Dr. Rudolf Hoermann, MD and PhD is a leading thyroid researcher, German endocrinologist and author of more than 100 publications. He has collaborated with two co-authors, Mel L. Rowe, and Peter S. Warmingham, to compile an excellent document published on the ThyroidUK website that covers many of the topics in our rationale. This is some of what they propose as a reasonable and flexible treatment strategy:
If hypothyroidism is diagnosed, the patient’s FT4 and FT3 levels should be increased enough to eliminate signs/symptoms of hypothyroidism without creating signs/symptoms of hyperthyroidism.
TSH should not be relied on to determine the medication dosage. [33 (p. 2)]
The aim of dose determination for a patient should be to get the patient on the required or optimum dose as quickly as possible. Dose and timing may vary by individual needs.
In an otherwise healthy patient the initial dose can be higher, whereas a patient with a history of cardiac problems may need more gradual and careful titration of the L-T4 dose under close clinical supervision.
Major determinants would be the presence of a residual thyroid gland or the size of the remnant, with athyreotic patients requiring a higher dose, and the weight or BMI of the patient. Some sets of rules have been proposed which may serve as an initial crude estimate to predict the final dose, which would equal the starting dose in unproblematic situations.
Dose adequacy should then be assessed and adjusted as needed, with relief of symptoms being the main concern.
While severe symptoms and free thyroid hormones may respond more quickly – within a month or so – achievement of final symptomatic relief may take several months, as time is needed for the body to heal.
As for TSH, it takes 6 to 8 weeks after initiation of treatment or change of the L-T4 dose until it reaches equilibrium levels with the peripheral hormones. Intermediate measurements are therefore of little value.
Contrary to widespread practice, TSH should not be relied on as the dominant determinant of treatment success or main gauge of dose adequacy; the equilibria established in a healthy population do not equally apply and are therefore not transferable to patients taking replacement thyroid hormone. This phenomenon, which has been long known to practitioners, has recently been documented by large clinical studies. [33 (p13)]
The response to a given hormone level as defined by measuring thyroid hormones in the circulation may be subject to variation and modification by various influences that determine the thyroid hormone tissue effects. Those influences may be genetic, but also include age, body weight, environmental temperature, toxic chemicals and many others. [33 (p.14)]
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