Dr Lowe Q & A Central Hypothyroidism
October 28, 2005
Question: I have some of the hypothyroid symptoms you list on your website. They aren’t severe but they’re strong enough to be annoying. I have a very healthy lifestyle, take vitamins, and exercise every day. Because of that, I disagree with the doctors who’ve told me that my symptoms are lifestyle related. Several doctors have tested me for hypothyroidism. My T4 and T3 levels are in the lower part of the normal range, but my TSH is always low. The doctors tell me I shouldn’t take thyroid hormone because my TSH shows that I’m hyperthyroid. If that’s true, why do I have symptoms of the opposite condition, hypothyroidism?
Dr. Lowe: Hyperthyroid patients do have low TSH levels, but a low TSH definitely does not always mean that a patient is hyperthyroid. In fact, despite your low TSH, you may be hypothyroid. If so, that will explain your hypothyroid symptoms.
We see this lab test pattern among patients who have “central hypothyroidism.” In this disorder, the patient has a thyroid hormone deficiency because her TSH is low. The TSH is low because of a problem with either the hypothalamus or pituitary gland. The hypothalamus normally sends the hormone TRH to the pituitary gland, stimulating it to secrete TSH. TSH then passes through the blood to the thyroid gland and stimulates it to secrete the thyroid hormone. But if the hypothalamus or pituitary gland dysfunctions for some reason, too little TSH may be secreted to properly regulate the thyroid gland. If so, the patient may have low or low-normal thyroid hormone levels, and her TSH level will also be low. An understanding of central hypothyroidism makes it clear that we can’t rule out hypothyroidism based on a low or low-normal TSH level.
We’ve had many patients with central hypothyroidism who suffered for years because their doctors falsely believed that their low TSH levels meant they were hyperthyroid. The doctors ignored the fact that the patients had clear-cut symptoms and signs of hypothyroidism.
Incidentally, that your symptoms aren’t severe but are mild or moderate is consistent with central hypothyroidism. As a group of Italian researchers pointed out, the symptoms and signs of patients with central hypothyroidism are usually milder than those of patients with “primary hypothyroidism” (thyroid hormone deficiency due to a problem with the thyroid gland itself).
In your circumstance, I think the best course of action is to get your resting metabolic rate measured. If its abnormally low, factors other than hypothyroidism may account for it. For example, calorie restriction, a testosterone deficiency, or lose of muscle mass may be responsible. If you rule out these and other such factors, then chances are you have central hypothyroidism. It will be useful for you to also undergo other tests to see if the results support the diagnosis. For example, low voltage of the QRS complex on an EKG is consistent with hypothyroidism.
Clearly, for doctors to depend only on TSH levels to rule out hypothyroidism can be a disservice to patients. You may learn that you’re among these disserved patients if you follow through with the testing Ive suggested.
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2. Tanaka, Y., Sawa, H., Inden, M., et al.: A case of idiopathic hypothalamic hypothyroidism. Jpn. J. Med., 20(3):222-226, 1981.
3. Ichida, T. and Kajita, Y.: A case of idiopathic thyrotropin (TSH) deficiency. Korean J. Intern. Med., 12(1):96-99, 1997.4. Miyai K.:Pituitary hypothyroidism. Ryoikibetsu Shokogun Shirizu, (1):190-193, 1993.
5. Collu, R.: Genetic aspects of central hypothyroidism. J. Endocrinol. Invest., 23(2):125-134, 2000.
6. Hershman, J.M.: Hypothalamic and pituitary hypothyroidism. In Progress in the Diagnosis and Treatment of Hypothyroid Conditions. Edited by P.A. Bastenie, M. Bonnyns, and L.VanHaelst, Amsterdam, Excepta Medica, 1980, pp. 40-50.
7. Asteria, C., Persani, L., and Beck-Peccoz, P.: Central hypothyroidism: consequences in adult life. J. Pediatr. Endocrinol. Metab., (14 Suppl) 5:1263-1269, 2001.
April 15, 1998
Question: After reviewing your T3 protocol for fibromyalgia, my endocrinologist agreed to put me on trial of Cytomel at 25ug/day. Six weeks later my fibromyalgia fog was beginning to lift and I could tell I was feeling better, but my TSH test fell to near zero on Cytomel and he took me off for about 2 weeks. My FM symptoms regressed. I convinced him to redo the blood work asked him to include T4, TSH, and T3 to prove to him that I was not “hyperthyroid” on T3.
He agreed, and this time he found my T4 and TSH near zero and my T3 very low. He agreed to put me back on Cytomel and retested for T4, T3, and TSH after 3 months. This time both T4 and TSH were nearly undetectable and T3 was normal, but I was beginning to feel much better. Much of my soreness was greatly reduced and most of my tingling (paresthesia) was gone. I was still easily fatigued physically and mentally, but I could tell I was much improved. My chiropractor measured only 3 of 18 FM pressure points!
Following this last thyroid test, my endocrinologist said my tests were more consistent with central hypothyroidism and that my TRH stimulation test had only been barely normal, and he put me on full thyroid treatment. Thankfully, my MRI was normal. Remarkably, he agreed to keep me on 25ug Cytomel since I was doing so much better and added 25mg Synthroid.
Although these levels are relatively low, I am feeling nearly normal. But, I’d like a little more improvement. At my last blood test a couple of weeks ago my TSH was 0.22, T4 was 1.07, T3 was 157 all indicating my T3/T4 medicine was doing well. My endocrinologist now – believes that I have had fibromyalgia/stress induced central hypothyroidism since my pituitary appears to be normal on the MRI and it is functioning normally with regards to its other hormone systems. He’s continuing Cytomel and Synthroid and plans to check my blood levels every 6 months for the next couple of years. He then would like to withdraw the T3 and T4. Is it reasonable that I could withdraw and be healed of FM and hypothyroidism?
Could my Synthroid and/or Cytomel be increased above 25mg and 25ug without overtreating me into “hyperthyroidism”? Is my T4 of 1.07 “optimal” (T4 test range 0.70-1.85)?
Thanks for your help.
Dr. Lowe: It is not likely that your central hypothyroidism was stress-induced. The high incidence of primary and central hypothyroidism in fibromyalgia patients is often dismissed as merely “stress-induced.” It is improbable, however, that this mechanism accounts for long-lasting fibromyalgia manifested as hypothyroid symptoms especially when the – symptoms last for more than a few weeks.
During stress (such as surgery or an auto accident), the adrenal glands increase their secretion of cortisol. The increase in cortisol inhibits the thyroid system in two ways: (1) it decreases TSH secretion by the pituitary gland, and (2) it decreases conversion of T4 to T3. However, these thyroid-inhibiting effects last only a few weeks at most. Despite Dr. Dennis Wilson’s claim that impaired T4 to T3 conversion becomes “stuck,” there is no evidence to justify this speculation. The available scientific studies and my laboratory testing deny that this occurs. Instead, that the thyroid-inhibiting effects of stress are a brief phenomenon has been well-documented. Even when a patient takes cortisol as a medication (such as prednisone) for months, full TSH secretion and conversion of T4 to T3 “recover” to normal within a few weeks. Because of this, it is not likely that “stress” sustained your symptoms over a prolonged time. I would predict that your symptoms would soon return if you were to stop taking exogenous thyroid hormone.
This leads to the question: What may account for your central hypothyroidism? Your normal MRI (presumably of your pituitary gland) rules out structural abnormalities, such as tumors or atrophy of the gland. But your pituitary may fail to synthesize enough TSH because of other abnormalities that cannot be detected by an MRI. For example, gene transcription for TSH mRNA may be impaired, possibly because of one or more mutations of the TSH subunit genes. This would result in abnormally low TSH synthesis and secretion. Verifying such abnormalities is technically difficult now, but such an abnormality would make it likely that you will always have to take thyroid hormone to maintain your improved state.
Regarding your dosage, keep in mind that the point to taking thyroid hormone is to normalize tissue metabolism. Unfortunately, blood levels of thyroid hormones and TSH are not measures of tissue metabolism. They are an assessment of the interaction of the pituitary-thyroid gland axis, and nothing more. (This assessment is helpful in diagnosing an untreated patient’s thyroid status. It is, however, useless as a gauge for adjusting dosage.)
There is no good evidence that the blood levels of these hormones correlate well with tissue metabolism. Because of this, if your goal is normal metabolism, the “optimal” blood levels of T3 and T4 must be determined on an individual basis. This is accomplished by adjusting your dosage so as to provide optimal health without tissue overstimulation. Imposing a predetermined blood level on an individual patient usually results in a poor clinical outcome.
The only effective method for most patients is for the clinician to abandon the blood tests altogether and adjust the dosage according to measures of tissue metabolism.