Hypothyroidism in Athletes: Causes and the Link with Training and Pharmacology
Fatigue, sensitivity to cold, weight gain on the same diet, and a “plateau” in results — symptoms that an athlete often writes off as overtraining. Sometimes reduced thyroid function really does stand behind them, and sometimes it is only the body’s adaptation to an energy shortage or a consequence of taking medications. The editorial team examines where hypothyroidism in people who train comes from and how training 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 the muscles and cholesterol metabolism.
The work of the gland is controlled by the “hypothalamus — pituitary — thyroid gland” axis. The hypothalamus releases thyrotropin-releasing hormone, and the pituitary in response releases thyroid-stimulating hormone (TSH), which stimulates the gland. T4 and T3, by the principle of feedback, suppress the production of TSH. So when the gland itself is damaged, TSH rises, trying to “nudge” it into working.
A distinction is made between primary hypothyroidism (the problem is in the gland itself, the most common variant), central (insufficiency of the pituitary or hypothalamus), and subclinical — when TSH is elevated but the level of free T4 is still within the norm. 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 precisely at this level that the body is able to quickly “regulate” the activity of the hormones in response to hunger, illness, and stress — which is crucial for understanding the situation in sport.
The main causes
In regions with sufficient iodine intake, the most common 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 can remain normal with elevated antibodies.
On a global scale, the main cause remains iodine deficiency. Ukraine historically belongs to regions with iodine deficiency, 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 dysfunction of the gland in predisposed people.
Other causes are the consequences of operations on the thyroid gland or treatment with radioactive iodine, past thyroiditis (in particular postpartum), irradiation of the neck, and also some drugs: amiodarone, lithium preparations, immune checkpoint inhibitors. Central hypothyroidism occurs rarely and is associated with tumors, injuries, or other lesions of the pituitary.
Training in 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 in which the tests and well-being imitate hypothyroidism — these are discussed further.
Energy deficit and low-T3 syndrome
When the energy obtained from food is insufficient to cover the costs of training and basic functions, the body switches into a saving mode. One of the first signals is a reduction in the T3 level due to decreased 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 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 of hypothyroidism with pharmacology is the self-directed use of thyroid hormones (pharmaceutical T4 or T3) for “cutting”. Exogenous hormones suppress TSH, and one’s own gland reduces its work. After abrupt discontinuation, temporary hypothyroidism may develop until the axis recovers. In parallel, against the background of intake, the risks of arrhythmias and loss of muscle and bone mass increase.
Anabolic-androgenic steroids reduce the concentration of thyroxine-binding globulin. Because of this, total T4 on the form may turn out to be reduced with normal free T4 and TSH. If the doctor does not know about the drug use, such a finding may be wrongly regarded as hypothyroidism. Estrogens, on the contrary, 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 interference of biotin with laboratory tests.
In addition, some drugs reduce the absorption of levothyroxine in people who are already receiving treatment: iron and calcium preparations, some antacids, soy products, and also coffee drunk at the same time as the tablet. For an athlete on therapy this is important when planning the intake of supplements.
How to distinguish it from overtraining
The symptoms of hypothyroidism are nonspecific: fatigue, drowsiness, sensitivity to cold, dry skin, constipation, puffiness, a slowed pulse, an increase in body weight, menstrual cycle disturbances, and a lowered mood. Most of them also occur in overtraining, lack of sleep, iron deficiency, or energy deficit.
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 the usual training period, rather than immediately after competitions;
- a few days before the test, stop supplements with high doses of biotin (after agreeing with a doctor);
- inform the doctor about all hormonal preparations, steroids, and fat burners;
- assess the diet: whether it covers the real energy expenditure.
| Condition | TSH | Free T4 | Free T3 | Key clue |
|---|---|---|---|---|
| Primary hypothyroidism | ↑ | ↓ or normal (subclinical) | ↓ or normal | Often antibodies to TPO |
| Energy deficit (low T3) | normal | normal / low-normal | ↓ | Calorie deficit, weight loss |
| Intake of exogenous hormones | ↓ | depends on the drug | depends on the drug | History of intake |
| After discontinuation of hormones | normal / ↑ transiently | ↓ | ↓ | Temporarily, until the axis recovers |
| Effect of biotin | falsely ↓ | falsely ↑ | falsely ↑ | Supplements with biotin |
This table is only a guide. The final interpretation is made by a doctor, taking into account all circumstances, often after a repeat test in a few weeks.
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 operations and drugs. Training in itself does not damage the thyroid gland.
Situations specific to sport are energy deficit with low-T3 syndrome, discontinuation of self-administered thyroid hormones, the effect of steroids on binding proteins, and of biotin on test results. All of them are able to imitate hypothyroidism but require a completely different approach.
Therefore, 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 oneself.
We also advise reading our articles on the prevention and diagnosis of hypothyroidism, on energy deficit in sport, and on hyperthyroidism in athletes.
References
- Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. Lancet. 2017;390(10101):1550–1562.
- 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.
- 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.
- 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.
- 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.
- U.S. Food and Drug Administration. Biotin (Vitamin B7): Safety Communication — may interfere with lab tests. FDA; 2017 (updated 2019).
Andriy Melnyk
A strength-sports coach and author of programs for beginner and intermediate levels. Writes about training planning.
