Hypothyroid patients often ask me whether I think they are actually resistant to thyroid hormone rather than hypothyroid. They usually ask after undergoing treatment with a T4/T3 product, such as Armour, that hasn’t gotten them completely well.

My answer to patients often differs. One reason is that the factors differ that I must consider in formulating an opinion. So many patients ask this question, though, that I believe our readers may find it interesting to consider one case, and the factors that I had to consider to come to a conjecture for her.

The patient in question had come to our clinic for a full metabolic evaluation. Every physiologic test gave abnormal results: Her resting metabolic rate was 42% below normal; her basal body temperature was 96.9 F (36.06 C); the voltage of her electrocardiogram was low; and the relaxation phase of her Achilles reflex was abnormally slow.

She also had classic symptoms of hypothyroidism. These included chronic back pain, fatigue, stiffness, coldness, anxiety, and intolerance of exercise. And she hadn’t had a menstrual period for more than two years. (In 2005, an endocrinologist had diagnosed the cause of her amenorrhea as thyroiditis, but he didn’t prescribe treatment.)

Laboratory test results were revealing: her cholesterol and LDL were high, and her thyroglobulin antibodies and especially her thyroid peroxidase antibodies were very high. Yet her TSH, free T3, and free T4 were "normal."

I did a deductive differential diagnosis to eliminate the possibility that anything other than autoimmune-induced hypothyroidism was the cause of her abnormal test results and symptoms. This deductive process showed only one rational conclusion: she was suffering from severe hypothyroidism caused by active autoimmune thyroiditis.

The year before, a doctor had treated her with 50 mcg of Synthroid. As any observant clinician with an open mind would anticipate, this treatment failed her.  Before she consulted me, another doctor treated her with 90 mg of Armour Thyroid. Armour, of course, is vastly superior to Synthroid. Nonetheless, the 90 mg of Armour left her with low metabolism, other abnormal test results, and troubling hypothyroid symptoms.

Knowing that this dosage range is safe for the vast majority of patients, I advised the patient’s doctor to increase her dosage of Armour. The doctor cooperated. At 150 mg (2.5 grains), she had improved. Her basal temperature had increased from an average of 96.9 F (36.06 C) to 97.45 F (36.36 C). Also, at long last, last month she had a menstruated. Her thyroglobulin level decreased from 35 to 31, and her thyroid peroxidase antibodies decreased from 703 to 573. Her exercise intolerance still depressed her somewhat, but now she could also exercise some; for example, unlike before, she was exercising by walking, and she had lost 2 lbs. She denied any indication of thyroid hormone overstimulation.

Then came the question I hear so often: "Do you think I’m resistant to thyroid hormone?" I got the impression that she asked the question because her doctor was concerned that her low TSH (0.03 mU/L) indicated that she was taking too much Armour. The implication, of course, would be that if she’s taking too much thyroid hormone and has improved so little, then maybe she’s thyroid hormone resistant.

I did some quick calculations and then told her that I see no reason at this point to think she is resistant. She may turn out to have some degree of resistance, but for now, its clear only that she’s hypothyroid. I say this because her dosage is only a short distance into the dosage range that, before lab tests came to dominate doctors’ decisions, was known to be safe and effective for patients. With that dosage (150 mg), she has improved somewhat. Of course, to fully recover, she may have to proceed—as many patients traditionally did—to 175 mg, 200 mg, or even a higher dosage.

I explained my reasoning to her: Most resistance patients don’t improve or recover with T4. They do so only with T3, and then only with fairly high doses. Her dosage of 150 mg of Armour contains 95 mcg of T4, but that’s really of no relevance to the question of whether she’s resistant. Few if any resistance patients improve with T4 therapy no matter how high their dosages.

The 150 mg of Armour, however, contains 22.5 mcg of T3, and that is relevant to the question of resistance. If she is resistant, chances are that the T4 was not responsible for her improvements. At the same time, the 22.5 mcg of T3 she was taking was too little to give a resistance patient the improvements she’d gotten so far. Most patients have to take far more T3 to improve or recover.