Is it Safe for TSH to Be Low or Suppressed on Thyroid Treatment – Research

I often get asked the question of whether it is safe to have zero (or suppressed TSH) when on T4/T3 treatment (or any thyroid treatment).

The research is very clear, but I wish more doctors and endocrinologists were aware of this research!

A suppressed TSH when on thyroid treatment is NOT a concern at all, as long as:

  • The person has no hyperthyroid symptoms and
  • FT3 is not above the range (but this last point also has caveats).

The above statement is true on T4, and I will provide the research references below to back it up.

What about T4/T3 or T3-Only therapy?

On any T4/T3 based treatment, I believe FT3 can creep up to and over the range also. There is a very clever but a little complicated explanation for this. It goes like this:

People who are healthy, or on T4 medication, have on-going T4-to-T3 conversion happening within their cells. Much of this intra-cellular-T3 that is converted from T4 remains in the cells and is used there. Little gets returned to the bloodstream. This is an IMPORTANT point. The FT3 population reference range is created by measuring blood levels of FT3.

So, for people who are healthy, or on T4-therapy, they have the FT3 that can be measured. However, they also have the EXTRA FT3 that is being constantly converted from T4 within their cells.

So, the FT3 reference range does not account for the extra intra-cellular FT3.

As soon as someone uses T4/T3 treatment or NDT, they have extra T3, but usually less T4 than previously had. So, the FT3 measured in blood is almost certainly going to be higher for someone on T4/T3 therapy than someone on T4 treatment. There will also be less intra-cellular T3 being converted from T4. The net result is that T4/T3 therapy patients are much more likely to have a higher FT3 – possibly close to the top of the FT3 reference range.

The thyroid lab ranges have not been developed based on a population of thyroid patients who are on some T3 – so this should not be a surprise.

The situation gets a whole lot worse for people on T3-Only. They have NO intracellular T4-to-T3 conversion at all. Their FT3 level is often well over the range. This is necessary in order to compensate for the lack of intracellular T4-to-T3 conversion.

Our UK reference range for FT3 is typically 3.3-6.6. My FT3, when tested, is often at or above the top of the FT3 reference range. I have zero FT4 and zero TSH. I am NOT hyperthyroid. This makes lots of sense when you understand the real endocrinology.

Unfortunately, most doctors do NOT understand the fundamentals.

I hope this helps to explain it.

The above is described in ALL my books now. The research papers and many other research findings are all discussed in The Thyroid Patient’s Manual.


Here are some of the research references from Chapter 14 of The Thyroid Patient’s Manual. I kept the same reference numbers as in the book – hence they aren’t sequential:


1. “Symptomatic Relief is Related to Serum Free Triiodothyronine Concentrations during Follow-up in Levothyroxine-Treated Patients with Differentiated Thyroid Cancer”
Larisch, Midgley, Dietrich, and Hoermann.
https://www.researchgate.net/publication/322914153_Symptomatic_Relief_is_Related_to_Serum_Free_Triiodothyronine_Concentrations_during_Follow-up_in_Levothyroxine-Treated_Patients_with_Differentiated_Thyroid_Cancer

This paper clearly proves that FT3 concentrations are the most important in clinical decision making, as they are most closely linked to residual hypothyroid symptoms in T4- Only treated patients. It also shows that in-range TSH is not sufficient for symptom relief.


2. “Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment”
Hoermann R1, Midgley JE, Giacobino A, Eckl WA, Wahl HG, Dietrich JW, Larisch R.
https://www.ncbi.nlm.nih.gov/pubmed/24953754

This is a great paper, although complex. It shows that it is the relationships of the thyroid hormones, and how they adjust during treatment, that counts. It also makes it crystal clear that TSH should only have a supporting role in the assessment process during treatment.


3. “Recent Advances in Thyroid Hormone Regulation: Toward a New Paradigm for Optimal Diagnosis and Treatment”
Hoermann, Midgley, Larisch, Dietrich.
https://www.frontiersin.org/articles/10.3389/fendo.2017.00364/full

This paper talks about the need for a new paradigm of thyroid treatment that accepts that the relationship between TSH and thyroid hormones are individual, dynamic and can adapt, i.e. the current practice of simply looking at numbers that do or do not fit in the population ranges is not sufficient.


12. Thyroid hormone replacement – a counterblast to guidelines – Dr A.D. Toft. See: 
http://www.rcpe.ac.uk/sites/default/files/jrcpe_47_4_toft.pdf


13. Consensus statement for good practice and audit measures in the management of hypothyroidism and hyperthyroidism – M P J Vanderpump, J A 0 Ahlquist, J A Franklyn, R N Clayton, on behalf of a working group of the Research Unit of the Royal College of Physicians of London, the Endocrinology and Diabetes Committee of the Royal College of Physicians of London, and the Society for Endocrinology See:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2351923/pdf/bmj00557-0041.pdf


I hope you found this interesting.

Best wishes,

Paul

Paul Robinson

Paul Robinson is a British author and thyroid patient advocate. The focus of his books and work is on helping patients recover from hypothyroidism. Paul has accumulated a wealth of knowledge on thyroid and adrenal dysfunction and their treatment. His three books cover all of this.

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