by Begoña Ruiz-Núñez, Rabab Tarasse, Emar F Vogelaar, D A Janneke Dijck-Brouwer, Frits A J Muskiet PMID: 29615976, PMCID: PMC5869352, DOI:10.3389/fendo.2018.00097, Front Endocrinol (Lausanne), 2018 Mar 20;9:97. doi: 10.3389/fendo.2018.00097. 2018.
CFS symptoms resemble a hypothyroid state.
ABSTRACT (I paraphrased this abstract, for brevity and clarity)
Chronic fatigue syndrome (CFS) is a heterogeneous disease with unknown cause(s). CFS symptoms resemble a hypothyroid state, secondary to chronic inflammation.
We studied 98 CFS patients and 99 age- and sex-matched controls.
We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation.
Remarkably, CFS patients exhibited:
Lower free T3 (FT3),
Lower total thyroxine (TT4),
Lower total T3 (TT3),
Lower %TT3 (4.7%),
Lower activity of deiodinases,
Lower secretory capacity of the thyroid gland (14.9%) and
Lower 24-h urinary iodine (27.6%).
The % of reverse T3 (rT3) was higher (13.3%), among the patients and FT3 below the normal range, consistent with the “low T3 syndrome,” was found in 16/98 CFS patients vs. 7/99 controls.
We also found evidence of low-grade metabolic inflammation (ferritin & HDL-C).
FT3, TT3, TT4, and rT3 correlated positively with hsCRP in CFS patients and controls. TT3 and TT4 were positively related to hsCRP in controls.
Low T3 and the shift from T3 to rT3 may reflect more depressed tissue T3 levels.
The findings in patients agree with studies suggesting a hypometabolic state.
They resemble “non-thyroidal illness syndrome” and “low T3 syndrome” experienced by a subgroup of hypothyroid patients receiving T4 monotherapy.
Our study needs confirmation by others: trials with,T3 and iodide supplements might be indicated.
Keywords: chronic fatigue syndrome, thyroid, “low T3 syndrome”, triiodothyronine, reverse triiodothyronine, urinary iodine, inflammation, high-sensitive C-reactive protein
My COMMENT REGARDING THIS ARTICLE:
This is a truly excellent paper.
It tends to agree with me, confirming that CFS symptoms resemble a hypothyroid state, or at least that there is a relationship between CFS and “Functional Hypothyroidism“, and it raises the obvious question: is therapy available?
My answer is as follows:
(1) CFS is “Low T3 syndrome” and “CFS” a manifestation of Functional (Intracellular) Hypothyroidism (IH).
(2) Those presenting with CFS, or other symptoms of Intracellular Hypothyroidism, should have Thyroid Profile tests, including TSH, free T4, free T3 and reverse T3:
(3) If the FT3/rT3 ratio is less than 20, all patients, male or female of whatever age, should be treated with T3 (Triiodothyronine), using a protocol of upward titration of the T3 dose * to achieve a serum T3 between 5.0 and 6.1 Picomoles/Litre.
(4) Treatment with slow-release T3 can be expected to be successful: if it is, the IH will be eliminated, “low thyroid” symptoms will be gone and the CFS will be CURED. **
- * Monitored with weekly retesting of FT3 and rT3, at 3-4 hours post-dose: since the half-life of Triiodothyronine is just 2-3 hours, there is no need for a 6-week dose-test interval, as is done with Levothyroxine.
- ** Weaning off Triiodothyronine can be attempted 3-6 months after confirming the curative dose. However IH is a stress-dependent condition and will quickly recur, with relapse of CFS, if and when the patient is subjected to stress.
In such cases, T3 therapy can be continued, with dose adjustment ad hoc, indefinitely.