In November 2021, I received a paper, 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.
the paper is entitled “chronic fatigue syndrome: a case control study”.
ABSTRACT (paraphrased, 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 Chronic Fatigue Syndrome 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 chronic fatigue syndrome 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 agrees with me, that Chronic Fatigue Syndrome symptoms resemble a hypothyroid state, or at least that there is a relationship between CFS and “Functional ( Intracellular) Hypothyroidism“.
It raises the obvious question: can Chronic Fatigue Syndrome be treated?
My answer is as follows:
(1) CFS, closely related to “burnout”, is “Low T3 syndrome“, aka “Functional”, or “Intracellular” Hypothyroidism (IH).
(2) Those presenting with CFS, or other symptoms of Intracellular Hypothyroidism, should have a “Thyroid Profile” test panel done (TSH, FT4, FT3 and reverse T3).
(3) A low T3/rT3 ratio (less than 20) confirms the presence of IH, indicating that the background etiology of the CFS is stress.
An effort is made to identify and eliminate stressors, so as to avoid post-treatment relapse.
(3) All patients are treated with T3 (Triiodothyronine): the protocol begins with a 5 or 10 µg dose of slow-release T3, with upward titration of the dose*, to achieve a serum T3 between 5.0 and 6.1 Picomoles/Litre. rT3 is expected to fall to less than 13 Ng/DL, while T3/rT 3 rises above 20.
(4) Slow-release T3 works well: the IH symptoms regress, and the CFS is cured.
(5) Therapy is continued for at least 3 months **.
- * Monitored with weekly retesting of FT3 and rT3, at 4-6 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 by repeating the thyroid profile and T3/are T3 ratio estimation. However IH is a stress-dependent condition and will quickly recur, with relapse of the Chronic Fatigue Syndrome, if and when the patient is subjected to stress.
In some cases, T3 therapy has to continue, with dose adjustment ad hoc, indefinitely.