Hypothyroidism in Athletes: Causes and the Link with Training Load and Pharmacology

Fatigue, sensitivity to cold, weight gain on the same diet, and results “stalling” are symptoms an athlete often writes off as overtraining. Sometimes they really do reflect reduced thyroid function, and sometimes just the body's adaptation to an energy shortage or a consequence of taking medications. The editorial team examines where hypothyroidism comes from in people who train and how load and pharmacology change the picture.

What hypothyroidism is

Hypothyroidism is a condition in which the thyroid gland produces insufficient amounts of the hormones thyroxine (T4) and triiodothyronine (T3). These hormones regulate the rate of metabolism in practically all tissues: from heart rate and thermogenesis to protein synthesis in muscles and cholesterol metabolism.

The gland's work is controlled by the “hypothalamus–pituitary–thyroid” axis. The hypothalamus releases thyrotropin-releasing hormone, the pituitary in response releases thyroid-stimulating hormone (TSH), which stimulates the gland. T4 and T3, by the feedback principle, suppress the production of TSH. So when the gland itself is damaged, TSH rises, trying to “push” it to work.

A distinction is made between primary hypothyroidism (the problem is in the gland itself, the most frequent variant), central (insufficiency of the pituitary or hypothalamus), and subclinical — when TSH is elevated but the level of free T4 is still within the normal range. Overt hypothyroidism is prevalent in about a few percent of the population and occurs much more often in women (Chaker et al., 2017).

Most T3 is formed not in the gland but in peripheral tissues from T4 with the participation of deiodinase enzymes. It is at this level that the body is able to quickly “regulate” hormone activity in response to hunger, illness, and stress — which is fundamental to understanding the situation in sport.

The main causes

In regions with adequate iodine intake, the most frequent cause of primary hypothyroidism is chronic autoimmune thyroiditis (Hashimoto's thyroiditis). The immune system produces antibodies to thyroid peroxidase and thyroglobulin and gradually destroys the tissue of the gland. The process lasts for years, and for a long time function may remain normal despite elevated antibodies.

On a global scale the main cause remains iodine deficiency. Ukraine has historically belonged to iodine-deficient regions, so the question of iodized salt for Ukrainian athletes is not a formality. At the same time, an excess of iodine — for example, from uncontrolled intake of supplements with kelp — can provoke gland dysfunction in susceptible people.

Other causes are the consequences of thyroid surgery or treatment with radioactive iodine, past thyroiditis (including postpartum), irradiation of the neck, as well as certain medications: amiodarone, lithium preparations, immune checkpoint inhibitors. Central hypothyroidism occurs rarely and is associated with tumors, injuries, or other damage to the pituitary.

Training itself does not cause hypothyroidism. Regular physical activity does not damage the gland and does not provoke an autoimmune process. However, an athlete's lifestyle can create situations where tests and well-being mimic hypothyroidism — more on those below.

Energy deficiency and low-T3 syndrome

When the energy obtained from food is insufficient to cover the expenditure on training and basic functions, the body switches into a saving mode. One of the first signals is a decrease in the T3 level due to reduced peripheral conversion of T4 into T3. Loucks and Heath (1994) showed that in women who trained, low-T3 syndrome arose when available energy dropped below a certain threshold.

This mechanism underlies the concept of relative energy deficiency in sport (REDs), described in the consensus of the International Olympic Committee (Mountjoy et al., 2023). Reduced T3 is considered there as one of the markers of low energy availability, alongside menstrual cycle disturbances, reduced testosterone, and reduced bone mineral density.

The laboratory picture in this case differs from true hypothyroidism: TSH is usually normal or low-normal, free T4 is normal or at the lower limit, and free T3 is reduced. This is an adaptation, not a disease of the gland, and it is treated not with hormones but by restoring the energy balance.

Such a situation is characteristic of sports with weight categories, aesthetic disciplines, long-distance running, and bodybuilding during the period of preparation for competitions. Taking thyroid hormones “to correct” low T3 in these cases does not remove the cause and creates new risks.

Pharmacology and supplements

The most direct link between hypothyroidism and pharmacology is the self-directed use of thyroid hormones (medicinal T4 or T3) for “cutting.” Exogenous hormones suppress TSH, and the person's own gland reduces its work. After abrupt withdrawal, temporary hypothyroidism can develop until the axis recovers. At the same time, against the background of intake, the risks of arrhythmias and loss of muscle and bone mass rise.

Anabolic-androgenic steroids reduce the concentration of thyroxine-binding globulin. Because of this, total T4 on the form may turn out to be reduced while free T4 and TSH are normal. If the doctor does not know about the drug use, such a finding may be falsely interpreted as hypothyroidism. Estrogens, by contrast, raise the level of the binding protein.

A separate trap is biotin in high doses, common in supplements for hair and skin and in some multivitamin complexes. It affects immunochemical methods that use the “streptavidin–biotin” system and can give a falsely low TSH and falsely high T4 and T3. The FDA has published a warning about such biotin interference in laboratory tests.

In addition, certain drugs reduce the absorption of levothyroxine in people who are already receiving treatment: iron and calcium preparations, some antacids, soy products, and coffee drunk at the same time as the tablet. For an athlete on therapy this is important when planning supplement intake.

How to distinguish it from overtraining

The symptoms of hypothyroidism are nonspecific: fatigue, drowsiness, sensitivity to cold, dry skin, constipation, puffiness, slowing of the pulse, weight gain, menstrual cycle disturbances, low mood. Most of them also occur with overtraining, lack of sleep, iron deficiency, or energy deficiency.

It is impossible to distinguish these states by well-being alone — tests are needed. The most important of them is TSH, supplemented by free T4, and if an autoimmune process is suspected — antibodies to thyroid peroxidase. In parallel it is worth checking ferritin, a complete blood count, and assessing the energy balance of the diet.

• take the test in the morning, during a usual training period, and not right after competitions;
• a few days before the test, stop supplements with high doses of biotin (after agreeing with the doctor);
• tell the doctor about all hormonal drugs, steroids, and fat burners;
• assess the diet: whether it covers the real energy expenditure.

This table is only a guide. The final interpretation is made by a doctor taking into account all the circumstances, often after a repeat test a few weeks later.

Editorial conclusions

True hypothyroidism in athletes most often has the same causes as in the general population: autoimmune thyroiditis, disturbances of iodine supply, the consequences of surgery and medications. Training itself does not damage the thyroid gland.

The situations specific to sport are energy deficiency with low-T3 syndrome, withdrawal of self-administered thyroid hormones, the effect of steroids on binding proteins, and of biotin on test results. All of them are capable of mimicking hypothyroidism but require a completely different approach.

So with a persistent loss of performance it is worth taking TSH and free T4, telling the doctor openly about all drugs and supplements, and not prescribing hormones to yourself.

We also recommend reading our articles on the prevention and diagnosis of hypothyroidism, on energy deficiency in sport, and on hyperthyroidism in athletes.

References

1. Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. Lancet. 2017;390(10101):1550–1562.
2. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014;24(12):1670–1751.
3. Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. Am J Physiol. 1994;266(3 Pt 2):R817–R823.
4. Mountjoy M, Ackerman KE, Bailey DM, et al. 2023 International Olympic Committee's (IOC) consensus statement on Relative Energy Deficiency in Sport (REDs). Br J Sports Med. 2023;57(17):1073–1097.
5. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
6. U.S. Food and Drug Administration. Biotin (Vitamin B7): Safety Communication — may interfere with lab tests. FDA; 2017 (updated 2019).