highly effective at one thing: suppressing TSH secretion by the pituitary gland. T4 can suppress pituitary TSH secretion while leaving the metabolism of other tissues so slow that the patient continues to suffer from hypothyroid symptoms. Consequently, the doctor concludes (from the lowered TSH) that the patient is well; in the mean time, the patient suffers from continuing hypothyroid symptoms. Even worse, if the T4 dose is too low, the patient’s symptoms may actually worsen. It's possible that the paltry amount of T4 you’re taking, by lowering your TSH level, has reduced your thyroid gland’s release of T4 and T3. The T4 you're taking may be far too little to compensate for your thyroid gland’s reduced thyroid hormone output. As a result, the small dose of T4 you’re taking may actually be worsening some harmful effects of your hypothyroidism. The Physician’s Desk Reference contains an important statement largely ignored by conventional doctors: "Inadequate doses of Synthroid [and by extension, any other brand of T4] may produce or fail to resolved symptoms of hypothyroidism."[1,p.1500] (Italics mine.) Doctors currently restricting their hypothyroid patients to small doses of T4 would do well by their patients to read and seriously consider the implications of this quote. Two possible mechanisms come to mind that could—at least theoretically—account for the visual problems that began after you began using T4. A possible harmful effect of a small T4 dose is myxedematous swelling behind the eyes that distorts the patient’s vision. (Myxedema is the swelling that occurs when too little thyroid hormone regulation of connective tissue cells causes an increase in water-binding molecules in connective tissues.) The swelling might cause you to feel pressure behind your eyes. And you may have other body areas that have become swollen or puffy since you began to use T4. If you have either of these symptoms, you should discuss this possibility with your doctor. Another possibility is that you have autoimmune thyroid disease, and as part of the disease, you have anti-thyroglobulin antibodies. The suppression of your thyroid gland by too small a dose of thyroid hormone may have augmented the autoimmune process by increasing your anti-thyroglobulin antibodies. In some patients, serum containing anti-thyroglobulin antibodies was found to bind to human eye muscles.[2] Apparently, an antigen within the thyroglobulin molecule is the same or similar to one in an enzyme (acetylcholinesterase) at the nerve-muscle junction in the eye muscles.[3] The anti-thyroglobulin antibodies apparently cross-reacts with this muscle enzyme. Destruction of the enzyme could cause the eye muscles to stay contracted too long. This would distort the eye ball’s shape and produce the fuzzy, blurred vision you described. The proper approach would be for your doctor to switch you to a more effective thyroid hormone preparation—one containing both T4 and T3, such as desiccated thyroid. Of course, if your doctor keeps your dosage as low as he has your T4 dose, you might not fair much better. So, if your present doctor won’t cooperate with your using a high enough dose of a more effective thyroid hormone preparation, prudence will lead you to another doctor who will. References
September 25, 2002 Dr. Lowe: Thank you for your very interesting email. Your internist is patently wrong about the thyroid peroxidase (anti-microsomal) antibodies—they do indeed impair thyroid gland function. The antibodies are considered "cytotoxic,"meaning they’re damaging to thyroid gland cells.[1,p.926] The antibodies interfere with the activity of the enzyme "thyroid peroxidase," and the interference impairs function of the thyroid gland.[2] Your elevated of antibodies indicate that you have "autoimmune thyroiditis," and that is clearly a process destructive to the thyroid gland. Your TSH level also suggests that the function of your thyroid gland is impaired. A few years ago, clinicians would’ve considered your TSH level of 4.15 "normal." Based on recent evidence, however, a TSH level that high suggests impaired thyroid gland function—especially in someone with elevated thyroid peroxidase antibodies. So your TSH, like your antibody titer, indicates hypothyroidism. Treatment with thyroid hormone usually suppresses anti-thyroid antibodies and slows or stops the process of autoimmune thyroiditis.[3][4] Based on your symptoms and your lab results, I have no doubt that you are hypothyroid and need treatment. References
November
18, 2001 Dr. Lowe: Many patients with silicone breast implants have fibromyalgia symptoms. These symptoms are the same as those of many patients with hypothyroidism caused by autoimmune thyroid disease. Some implant patients have positive immune function test results. The most common positive immune test result is a high level of anti-nuclear antibodies. This test result, however, isn’t specific to any of the body's organ systems. Some implant patients have high levels of "anti-thyroglobulin" and "thyroid peroxidase" antibodies. These antibodies, of course, are highly specific to the thyroid gland. As I wrote at length in The Metabolic Treatment of Fibromyalgia, studies clearly show that silicone implants commonly rupture and leak, and bacteria often colonize the implants. These findings make it plausible that decomposing implants activate the immune system, and that this activation leads to autoimmune disease in susceptible women. It’s equally tenable that the autoimmune disease in some breast implant patients involves the thyroid gland. If the autoimmune disease suppresses thyroid gland function, the women may develop so-called "fibromyalgia" symptoms. If the women had fibromyalgia before getting the implants, their symptoms may worsen. In 1997, researchers published a report of two patients who developed Hashimoto’s thyroiditis after receiving silicone breast implants for cosmetic purposes.[1] A 45-year-old woman received her implants 1976. In 1991, she developed Hashimoto’s thyroiditis that led to a deficiency of thyroid hormone. For treatment, she took T4 alone. As often happens, the T4 alone was ineffective, and her symptoms continued. She was chronically fatigued and had joint pain and morning stiffness; her eyes were so dry that she had to use artificial tears. In 1995, she had a high level of both antinuclear antibodies and thyroid peroxidase antibodies. Her gamma globulin level was elevated by 22.6%, and her thyroid gland was diffusely enlarged. Because her implants were painful, she had them removed in 1996. A pathologist performed a microscopic exam of the implant materials from the woman. He reported that each implant had a fibrous capsule with extremely dense connective tissue and fibrosis. This, of course, is evidence of immune reaction to the implant materials. The second patient was 55 years old. She received silicone breast implants in 1984. In 1995, she developed Hashimoto’s thyroiditis. Her thyroid gland was painful and tender when palpated. She had mild hyperthyroidism and positive anti-thyroglobulin antibodies. She underwent corticosteroid treatment for five months. In 1996, her test for antinuclear antibodies was positive. She had the implants removed because her breasts were painful. The researchers who reported these two cases wrote that Hashimoto’s thyroiditis is only rarely associated with silicone breast implants. They also wrote that the patients’ implants may have had nothing to do with the thyroiditis.[1] If silicone implants have nothing to do with patients' autoimmune thyroiditis, however, we could accurately predict that women with breast implants would have no higher incidence of anti-thyroid antibodies than women in the general population. But this prediction is refuted by a report I just read from AAL Reference Laboratories. The report states, "We have found [thyroglobulin and thyroid peroxidase antibodies] present in the sera of 24% of patients with silicone gel breast implants."[2] For comparison, let's consider the percentages of 1,314 health individuals with high levels of the antithyroid antibodies. Of 870 males, 2.6% had high thyroglobulin antibodies, 3.9% had high thyroid peroxidase antibodies, and 2.2% had high levels of both. Of 484 females, 6.2% had high thyroglobulin antibodies, 9.5% had high thyroid peroxidase antibodies, and 6.0% had high levels of both.[3] Obviously, by comparison, the 24% incidence of antithyroid antibodies among implant patients is a far higher than in the population at large. The higher percentage suggests that silicone implants leads to autoimmune thyroid disease in a significant percentage of women. We certainly need more studies of this issue by unbiased researchers. For the time being, though, I personally believe women with silicone implants have reasonable concerns—despite firm reassurances of medical researchers with financial ties to the silicone implant industry. References October 5, 2000
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. October 15, 1997 |
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