Some doctors unfortunately deny patients with delicate cardiovascular conditions any use of thyroid hormone. This is unfortunate because many of these patients can safely use and benefit from thyroid hormone; in fact, many cardiac patients must use thyroid hormone therapy to recover cardiac health.

I agree with this cautious approach except for two things. First, the company mentioned the patient reaching a euthyroid state. This implies using a thyroid hormone dosage that keeps the TSH, free T4, and free T3 within their reference ranges. Bringing these hormones into their reference ranges, however, does not render most patients well. At its website, Erfa tells what does: "The principal pharmacologic effect of exogenous thyroid hormones is to increase the metabolic rate of body tissues." The safest and most efficient way to help patients get well is to free them from their symptoms by normalizing their metabolic rates. Hence, rather than a euthyroid state, we should instead strive for a eumetabolic state.

What I next disagree with is the company's advice that some cardiac patients start treatment with a T4 product. These products may not work at all for many cardiac patients, regardless of the dosages they use. If the patient is hypothyroid, I recommend a T4/T3 product with a T4 to T3 ratio of 4:1, or T3 alone. Some T4/T3 products with the proper ratio are Armour Thyroid, Nature-Thyroid, and Westhroid. I prefer the latter two products for two reasons. First, an occasional patient reports to me that when she takes  Armour, she develops itching, which I assume is an allergic reaction. Switching to Nature-Throid or Westhroid relieves the itching. Second, the manufacturer of Nature-Throid and Westhroid, RLC Labs, goes to great lengths to ensure the quality, safety, and evidential basis of their therapeutic products. This is obvious in their description of how they formulate a variety of therapeutic products.

I always do an electrocardiogram (ECG) when I see patients personally. If I consult with a patient long distance, I also ask that he or she get an ECG from a local clinician and fax a copy of the tracing to me. I have two purposes for obtaining the ECG. First is to study the tracing for any evidence that aggressive thyroid hormone therapy is contraindicated. For example, my 12-lead electrocardiograph occasionally shows evidence of right heart damage and pulmonary hypertension in a patient who has used various weight-loss  drugs. Second is to see whether the voltage of the patient’s R wave is low. If it is, increasing voltage may serve as a useful physiologic barometer of metabolic improvement.

Erfa, in a statement I quoted above, suggests that thyroid hormone therapy may reveal "occult cardiac disease." This is true and important. Rarely, thyroid hormone therapy does unveil a cardiac problem that has been obscured over time by inadequate thyroid hormone regulation of the cardiovascular system. You mentioned that you have a copy of The Metabolic Treatment of Fibromyalgia. I recommend that you read the section on the heart (pages 875-888), especially the subsection titled "Worsening of the Manifestations of Coronary Heart Disease" on page 877. The entire chapter is about the safe use of thyroid hormone, but it’s the heart that most practitioners are concerned about. I address those concerns and explain how to avoid adverse cardiac effects in patients using thyroid hormone. Except in the rarest cases, patients with fragile heart conditions can use thyroid hormone. But, again, caution is the key.

Erfa also mentions other precautions I strongly agree with: "Thyroid hormone therapy in patients with concomitant diabetes mellitus or insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required."

Diabetes: I ask my patients to check their blood sugar regulation in two ways: (1) by taking several random measurements of their fasting blood sugar levels, and (2) by doing a 6-hour home glucose tolerance test (hGTT). These tests often show that a patient has glucose dysregulation. Some have fasting or reactive hypoglycemia, but most, in my clinical experience, have glucose intolerance.

In either case, too little glucose reaching a patient’s cells can cause what I view as an energy crisis. This occurs when thyroid hormone therapy accelerates intracellular energy metabolism by increasing a wide range of enzymes, but the increased energy demand conflicts with too little energy substrate in the form of glucose. Clinicians and patients often misinterpret the resulting symptoms as thyrotoxicosis. In fact, glucose dysregulation is the primary source of the symptoms. And the symptoms block the patient from using a fully therapeutic dosage of thyroid hormone.

Cortisol Deficiency: I recommend salivary testing for ruling out a cortisol deficiency. Bear in mind, though, that if a patient’s liver is underregulated by thyroid hormone, it may not clear cortisol from the body at a normal rate. The person’s adrenal cortices are producing too little cortisol, but the slowed liver clearance leaves the body fluids with a reference range concentration of cortisol. But as thyroid hormone increases the patient’s liver clearance of cortisol to a normal rate, the patient begins to develop cortisol deficiency symptoms. In this case, thyroid hormone therapy has unveiled an adrenocortical insufficiency. This phenomenon is similar to thyroid hormone therapy unveiling an occult cardiac disorder, which I mentioned above.

The precautions Erfa recommends are indeed important ones. However, in addition to those precautions, I also ask my patients to take two other precautions; that is, to  exercise and take nutritional supplements.

Exercise: I ask my patients to regularly engage in stretching, resistance, and cardiovascular exercise to tolerance. Some patients have especially low cardiovascular and muscular fitness. Despite their low muscle fitness, their muscles tend to be chronically too tight. Most of these patients must begin exercise with baby steps, increasing the intensity of their workouts only after light exercise and thyroid hormone therapy increase their tolerance for the three types of exercise.

Stretching is helpful in temporarily reducing the excess muscle tightness caused by low muscle energy from too little thyroid hormone regulation. Muscle bulking exercise is important because lean body mass is the only factor that increases the resting metabolic rate more than does thyroid hormone. And aerobic exercise gradually increases the patient's level of cardiovascular fitness. This makes the heart more resistant to adverse effects from a dosage of thyroid hormone high enough to enable the patient to get well.

Nutritional Supplements: Next, I ask each patient to take a wide array of nutritional supplements, especially B complex vitamins. The importance of this can hardly be overemphasized.

If a patient hasn’t been taking supplements, he or she may have borderline nutritional deficiencies. Many micronutrients function in cells as coenzymes. Thyroid hormone increases the production of many enzymes, causing a faster expenditure of their micronutrient coenzymes. When a patient doesn’t take nutritional supplements, as thyroid hormone accelerates his or her metabolic rate, borderline nutritional inadequacies may become severe deficiencies. A deficiency of some B complex vitamins, calcium, or magnesium can cause nervous system and muscle hyperirritability. Clinicians and patients may mistakenly believe that too much thyroid hormone is at fault. In fact, the patient isn’t even taking a fully therapeutic dosage of thyroid hormone.

A particularly harmful nutritional deficiency involves depletion of vitamin B1 from accelerated energy metabolism caused by thyroid hormone. The patient must regularly take in enough vitamin B1 to compensate for its increased intracellular expenditure. If he or she doesn't, a resulting B1 deficiency can cause beriberi-type cardiomyopathy—even though he or she is still taking too little thyroid hormone to recover from the hypothyroid symptoms.

Subject: About Thyroid Science
From: Anonymous Reader
Date: Thu, June 19, 2008 10:21 am
To: Editor@thyroidscience.com

Dear Editor: I have been taking Eltroxin then later Synthroid since 1974. I discovered Thyroid Science just today. It is apparently a new publication? I would like information regarding the journal. Thank you

Dear Reader: Thyroid Science is an open-access electronic journal started a couple of
years ago by Dr. John C. Lowe's publisher, McDowell Publishing Company,
LLC. It is committed to providing a publishing outlet for scientifically-oriented patients, clinicians, and researchers whose writings are usually censored by conventional endocrinology journals. The latter journals usually publish only papers that, as Dr. Lowe says, favor the financial interests of the drug companies that advertise in the journals. For all practical purposes, he says, those journals are ruled by adverting drug companies with the complicity of the endocrinology specialty. In contrast to those journals, Thyroid Science is dedicated to publishing papers without censoring their content to facilitate  commercial interests. You are welcome to read anything published in Thyroid Science, and, if you wish, to contribute to the journal. I hope this answers your question.

Sincerely,
Tracy Majors
Assistant Editor
Thyroid Science (www.ThyroidScience.com)

Subject: Fine-needle aspiration and thyroid hormone resistance
Date: February 23, 2008
To: Editor@ThyroidScience.com
From: peter.warmingham@whsmithnet.co.uk

Dear Dr. Lowe: Are you aware of the paper by E Tjørve, KMC Tjørve, JO Olsen, R
Senum, H Oftebro titled "On commmonness and rarity of thyroid hormone
resistance: A discussion based on mechanisms of reduced sensitivity in
peripheral tissues" (Medical Hypotheses, (2007) 69, 913-921)? In it the
authors call for a test for peripheral resistance. Since the standard thyroid function blood tests don't serve this purpose. which of course the standard thyroid function blood tests don't. Maybe the fine-needle aspiration (FNA) technique used by Dr Bo Wikland and his colleagues would fit the bill? 

Peter Warmingham, Thyroid UK Committee

Dear Peter: I have read the E Tjørve paper. I was pleased that Dr. Tjørve and his coauthors mentioned measuring the basal metabolic rate as a method for testing for resistance. I have used the test in my clinical practice for several years and published two studies so far using the method:

Report at Medical Science Monitor:

http://www.medscimonit.com/abstracted.php?level=4&id_issue=40182

(When you reach the page at Medical Science Monitor, scroll down to the second paper under "Clinical Research".)

Report at Thyroid Science: http://www.thyroidscience.com/studies/lowe.2006/lowe.2nd.rmr.fms.htm

Along with Tjorve et al, I believe that the basal or resting metabolic rate measurement is most useful clinically for identifying resistance patients, at least those with peripheral resistance. (Having peripheral resistance, of course, means that a patient's pituitary gland is normally or almost normally responsive to thyroid hormone, but most tissues peripheral to the pituitary are partially resistant.) Dr. Wikland’s FNA identifies patients who have autoimmune thyroiditis despite reference range antithyroid antibody levels. Most of the patients are hypothyroid, which is the reason he and his colleagues term the disorder “subchemical hypothyroidism.”

Some of these patients may also have peripheral resistance. But if they improve or recover with doses of thyroid hormone that are lower than supraphysiologic amounts, that would indicate that they are only hypothyroid and not resistant.

Most thyroid hormone resistance patients have to use supraphysiologic dosages of T3 to get well. Even T4/T3 products such as Armour usually don't work for them, not unless they use huge dosages, such as 12 grains or more. I have a book published in 1962 written by an endocrinologist—an endocrinologist from the time when many of them practiced clinical medicine rather than the extremist technocratic medicine of most endocrinologists today. In the book, the endocrinologist wrote that some of his “hypothyroid” patients didn't recover until they took as much as 60 grains of desiccated thyroid per day. I assume those patients really had peripheral resistance, as that amount would contain roughly 540 mcg of T3. That's truly a supraphysiologic daily dosage!

As I have, Dr. Wikland has found that most hypothyroid patients must suppress their  TSH levels before they recover. I don't know the dosages his patients typically use, but if some of them use dosages that are well into the supraphysiologic range, the patients are probably partially resistant to thyroid hormone.

I use the following criteria to diagnose peripheral resistance: the patient has before treatment (1) hypothyroid-like symptoms before treatment, (2) reference range TSH and thyroid hormone levels, and (3) an abnormally low resting metabolic rate; and after treatment, he or she (4) recovers from his or her symptoms with a supraphysiologic  dosage of plain T3 (5) with no evidence of thyrotoxicosis.

There are laboratory methods for testing for resistance. For example, we can use fibroblasts from a patient’s skin. If a supraphysiologic amount of T3 is needed to inhibit the fibroblasts' synthesis and secretion of connective tissue constituents such as fibronectin, then the patient's cells (at least his or her fibroblasts) are resistant to thyroid hormone. I don’t use this particular test for two reasons: first, it isn't available commercially; and second, even if it was, it requires a painful punch biopsy of the skin that I would prefer not to subject patients to.

To sum up, Dr. Wikland's FNA can certainly identify patients who are hypothyroid due to autoimmune thyroiditis. However, the procedure would not identify or rule out peripheral resistance to thyroid hormone.

Dr. John C. Lowe
Editor-in-Chief

Subject: Re: Thyroid Science: Jan. 18, 2008, New Publications
Date: Fri, January 18, 2008 4:53 pm
To: Editor@ThyroidScience.com

Dear Dr. Lowe:  Dr. Bo Wikland's paper (regarding treating euthyroid Hashimoto's patients with thyroxine) is unbelievably timely. I am seeing my doctor for the first time in over a month. I will be getting the results from my last full thyroid panel and hope to see a lowered antibody count.

I recently dosed up to 120mg of Armour and remained on the dose for three weeks prior to testing. At this point I need to bring my doctor up to date on what I've been trying to accomplish. I'm now up to 150mg of Armour and with the addition of Cortef to my program believe I may be beginning to get the improvement that I hoped for.

As my doctor views me as a "euthyroid Hashimoto's patient," it will be helpful to come armed with research as I try to get him onboard with my current strategy. My doctor and I have a good working relationship, and we go back many years. He's a long standing alternative doc and a good listener—so I am cautiously optimistic that all will go well. Thank you again for all that you, Tammy, and your staff do. Regards . . .

Dear Chris: I hope you're doctor responded well to Dr. Wikland’s paper. One of our purposes at ThyroidScience.com is to provide patients like you with publications by experts in the thyroid field whose publications are often truncated and placed in inconspicuous places in endocrinology journals, or rejected for publication altogether to avoid offending the journals' advertisers—usually ones that profit from T4-replacement therapy. I appreciate you writing. Your email lets us know that we're on the right track in publishing ThyroidScience.com.

Dr. John C. Lowe
Editor-in-Chief