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Dr. Lowe How to Prepare Patient-to-Patient Fibromyalgia Research Foundation
The Metabolic Treatment |
My years of focus on this issue boil down to a few evidence-based
beliefs. Arrhythmias occur in some patients with hypothyroidism and thyroid
hormone resistance. They occur when the patients’ doctors deny them
thyroid hormone therapy, or when their doctors under-treat them with thyroid
hormone. We usually say these patients' arrhythmias result from
"hypothyroid heart." Some researchers have reported an association of suppressed TSH levels
with heart arrhythmias. These studies, however, included only elderly,
sedentary individuals, some of whom were bedridden in nursing homes. None of
the researchers controlled for the influence of most of the important
heart-protective lifestyle factors. Because of this, the arrhythmias may
have been more strongly or wholly associated with unwholesome diet,
nutritional deficiencies, or low levels of cardiovascular fitness. Talking out of both sides of its collective mouth, the endocrinology
specialty continues to treat thyroid cancer patients with TSH-suppressive
dosages of thyroid hormone, while authoritatively warning hypothyroid
patients and other doctors that TSH-suppressive doses are likely to cause
arrhythmias and heart attacks. The specialty's self-contradicting
inconsistency is so glaring that it unveils conflicts of interest that
honorable people would be ashamed to be caught in. It's my belief that the specialty uses the theoretical possibility of
cardiac arrhythmias as a scare tactic to intimidate other doctors into
ordering more-and-more of these lab tests, especially TSH tests. The
intimidation ensures the continuing huge sales of these tests. The sales
please the corporations that market the tests, and as a quid pro quo,
the corporations generously share their profits with the specialty. (As
others have noted, the sharing comes as huge financial grants, speaking
fees, sponsoring of speaking appearances, research funds, free drug samples
and patient literature, and logo gift items.) For documentation, see: Unrealistic Worries About Thyroid Hormone Therapy and Heart Problems: The Source. August 17, 2004 Dr. Lowe: I apologize, but I can’t find it on the website either. However, I explained it in great detail in my book The Metabolic Treatment of Fibromyalgia. It’s a complicated phenomenon, since it involves certain genes, the proteins they code for, a specialized part of nervous system, and the heart muscle. But I’ll give you as short an explanation as I can, with the understanding that it’s greatly oversimplified. Let’s consider a female patient. She had Graves’ disease and her thyroid doctor destroyed her thyroid gland with radioactive iodine. Like most such patients, despite using T4-replacement, she’s since gained a troubling amount of weight. She’s gained it despite a diet that’s wholesome and fairly low in calories. She’s trying to stop or reverse her weight gain with aerobic exercise. Before developing Graves’, exercise was easy for her. But now she can’t exercise intensely enough to reduce her weight. Her doctor orders a heart stress test, and it shows that her heart just doesn’t beat fast and hard enough, no matter how much effort she exerts. Her trouble is that the T4-replacement is ineffective for her, just as it isn't for many other patients. As a result, thyroid hormone is under-regulating a certain set of her genes, called the "adrenergic genes." A physiological effect of the under-regulation is that her heart has a "blunted" response to vigorous exercise. By blunted, I mean that her heart doesn’t respond vigorously enough to the exercise-induced rise in her body of two stress hormones, adrenaline and noradrenaline; the hormones fail to make her heart muscle contract as fast and hard as it does in people who have normal thyroid hormone regulation. Because her heart’s response to the stress hormones is blunted, the heart pumps too little blood into her general circulation. The resulting less-than-adequate flow of blood to her exercising muscles leaves them deficient of oxygen. And the oxygen deficit renders the muscles unable of accommodating her desire to exercise hard enough to lose weight. Inadequate thyroid hormone regulation of her adrenergic genes is causing her blunted heart response through two molecular changes on her cell membranes. One is a reduced number of excitatory proteins called "beta-adrenergic receptors"; the other is an increased number of inhibitory proteins called "alpha2-adrenergic receptors." Exercising vigorously raises her levels of the two stress hormones, but because of her receptor imbalance, the hormones don’t have the same effect they do in someone with normal thyroid hormone regulation of the adrenergic genes. In the normal person, the hormones bind to more excitatory proteins and fewer inhibitory ones. This increases his heart’s force and rate of contraction. But our patient has too few excitatory proteins and too many inhibitory ones. So when the stress hormones bind to the proteins, her heart’s force and rate of contraction fail to increase normally. No matter how hard she tries, her heart won’t pump enough blood; it can’t, since inadequate thyroid hormone regulation is holding a molecular brake down on it. For her, as for many hypothyroid patients, there’s only one way to recover a normal heart response to exercise: switch from T4-replacement to either a T4/T3 combination or T3 alone. For an optimal therapeutic effect, she, like many hypothyroid patients, may have to find a slightly TSH-suppressive dose that’s not overstimulating. I hope this makes sense to you and your naturopathic physician and that you find it of some use in your treatment. May 23, 2004 I was then immediately put on Synthroid. The doctor changed my dose once every couple of months, up and down. But I never felt better and began to get sicker and sicker. I was 22 and had just graduated college, and I couldn’t get out of bed in the morning. I’d gained 10-to-20 pounds a year since the surgery, so I was very overweight. I had joint pain, brain fog, cold extremities, low body temp, and the list goes on and on. I saw many doctors who told me nothing was wrong because my TSH was normal. Then I got fed up and did research of my own. I found a doctor nearby who prescribes T3 for his fibromyalgia patients. I’m now taking 100 mcg per day and feel great. I’ve lost 30 pounds and all my other symptoms have faded away. It’s been wonderful to have a local doctor who responds to your research. But now he’s concerned because my heart rate is a little elevated, and he wants to lower my dose. I have no other symptoms of overdose and great blood pressure. Should I be concerned? I was on 75 mg before. At that dose, I had some fatigue and didn’t feel nearly as good. What do you think? Dr. Lowe: Congratulations on your remarkable improvement! I'm happy to hear that our research led to you getting effective treatment for your fibromyalgia symptoms. We’ve heard from hundreds of patients such as you who’ve freed themselves from fibromyalgia symptoms by switching from Synthroid or other brands of T4 to T3; I’m pleased you’re among them. If you went from 75 to 100 mcg of T3 in one dosage increase, you may have overshot slightly; your safe and effective dose may be somewhere between those two doses. If your doctor decreases your dose, I suggest that he do so only by a small amount, say 10 mcg, to see if that will slow your heart rate enough. His aim should be to lower your dose enough to slow your heart rate, but not so much that your fibromyalgia symptoms return. You didn’t say whether you’re doing regular aerobic exercise. If you’re not, your rapid heart rate may not be from too much T3. Instead, the mechanism may be a weak heart from deconditioning. A deconditioned heart contracts more weakly than a well-exercised one. If the weak heart contractions pump too little blood into the circulation, the heart will compensate by contracting faster. The faster contractions will keep enough blood entering the circulation so that sufficient oxygen reaches the tissues. When the weak heart is driven by T3, it will contract even faster. It may contract so rapidly that it alarms the patient’s doctor. The solution to this problem is for the patient to do regular aerobic exercise to strengthen her heart muscle. With stronger contractions, her heart rate will decrease, possibly without her lowering her dose of T3. Of course, if you’re already doing regular aerobic exercise, your doctor will most likely have to lower your dose of T3. Again, he should find a dose that slows your heart rate enough but still keeps you free from fibromyalgia and other hypothyroid symptoms. Please give him my best wishes for having rescued you from T4-replacement therapy.
June 28, 2001
Dr. Lowe: As I emphasized in The Metabolic Treatment of Fibromyalgia,[1] all doctors who treat patients with thyroid hormone should cautiously protect the patients from adverse effects on the heart. The only accurate way to assess the effect of thyroid hormone on a patient’s heart is to directly monitor cardiac status. At minimum, monitoring should involve the doctor’s attention to any symptoms the patient may have that suggest cardiac over-stimulation and EKGs. If the doctor is in doubt, he should refer the patient for evaluation by a cardiologist. I want to emphasize that the TSH test has nothing whatever to do with guarding a patient’s cardiac safety. To infer that a patient has cardiac over-stimulation because the TSH level is low is scientifically unjustified and logically unsound. It is ludicrous for a doctor to make this inference when he can easily and directly monitor how the patient’s heart is responding. Let me emphasize another important point: Some conventional endocrinologists have grossly exaggerated the cardiac risks of TSH-suppressive doses of thyroid hormone. When compared to replacement doses of thyroid hormone, TSH-suppressive doses are not associated with an increased incidence of ischemic heart disease. In fact, TSH-suppressive doses of thyroid hormone protect the heart. TSH-suppressive dosages lower the levels of blood fats more than replacement doses do. And higher-end doses of thyroid hormone can halt the progression of coronary artery disease. In patients who don’t have coronary artery disease, myocardial ischemia and/or infarction are rare even in those who are thyrotoxic. Moreover, restricting many patients to replacement doses predisposes them to cardiovascular disease and premature death. With these patients, erring on the side of safety means one thing—allowing them to use higher-end rather than lower-end doses of thyroid hormone. In most patients, then, TSH-suppressive doses of thyroid hormone don’t harm the heart. This justifies Dr. L.E. Shapiro writing in 1997, "In the absence of symptoms of thyrotoxicosis, patients treated with TSH-suppressive doses of L-T4 may be followed clinically without specific cardiac laboratory studies."[2] Dr. Gordon Skinner recently wrote that patients with normal thyroid test results who have symptoms and signs of hypothyroidism should be permitted undergo a trial of thyroid hormone therapy. Anticipating objections, Skinner wrote, "The dangers of osteoporosis and cardiac catastrophe—particularly during a three-month trial—are sometimes quoted, but these worries are unfounded and condemn many patients to years of hypothyroidism with its pathological complications and poor quality of life."[3] A correct interpretation of the available scientific evidence compels one to agree with Dr. Skinner. As I said, some conventional endocrinologists have grossly exaggerated the cardiac risks of TSH-suppressive doses of thyroid hormone. When doctors exercise reasonable precaution with their patients, they can safely ignore these endocrinologists’ exaggerations. References February 25, 2001 I recently treated a patient with T3 who lives in another city. When her local GP ran thyroid function tests, he was horrified at the free T3 level. He referred the patient to her local endocrinologist. The endocrinologist apparently didn’t agree himself with the treatment, but he referred the patient to one his colleagues who is interested. The only problem this patient has is a slightly labile pulse. When she gets stressed or anxious, her pulse goes up to 120 beats per minute. Otherwise, her resting pulse rate is 74. This isn’t the only patient of mine who feels better on high dosages of T3 but experiences episodes of a high pulse rate. Because your protocol isn’t mainstream medicine and it’s all new to me, I do feel slightly anxious in case I should run into problems with any patient. This would lead to complaints. But I am pretty convinced about your protocol. I have suggested that these patients with episodic high pulse rates reduce their T3 dosages slightly. Is there anything else you would suggest? Dr. Lowe: I appreciate both your concern for patient safety and the need to avoid complaints. Those of us with the Fibromyalgia Research Foundation are committed to the Hippocratic principle of doing no harm. The safety of our patients is our foremost concern. In addition, we’re fully aware of how "the system" works: If we made a mistake that harmed a patient under our care, some of our politically-motivated detractors wouldn’t view it as an isolated mishap. Instead, they’d unjustly use it to try and discredit our entire line of research. Hence, for more than one reason, patient safety is supremely important to us. To avoid adverse effects on patients’ hearts, we insist that they do everything known to confers cardiovascular health. Specifically, we insist that each of our patients do at least four things: !First, the patient must engage in cardiovascular exercise to tolerance. Tolerance increases as the patient’s metabolic health improves, and she is then able to increase both her intensity of exercise and the fitness of her heart. ! Second, unless her diet is already one that favors cardiovascular health, she must modify it so that it does. A diet that favors cardiovascular health, for example, includes substantial daily amounts of vegetables, fruits, and grains, and it includes low amounts of red meat and sugar-laden and fatty foods. ! Third, the patient must take a full array of heart-protective nutrients. We provide online the list of nutritional supplements we insist our patients take. These supplements include nutrients that take part in protecting the heart against disease and adverse cardiac events. The supplements we recommend make up our own nutritional supplement regimen. We based this supplement list largely on the beliefs of Prof. Linus Pauling. ! Fourth, the patient must take sufficient time for rest and relaxation. These are intended to reduce the overall stresses the patient’s cardiovascular system is subjected to. Let me emphasize that we insist that our patients use these heart-protective methods. We are as collaborative in our relationships with patients as any clinicians can be. However, using these methods is not optional for our patients. Their safety is more important to us than the principle of collaboration. In fact, I’ve ended my clinical relationships with a few patients who carried on with large dosages of T3 while declining to use these heart-protective methods. I considered these patients and the physicians who continued their T3 prescriptions foolhardy. Fortunately, most of our patients have been fully cooperative and safety minded. From experiences with these latter patients, I’m convinced that their use of these protective methods is responsible for none having had adverse cardiac effects. |
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