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Frontiers, Press Release, 20th March 2018.
Discovery of a crucial link between chronic fatigue syndrome and lower levels of key thyroid hormones raises hopes for treating this common yet debilitating disease
Frontiers in Endocrinology
New research demonstrates a link between chronic fatigue syndrome (CFS) symptoms and lower thyroid hormone levels. Published in Frontiers in Endocrinology, the study indicates that CFS, a condition with unknown causes, can be explained by lower thyroid hormones — but may be distinct from thyroidal disease. This finding can be seen as a first step to finding treatment for a debilitating illness for which there is no recognized treatment.
Chronic fatigue syndrome is a common disease marked by lengthy spells of weakness, fatigue and depression. Its diagnosis is predominantly based on symptoms and on ruling out any underlying medical condition, rather than on laboratory tests and physical examination.
Interestingly, several symptoms resemble those of hypothyroidism — a condition where the thyroid gland does not produce enough thyroid hormone. In hypothyroidism, the body tries to encourage thyroid hormone activity by releasing more thyroid-stimulating hormone — however, this does not happen in patients with chronic fatigue syndrome.
This contrast in thyroid-stimulating activity led the study's authors to hypothesize that chronic fatigue syndrome is caused by low activity of thyroid hormones in the absence of thyroidal disease.
Led by Dr. Begoña Ruiz-Núñez at the University Medical Center Groningen, The Netherlands, the researchers compared thyroid function and markers of inflammation between 98 CFS patients and 99 healthy controls. Remarkably, the CFS patients had lower serum levels of certain key thyroid hormones such as triiodothyronine (T3) and thyroxine (T4), but normal levels of thyroid-stimulating hormone.
Additional analyses indicated that CFS patients had a lower urinary iodine status and low-grade inflammation, which possibly mirrored the symptoms of patients with hypothyroidism. These CFS patients, however, had relatively higher levels of another thyroid hormone called “reverse T3” or rT3. This appeared to be due to a shift in hormone production, where the body preferred to convert T4 to rT3 instead of producing T3. The low T3 levels found in CFS patients coupled with this switchover to rT3 could mean that T3 levels are severely reduced in tissue.
“One of the key elements of our study is that our observations persisted in the face of two sensitivity analyses to check the strength of the association between CFS and thyroid parameters and low-grade inflammation,” says Dr. Ruiz-Núñez. “This strengthens our test results considerably.”
The researchers believe inclusion of patient information, such as duration of illness, would enable a correlation with their biochemical profiles. Further, even though the study demonstrates a link between chronic fatigue syndrome symptoms and low levels of key thyroid hormones, a definitive cause for CFS remains unknown.
If the study findings are confirmed by additional research, it may pave the way for a treatment for chronic fatigue syndrome.
For more details, and the full journal report, contact Frontiers:
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ME Association Comment:
Dr Charles Shepherd, Hon. Medical Adviser, ME Association.
This new research into thyroid gland hormones in ME/CFS represents an important advance in our understanding of hormonal abnormalities in this illness.
We already know that there are abnormalities involving the hormone cortisol in ME/CFS. However, routine blood tests for thyroid function have always indicated that thyroid gland hormones are not affected.
Consequently, thyroid hormone treatment (i.e. thyroxine) is not recommended for ME/CFS – as this can cause serious side effects in people who have normal thyroid function.
This new research demonstrates a defect in thyroid hormone activity (involving the conversion of one thyroid hormone to another – T4 to T3) rather than actual thyroid gland disease.
If these findings can be replicated by other independent research groups, it suggests that the cautious use of thyroid hormone treatment needs to be assessed in a clinical trial – as it could be an effective form of treatment for at least a subgroup of people with ME/CFS.
The ME Association Ramsay Research Fund funds research into the cause and management of ME/CFS and would welcome research grant applications that aim to follow up these findings.
The current ME Association position on thyroid gland function and the use of thyroxine in ME/CFS can be read in a new leaflet that is available to download from our website.
We also featured information relation to thyroid function and hypothyroidism, on our website last year.
The research:
Authors:Begoña Ruiz-Núñez1, 2*, Rabab Tarasse1, Emar Vogelaar3, Janneke Dijck-Brouwer1, FritsMuskiet1
Laboratory Medicine, University Medical Center Groningen, Netherlands,
Healthy Institute, Spain,
European Laboratory of Nutriënts (ELN), Netherlands.
Abstract:
Chronic fatigue syndrome (CFS) is a heterogeneous disease with unknown cause(s). CFS symptoms resemble a hypothyroid state, possibly secondary to chronic (low-grade) (metabolic) inflammation.
We studied 98 CFS patients (21-69 years, 21 males) and 99 age- and sex-matched controls (19-65 years, 23 males). We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation.
Most remarkably, CFS patients exhibited similar TSH, but lower FT3 (difference of medians 0.1%), TT4 (11.9%), TT3 (12.5%), %TT3 (4.7%), SPINA-GD (14.4%), SPINA-GT (14.9%), 24-hour urinary iodine (27.6%) and higher %rT3 (13.3%). FT3 below the reference range, consistent with the ‘low T3 syndrome', was found in 16/98 CFS patients vs. 7/99 controls (OR 2.56; 95% CI=1.00 – 6.54). Most observations persisted in two sensitivity analyses with more stringent cut-off values for BMI, hsCRP and WBC.
We found possible evidence of (chronic) low-grade metabolic inflammation (ferritin and HDL-C). FT3, TT3, TT4 and rT3 correlated positively with hsCRP in CFS patients and all subjects. TT3 and TT4 were positively related to hsCRP in controls. Low circulating T3 and the apparent shift from T3 to rT3 may reflect more severely depressed tissue T3 levels.
The present findings might be in line with recent metabolomic studies pointing at a hypometabolic state. They resemble a mild form of ‘non thyroidal illness syndrome' and ‘low T3 syndrome' experienced by a subgroup of hypothyroid patients receiving T4 monotherapy.
Our study needs confirmation and extension by others. If confirmed, trials with e.g. T3 and iodide supplements might be indicated.
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