Dr. John E.M. Midgley, one of the study's researchers, was interviewed by Thyroid UK and stated the following:
"What it proves is that there is no such thing as a TSH range that is suitable for everyone, and that the range is different according to the effect of independent influences such as age, body mass, size of working thyroid volume and whether someone is on T4 or not.
The T4 therapy range is very much lower than the "normal" untreated and sits around the 1 or lower mark. The 3-4 upper level that works for the normal person is not satisfactory and can indicate undertreatment.
Also we're finding that people with no thyroid working at all cannot easily regain normal FT3 with T4 alone and that TSH suppression often has to happen, and in some people no amount of T4 will regain normal FT3 levels. Recent reviews by the gurus now admit that some people cannot handle T4 only and regain health. Just thought you'd like to know that the avalanche is beginning."
The study's findings are listed below and were originally reported here. To download the full paper in PDF format, please click here.
Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment
Rudolf Hoermann*, John E.M. Midgley†, Adrienne Giacobino*, Walter A. Eckl*, Hans G€unther Wahl‡,
Johannes W. Dietrich§ and Rolf Larisch
Article first published online: 7 JUL 2014
We examined the interrelationships of pituitary thyrotropin (TSH) with circulating thyroid hormones to determine whether they were expressed either invariably or conditionally and distinctively related to influences such as levothyroxine (L-T4) treatment.
Design and methods
This prospective study employing 1912 consecutive patients analyses the interacting equilibria of TSH and free triiodothyronine (FT3) and free thyroxine (FT4) in the circulation.
The complex interrelations between FT3, FT4 and TSH were modulated by age, body mass, thyroid volume, antibody status and L-T4 treatment. By group comparison and confirmation by more individual TSH-related regression, FT3 levels were significantly lower in L-T4-treated vs untreated nonhypothyroid autoimmune thyroiditis (median 4·6 vs 4·9 pm, P < 0·001), despite lower TSH (1·49 vs 2·93 mU/l, P < 0·001) and higher FT4 levels (16·8 vs 13·8 pm, P < 0·001) in the treated group. Compared with disease-free controls, the FT3-TSH relationship was significantly displaced in treated patients with carcinoma, with median TSH of 0·21 vs 1·63 (P < 0·001) at a comparable FT3 of 5·0 pm in the groups. Disparities were reflected by calculated deiodinase activity and remained significant even after accounting for confounding influences in a multivariable model.
TSH, FT4 and FT3 each have their individual, but also interlocking roles to play in defining the overall patterns of thyroidal expression, regulation and metabolic activity. Equilibria typical of the healthy state are not invariant, but profoundly altered, for example, by L-T4 treatment. Consequently, this suggests the revisitation of strategies for treatment optimization.