withdrawal of liothyronine (T3) in a symptomatic tired, depressed and vulnerable patient with CFS or long COVID, 2022, Meeran

how do i rationalise withdrawal of liothyronine (T3) in a symptomatic tired, depressed and vulnerable patient with chronic fatigue syndrome or long COVID who may or may not have hypothyroidism?

https://www.endocrine-abstracts.org/ea/0086/ea0086hdi2.2

Endocrine Abstracts (2022) 86 HDI2.2 | DOI: 10.1530/endoabs.86.HDI2.2

Society for Endocrinology BES 2022

Karim Meeran


Author affiliations
Imperial College, London, United Kingdom

Patients on thyroxine have lower psychological well-being than controls using the GHQ12 questionnaire, which gives patients a score between 0 (very happy and well) and 36 (profoundly exhausted and feeling worthless).

Average GHQ was 11.39 in controls and 12.09 in patients optimised on thyroxine(P=0.028)1.

Liothyronine has a large and sustained placebo effect with the GHQ improving from 13.5 to 11.0 in the WATTS study2.

This placebo effect needs careful explaining to patients.

A genetic reanalysis of the WATTS study suggested an association between one point mutation and response to liothyronine in the subset of patients with one particular allele3.

Various websites wrongly interpret this and suggest that those patients with "the gene" (allele CC in the SNP rs225014 which was associated with a Thr92Ala mutation) would be tired unless they were given liothyronine, despite having normal plasma T3 levels.

A trial of liothyronine for patients who are tired despite adequate thyroxine replacement is fraught with the placebo effect, and benefit is also seen with placebo when patients are blinded but not in open label studies.

Further studies have found no linkage of this gene with tiredness, even in those who are particularly tired on levothyroxine and apparently responded to liothyronine4.

Resolution of life events that may have occurred after patients started liothyronine makes patients associate liothyronine with improvement in quality of life.

They are often taking other placebos such as Ashwaganda, Turmeric and Co-enzyme Q.

Listening to their story, reassuring such patients, and monitoring thyroid function while slowly weaning liothyronine has been the most successful method.

It is essential that any future studies of liothyronine are carefully planned and properly randomised and blinded to avoid all the biases of previous studies.

Open label studies of liothyronine are misleading and should not be carried out.

 

Current standards for treating hypothyroidism rely almost exclusively on a single measure - the TSH (Thyroid Stimulating Hormone). Once that is within range, anywhere in range, or even slightly over the range, the hypothyroid patient is considered to be adequately treated. Their levels of actual thyroid hormones, Free T4 and Free T3, are often not measured because the TSH is considered to be so perfect as an indicator of thyroid health. There is an assumption behind this that the pituitary (which produces TSH at the behest of the hypothalamus, which produces TRH - Thyrotropin Releasing Hormone) is never at fault, can never be wrong, and is a perfect measure of thyroid health. But the hypothalamus and pituitary respond to levels of thyroid hormones in their own neighbourhood, they don't respond to levels in the kidneys, the muscles, the liver etc. Parts of the body may have adequate levels of thyroid hormones while other parts are deficient.

Anyone with an interest in the functioning of the thyroid and its treatment should have a poke around this website - it has many very good articles, all referenced: https://thyroidpatients.ca/

Regarding "psychological well-being", a personal anecdote... I feel dreadful with a ferritin (iron stores) level which is low in range, but doctors think I'm fine when my level is anywhere in range. I also feel best with a vitamin B12 level which is top of range. So am I just a hypochondriac and a drug-seeker? Doctors have been saying yes to that all my life and recorded it in my medical records so that no new doctor is ever unaware of how other doctors have viewed me for the last 50 years. So I have to test and experiment by myself within the limits of legality and my knowledge. I've discovered for myself that keeping my ferritin level at about 70% through the range and my B12 at the top of the range works well for my mental health. It turns out that I'm not deficient in anti-depressants after all.

There is no explanation in the abstract explaining why they think T3 is a placebo. Every single cell in the human body needs T3 to function. If the level is too low it is bound to make the patient feel unwell and depressed.

Another factor is the reference range. In the UK a common reference range for Free T3 is 3.1 - 6.8 pmol/L. So if Patient A has a Free T3 level of 3.5 pmol/L they must be well, yes? But what if Patient A only feels well with a level of 6.0 pmol/L? Is that a sign that the patient is mentally ill? A hypochondriac? Addicted to T3? A drug seeker? Or is it a sign that individual patients have a personal reference range which is much narrower than the lab reported reference range? Patient B may feel best with a Free T3 level of 5.0 pmol/L. But modern medicine thinks both patients are well when Free T3 is low in range, or lower than their "personal optimal" level of T3.

But personalised medicine is something that is just a pipe dream as far as I can tell. It costs too much, so it is easier to blame the patient and say they must be being non-compliant with their treatment.

One common feature of research into hypothyroidism is that often patients are lumped in together and treated as an amorphous lump. Reasons for being hypothyroid (list not complete) are not taken into account :

1) Patient has thyroid removed due to uncontrollable Graves' Disease

2) Patient has thyroid removed due to thyroid cancer.

3) Patient has thyroid removed because of various kinds of nodules.

4) Patient was born without a thyroid.

5) Patient was born with a small thyroid.

6) Patient develops Hashimoto's Thyroiditis, an autoimmune condition which destroys the thyroid, beginning with the development of a goitre.

7) Patient develops Ord's Thyroiditis, an autoimmune condition which destroys the thyroid but without a goitre - the thyroid shrivels up and may almost completely disappear.

8) Patient is iodine deficient.

And another factor which is almost always ignored - treatment.

1) The vast majority of patients are on T4-only.

2) Other patients may be on T4 + T3, or NDT. These two options usually result in under-medication because exogenous T3 has a huge effect on TSH and makes it drop dramatically, thus persuading the doctor the patient is over-medicated.

3) Some patients only do well on T3-only.

So, thyroid research treats someone on T4-only because of some form of autoimmune thyroiditis as being the same as someone who has never been hypothyroid or hyperthyroid but developed thyroid cancer and had their thyroid removed.

And given that statistics suggest that for every hypothyroid patient treated with T3 or T4 + T3 or NDT there are 10 patients treated with T4-only, that is another reason for thyroid research to be of incredibly poor quality.

So this author knows better than all these other researchers? And again there is a reference to "normal" T3 levels, so the reference range is all that matters.

I find the reference to CoQ10 as a placebo amusing since other researchers are taking it seriously enough to test it in Long Covid :

https://www.s4me.info/threads/high-...se-2-crossover-trial-2022-hansen-et-al.30299/

Also, statins reduce levels of CoQ10 and lots of research effort has been put into working out the effect on patients. Advice to patients on statins to take supplementary CoQ10 is commonly reported.

...

This whole abstract suggests that many medical myths related to thyroid are still alive and well :

1) TSH tells you everything you need to know about the thyroid.

2) T3 isn't important, and is a placebo, and doesn't need to be tested. This is despite the fact that doctors have T3 flowing through their veins and arteries while they sit and tell the patient that they don't need as much T3 as the doctor does, or the patient's levels are irrelevant.

3) There is an underlying suggestion in the wording ("slowly weaning liothyronine") that T3 is addictive.

 

Do you mean keeping B12 and ferritin in the ranges you quoted helps your ME/CFS?

 

I have never been diagnosed with ME/CFS, probably because I don't give doctors the opportunity to do so by hardly ever seeing them, and restricting my doctor visits to occasions when the problem I have is visible and/or is easily tested.

I treat myself for anything and everything that I can think of, and can test privately (if I can afford to).

I am mostly limited to treating my nutrient levels and I also treat my own thyroid - but doing so makes my quality of life far better than it was before I started doing these things.