According to the CDC, between 836,000 and 2.5 million people live with chronic fatigue syndrome, yet many do not receive an official diagnosis or adequate treatment due to the ill-defined nature of the condition.
Characterized by extreme fatigue, impaired functioning, and sleep disturbances which are not improved by rest and are unrelated to underlying medical conditions, the root cause of CFS is yet to be determined—but the condition may be tied to lower levels of key thyroid hormones in the body.
CFS symptoms resemble those associated with the thyroidal disease hypothyroidism, with similar primary complaints present including fatigue, impaired cognitive functioning, and sleep issues. In hypothyroidism, the thyroid gland produces insufficient levels of thyroid hormones, which are essential to proper metabolism regulation. To combat this, the body releases increased amounts of thyroid-stimulating hormones (TSH), which does not occur in patients suffering from chronic fatigue syndrome.
Despite similarities between the two conditions, new research reveals key differentiating elements that provide key insight into CFS. While the examination of CFS and its causes is ongoing, a recent study published in Frontiers in Endocrinology reports a potential link between lowered levels of thyroid hormones and CFS: unrelated to thyroidal disease. Led by Dr. Begoña Ruiz-Núñez, a team of researchers at the University Medical Center in the Netherlands tested thyroid functioning and markers of inflammation in healthy individuals and patients with chronic fatigue syndrome.
Impaired thyroid functioning was found in CFS patients, who had lower levels of thyroid hormones triiodothyronine (T3) and thyroxine (T4) but normal production rates of TSH, eliminating the possibility of thyroidal disease. Individuals with CFS additionally exhibited low-grade inflammation and decreased urinary iodine levels, both of which are associated with thyroid gland-related issues.
Dr. Ruiz-Núñez’s study also revealed that participants with CFS showed higher levels of the reverse T3 (rT3) hormone as another consequence of the shift in thyroid hormone production. Patients with CFS were found to convert T4 hormones into rT3, rather than regularly producing T3 hormones. This could potentially explain the significantly lower levels of T3 found in the affected participants.
One of the most significant findings of the study is that the results persisted alongside two sensitivity analyses, strengthening the connection between CFS and thyroid functioning as well as low-grade inflammation. Dr. Ruiz-Núñez’s findings symbolize a major step toward the development of treatment for this previously unmanageable condition. Nevertheless, while the study links CFS with low levels of key thyroid hormones, a definitive cause still remains unknown. Additional studies will need to be conducted to further investigate this new research, confirm the relationship between CFS and underperforming thyroid glands, and develop more effective treatment methods.