DIAGNOSIS AND TREATMENT OF HYPOTHYROIDISM: MYTHS, MAGIC, AND MISCONCEPTIONS

Recently, I have been contacted by a number of acquaintances, all of whom have been diagnosed with hypothyroidism.  That in and of itself is not so strange; hypothyroidism is acually quite common, especially in women, and mostly due to chronic lymphocytic thyroiditis, aka Hashimotos thyroiditis.  The strange thing was what they told me about their medical histories.   All of them had been diagnosed with hypothyroidism in their 20’s.  They presented with fatigue, weight gain, and depression (I do not think any of them had a mood disorder such that a psychiatrist would have called it depression).   Anyway, I do not know how the diagnoses of hypothyroidism were made and what the various etiologies were.  I do know that each of these people were initially treated with Synthroid, the most widely-used  brand name of L-thyroxine or T 4.   After a few months of treatment, none of the people felt any better.  For that reason, their doctors switched them to Armour thyroid and Cytomel, brand names for desiccated thyroid and triiodothyronine, liothyronine,  or T 3 (the 3 means that the compound has 3 iodines attached- guess what the 4 in T4 means?).  Within a few weeks, all of the people felt much better and they have remained on the Armour/Cytomel mixtures for quite a number of years.  All of them are convinced that Synthroid doesn’t work for them.

A few weeks ago, one of the people, Susan, came to me very upset and asked if I would review some thyroid lab tests she had obtained recently.  The tests were performed as part of a routine health care check-up with a new doctor (her previous doctor had recently moved away).  The test results showed unmeasurable serum TSH, and both elevated free T4, and T3 levels.  The doctor recommended that Susan stop the Armour and Cytomel and come back for a follow-up blood test in 6 weeks.  Susan explained to me (through her tears) that there was no way she could make it 6 weeks since she had already gained 10 pounds and had much less energy.  She was particularly upset that the doctor told her that depending on the follow-up test results she might or might not need treatment with thyroid hormone; if she did need treatment with thyroid hormone, it would be with Synthroid or the generic equivalent, not Armour and Cytomel.  So, what is this all about?  Was the doctor’s approach correct or was Susan being treated appropriately before her visit to the new doctor?

Back to Basics

First of all, the thyroid gland synthesizes two major hormones, T4 and T3.  If the thyroid gland were in an automoboile, it would be the gas pedal, controlling the speed of the vehicle.  In much the same way,  T4 and T3 control the basal metabolic rate, more or less, how fast the body runs.  Too much circulating thyroid hormone, and the body “drives” too fast; to little, and the body goes about its business at a very slow pace.  Normally, we don’t have to do anything to be certain our bodies are moving along at just the right speed.  This is how the system works (if you are already, very familiar with this stuff, just speed-read it).  Up in the brain, the hypothalamus sends hormone signals (thyroid-releasing hormone or TRH) to the pituitary gland telling it to whether to send signals to the thyroid gland (via the hormone  thyroid-stimulating hormone TSH, also called thyrotropin) to increase production of T 4 and T3.  If the blood level of T4 or T3 is too low, the thyroid gland is stimulated to produce enough T4 or T3 to achieve normal blood levels.  It is what is called a classic negative feed-back system, one that is very common with endocrine glands.  It is really like the thermostat in my living room that will do its best to keep the temperature in my living room at whatever temperature I set.

Actually, it is a bit more complicated than what I implied above.  The thyroid gland “factory”  produces mostly T4 and only a small amount of T3 (about 20% of the total hormone production); most T3 is synthesized from T 4 in various body tissues, particularly the liver.  T3 is actually the predominant active thyroid hormone.  But the body is so smart that it can even “adjust” the amount of T3 which is made from T4, based on the blood level of T3; the body can make either T3 from T4 or an inactive hormone, reverse T3 (it is called reverse T3 because although there are 3 iodines on the compound, they are arranged differently than on the “real” T3).

The Bottom Line

What this all means is that in patients with hypothyroidism, it is not necessary to treat them with T3, the active hormone, since giving them T 4 will do the trick unless they have a very, very rare genetic disease in which a person cannot convert T 4 into T3 (this condition is typically diagnosed in early infancy and has very serious consequences for the patient).  Also, it is not necessary to treat them with a mixture of T4 and T3, which is what desiccated thyroid contains.  Nor is it necessary to treat  them with desiccated thyroid and T3, which is what Susan was being treated with.  In Susan’s case, her treatment actually had made her hyperthyroid.  That is why she “felt better” on the earlier treatment.   Her overtreatment made it far easier for her to keep from gaining weight and helped with her energy level (hyperthyroid = hyperactive).  Unfortunately, hyperthyroidism, whether it is caused by an overactive thyroid gland or by too much medication, is not good for a person.  It can cause hypertension, cardiac arrhythmias, and osteoporosis and many other health problems.

I forgot to tell you anything about desiccated thyroid.  It is ground up animal thyroid, all from pigs these days and is FDA-approved to treat hypothyroidism.  It was first used in the 1800s and was an incredible medical advance.  When I started treating patients with hypothyroidism, desiccated thyroid was the drug of choice.  These days, it has a set amount of T4 and T3 (80-20 mixture) and works, but I find it hard to understand why it might be better to take ground up pig thyroid (of each 60 mg tablet, more than 59 mg is non-thyroid hormone pig parts) than synthetic T4.  I do not know of any reputable studies that have shown any benefit (or harm) from using desiccated thyroid rather than synthetic T4, which is identical to the T4 synthesized in the thyroid gland..  The only “studies” I have seen are basically testimonials from patients swearing that they didn’t get any better on T4, but that all of their symptoms disappeared after they started the desiccated thyroid.  You would be amazed at the stuff on the internet!  I would only say that health care professionals who prescribe dessicated thyroid, and particularly those who prescribe T3,  need to make certain that a patient’s improvement on desiccated thyroid (with  or without the addition of synthetic T3), is not because the patient has iatrogenic hyperthyroidism (like Susan).

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