One of the outstanding deficiencies in thyroidology is well conducted studies of Quality of Life (QoL) against FT3 levels in T4 treated patients. A recent study (Pol. Arch Med. Wewn 2016; 128 (4) 293-296, doi: 10 20452/parriw.3392) has shown very clearly that there is a strong relation between T4 dosage (thus FT3 production) and QoL. It further shows that in a few subjects FT3 does not rise when T4 dose is increased and thus such people would benefit from T3 supplementation.. This is a very well conducted prospective study. It shows clearly that TSH levels should not be much of a concern in setting a dose level for better QoL and that many subjects had below range TSH to get there. Though this is only a small paper, it is of major significance in the battle to understand and treat thyroid deficiency more effectively.
If you cannot access the paper direct, then I've sent Louise Warvill a copy.
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It's an open access journal. Type in Pol. Arch.Med. Wewn and the appropriate archive websites come up. You just have to wade through to find the right issue.
This study selected those patients who still had symptoms, about 10%. They had average fT4 16.52 (11.5 - 21.0), fT3 3.94 (3.9 - 6.7). Furthermore 18 were Hashimoto's, 11 thyroidectomized and 8 RAI. It's pretty dreadful that these patients, many without active thyroid tissue should have been so undermedicated, average 79 mcg L-T4. This is not unique to Poland, we see many posts on this forum where patients are told to go away when there TSH drops to e.g. 4.5. The patients improved with fT4 19.76 (11.5 - 21.0) and fT3 4.67 (3.9 - 6.7).
A disadvantage of this study is that it was not placebo controlled. They did however find correlations with fT3 and fT4 levels. It is unlikely that patients would modify their placebo response according to fT3 and fT4 levels.
The authors referred to a Saravanan paper which only found correlations with fT4. They suggest this might be due to the Total Symptoms Questionairre used by Saravanan. I suspect it is due to differences in the studies. Saravanan selected a broad range of subjects, all of whom were on at least 100 mcg L-T4. This latest study was restricted to patients who still had symptoms, consequently it would be easier to achieve statistical significance in this specific group. Furthermore, the subjects in this study were quite obviously undermedicated, 79 mcg L-T4 is not sufficient for patients without a thyroid gland.
I suspect that in patients receiving adequate L-T4 there may not be a simple link with QOL and fT3. This is because as fT4 rises above the upper limit of the reference interval type-1 deiodinase activity increases leading to higher rT3 levels.
It must be true that when QoL is maximum, it will not correlate with FT3. This is because having reached optimum, the natural patient variation in FT3 achieving that optimum will now predominate and randomise the sample correlation. Only in cases of insufficient (and too much?) T4 dosage will the correlation kick in. Overdosage of course will elevate rT3, since the body is suffering overload and gets rid of some of the excess that way.
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Does T3 always suppress TSH?
TSH, FreeT4 & Free T3
