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Transcript
For Physicians of
Patients Taking
Thyroid Hormones
I have prescribed thyroid hormone for your patient because his/her symptoms, physical signs,
and/or blood tests suggested that he/she had inadequate levels for optimal quality of life and longterm health. Mild-to-moderate thyroid insufficiency, often secondary in origin, is common and is
causes of depression, fatigue, weight gain, high cholesterol, cold intolerance, atherosclerosis, and
fibromyalgia. Effective thyroid optimization can help with all these problems.
I have prescribed natural dessicated thyroid for your patient (Armour or Nature-Throid). These
products contain T4 and T3 (40mcg and 9mcg respectively per 60mg). They are more effective
than T4 therapy for most patients. Since they provide more T3 than the thyroid gland produces,
the well-replaced patient’s free T4 will be around the middle of its range or lower, and the FT3
will be high-“normal” or slightly high before the next AM dose. If your patient had clear
improvements on TRT, I continued the therapy, adjusting the dose by symptoms and free thyroid
hormone levels, not by the TSH level. Your patient’s TSH may be low or undetectable. This is
not hyperthyroidism as the free T4 and Free T3 levels are normal 24hrs post dose.
I know that the standard approach to thyroidology is to use the TSH to both diagnose and treat
hypothyroidism. The approach is, however, a practice of convenience, even of ignorance. It is not
supported by any evidence—the best evidence actually argues against using the TSH in this way.i
Clinical medicine, and medical ethics require us to make the diagnosis of thyroid insufficiency,
and the determination of replacement dosing, based upon the patient’s symptoms first, and on the
free T4 and free T3 levels second. The TSH is an indirect test of no help unless it remains high.
Also, the labs’ reference ranges for free T4 and free T3 are not optimal ranges; but only 95%inclusive statistical population ranges, often including physician-ordered results. The lower limit
for free T4 seen in studies of health adults is 1.0ng/dL, not 0.8 or 0.6 as reported by many labs.
Studies show, and I have found that T4-only therapy (Synthroid, Levoxyl), to merely
“normalize” the TSH is inadequate therapy for most persons. The person may have some H-P
axis hypoactivity to begin with, and it’s clear once-daily oral dosing over-suppresses TSH
production. TSH-normalizing T4 therapy often leaves both FT4 and FT3 levels relatively low,
and the patient symptomatic. Recognizing this, NACB guidelines call for dosing T4 to keep the
TSH near the bottom of its RR (<1) and the FT4 in the upper third of its RR; but even this may
not be sufficient. The ultimate criterion for dose adjustment must always be the clinical response.
Excessive thyroid dosing causes many negative symptoms, and overdosed patients do not feel
well. I suggest lowering the dose in any patient who has developed insomnia, shakiness,
irritability, palpitations, overheating, excessive sweating, etc. The most serious problem that can
occur is atrial fibrillation. It can occur in susceptible patients with any increase in their thyroid
levels, and is more likely with higher doses. It should not recur if the dose is kept lower than their
personal threshold. Thyroid hormone does not cause bone loss, it simply increases metabolic rate
and therefore the rate of the current bone formation or loss. Menopausal women are losing bone.
The solution is to correct the sex steroid, DHEA, Vitamin D, and growth hormone deficiencies.
i
Fraser WD et al., Are biochemical tests of thyroid function of any value in monitoring patients
receiving thyroxine replacement? Br Med J (Clin Res Ed). 1986 Sep 27;293(6550):808 -10.
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