August 1, 2011

Question: Why can't my heart tolerate even low-dose thyroid hormone?

Note: We often received versions of this question. The question is an extremely important one to answer. The reason is that without proper answers, many people stop taking thyroid hormone and likely suffer from the multiple harmful effects of too little thyroid hormone regulation for prolonged times. To answer the question as comprehensively as I can,  we have posted it to my commentary section. Please see the heart page in that section to read my answers.  

December 12, 2005

Question: I'm a physician in North Carolina who uses your book The Metabolic Treatment of Fibromyalgia as a manual for treating my fibromyalgia patients. I have now gotten many of these patients well by using doses of Armour or Cytomel that my partners consider excessive. Their main concern is that the doses I use may cause heart arrhythmias. A local endocrinologist recently told one of my partners that sooner or later, I'm going to cause some of these patients to have heart attacks. Because of the documentation you give in the book, I'm comfortable using doses of thyroid hormone that are obviously necessary for the patients to get well. I am curious, however, what your current position is on the issue of thyroid treatment and arrhythmias.

Dr. Lowe: Hardly a week passes that I don't receive an email from a physician asking the same question you have. My answer here is typical of what I send to them.

The major concern of our research and treatment team over the years has been the safety of our patients. Out of that concern, I've given the subject of thyroid hormone therapy and heart arrhythmias intense focus. I have studied the entire research literature on the subject. In addition, our research and treatment team may have run more ECGs (EKGs) and ordered more advanced cardiac testing than any other clinic not specializing in cardiology.

We ran so many in years past that the results forced us to a conclusion: it's the rarest exception when the ECG rhythm of a patient is of concern. We've referred for cardiac consults the few patients who had rhythms we were concerned about. Only once did a cardiologist advise that the patient undergo cardiac rehab before beginning the use of thyroid hormone. In every other case, the cardiologist said that thyroid hormone therapy was safe for the patient. Some cardiologists said that the therapy would most likely improve the patient's cardiac health.

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."

Arrhythmias also occur in some patients with suppressed TSH levels. It's not clear at all, however, that excessive thyroid hormone stimulation causes these patients' arrhythmias. Unfortunately, the endocrinology specialty has concluded from these studies that anyone taking TSH-suppressive doses of thyroid hormone is likely to have heart arrhythmias. But this conclusion is simply illogical, and it is self-contradictory for the specialty, as I explain below.

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.

Also, the suppressed TSH levels of people in the studies weren't caused by thyroid hormone therapy; researchers only found the low TSH levels upon reviewing medical records of the people. This raises the possibility that factors other than too much thyroid hormone were responsible for the people's suppressed TSH levels.

For example, some of the people in the studies may have had pituitary hypothyroidism. This is a condition in which the pituitary gland doesn't produce a normal amount of TSH; as a result, patients have abnormally low TSH levels. It’s important to note that these patients have deficiencies of thyroid hormone, so thyroid hormone overstimulation couldn’t be the cause of their arrhythmias. Other patients in the studies may have had some degree of Graves' diseases. If so, then it's possible that their arrhythmias were caused by some sort of cardiac cross-reaction with thyroid stimulation antibodies.

For real clarity on this issue of arrhythmias, we must compare patients in the studies I just mentioned (elderly, sedentary, often bedridden people) to thyroid cancer patients. The comparison reveals an outrageous double standard of therapy by the endocrinology specialty.

Nearly all thyroid cancer patients use TSH-suppressive dosages of thyroid hormone. Through meta-analyses of many studies, researchers looked at the heart condition of these patients—some of whom have suppressed their TSH levels with thyroid hormone for decades. The researchers found that the suppression has not compromised the health of the patients’ hearts.

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.

From my study and clinical experience of this issue over the years, I've derived a distinct impression that I justify in my forthcoming book Tyranny of the TSH: The endocrinology specialty is unyielding in its endorsement of T4-replacement, and this appears to me to be a commitment to stabilize the financial market for the associated products of T4 replacement. Those products in the U.S. include Synthroid, and importantly, they also include the TSH, free T4, and free T3 tests provided by labs.

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.)

The endocrinology specialty's obvious financial conflicts of interest are a devastating blow to its credibility. In my mind, it has none left. I hold suspect anything and everything that flows from the mouths or pens of the specialty. And that certainly includes its scientifically-indefensible claim that TSH-suppressive doses of thyroid hormone are likely to cause cardiac arrhythmias. 

For documentation, see: Unrealistic Worries About Thyroid Hormone Therapy and Heart Problems: The Source.

August 17, 2004

Question: You explained somewhere on your website why hypothyroid patients have a slow heart rate response to exercise. I can't find the explanation now. I want to share it with my naturopath, so can you please help me find it? Thank you.

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.

If your doctor won't order thyroid antibody lab tests for you, order the tests yourself. In fact, order any lab test you want at discounted fees through our arrangement with Direct Labs. www.directlabs.com/drlowe

 

 

Our Educational Consulting Service We provide educational consulting to both patients and clinicians. Phone us at 603-391-6061, or preferably, write to us at  Tammy@drlowe.com. Our fax number is 303-496-6200. —Tammy Lowe

May 23, 2004

Question: I am a huge fan of your thyroid research. It’s because of your research that my doctor put me on Cytomel, which has changed my life. At age 17, I was diagnosed with thyroid cancer. My thyroid gland was removed and then I had radiation treatment.

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.