Hypothyroidism: Causes, Symptoms, Diagnosis, Treatment, and What It Means for Athletes
Table of Contents
Key Takeaways: Hypothyroidism
- Hypothyroidism means the body has too little thyroid hormone. Overt hypothyroidism combines a raised TSH with a low free T4; subclinical hypothyroidism is a raised TSH with free T4 still inside the reference range.
- It is common, especially in women. In iodine-sufficient countries, roughly 1–2% of people have overt hypothyroidism, and hypothyroidism is about ten times more common in women than in men.
- Hashimoto’s thyroiditis is the leading cause in iodine-sufficient countries. Thyroid surgery, radioactive iodine, and medicines such as amiodarone, lithium, and immune checkpoint inhibitors are other frequent causes.
- Symptoms alone cannot make the diagnosis. Fatigue, weight gain, cold intolerance, and dry skin are non-specific, so the diagnosis rests on blood tests, and a mildly raised TSH should be repeated before anyone is labelled hypothyroid.
- Hypothyroidism is an important differential diagnosis. In practice, it can resemble, and coexist with, depression, burnout, and overtraining, which is why thyroid tests are often part of fatigue work-ups.
- Overt hypothyroidism should generally be treated; routine treatment is not recommended for most adults with subclinical hypothyroidism. Guidelines allow treatment to be considered in selected situations, but randomised trials have not shown that levothyroxine improves quality of life or symptoms in most adults with subclinical hypothyroidism.
- A mildly raised TSH is often followed rather than treated straight away. Repeat testing shows whether thyroid function is changing, and positive TPO antibodies indicate a higher risk of progression to overt hypothyroidism.
- Levothyroxine is the standard treatment, and getting the dose right matters. In a large observational cohort of treated patients, mortality was higher when TSH was below 0.1 mIU/L or above 4 mIU/L than when it sat in the middle of the reference range.
- Treated hypothyroidism still needs follow-up. Testing is more frequent while the dose is being adjusted and can usually be reduced to about once a year once it is stable, but levels can drift over the years if they are not checked.
- For athletes, two traps stand out. Exercise intolerance can persist even when blood tests look normal on treatment, and low T3 caused by low energy availability is not the same thing as hypothyroidism.
- Athletes are treated in the same way as everyone else. They may simply seek testing sooner because they notice a drop in performance. Low energy availability can lower T3 without thyroid disease, whereas low TSH together with low free T4 needs careful interpretation, because central hypothyroidism is one possible cause.
Introduction: Hypothyroidism
Hypothyroidism, a deficiency of thyroid hormone, is a common condition worldwide [1]. Thyroid hormones act on almost all body systems, and the classic symptoms of deficiency, such as fatigue, weight gain, and cold intolerance, are non-specific [1]. Hypothyroidism is therefore diagnosed mainly with blood tests rather than on symptoms alone [1].
From a clinical perspective, hypothyroidism is a common diagnosis, and thyroid tests are ordered in many different situations. In my clinical experience, I see it more often in women than in men, although men are affected as well, and most of these patients are treated with levothyroxine. In my practice, TSH is also part of almost all the basic laboratory packages used for routine periodic check-ups, so it effectively works as a common screening test and is measured very often, although routine screening of the general population is not recommended in UK NICE guidance [1].
For athletes, there is an extra layer of complexity: energy availability and acute illness can both shift thyroid hormone levels without any thyroid disease, as discussed below, so a thyroid result has to be read in context. This article explains what hypothyroidism is, what causes it, how it is diagnosed and treated, and, in a shorter dedicated section, what it means for training and performance. It is the counterpart to the article on Graves’ disease, which covers the opposite problem: an overactive thyroid.
What Is Hypothyroidism?
Most cases are primary hypothyroidism, meaning the thyroid gland itself cannot produce enough hormone [1]. The pituitary gland responds by releasing more thyroid-stimulating hormone (TSH). Because modest changes in free T4 and free T3 produce much larger changes in TSH in the opposite direction, TSH is the accepted main marker of thyroid status [1].
Two biochemical categories are used [1]:
- Overt hypothyroidism: TSH above and free T4 below the laboratory reference range.
- Subclinical hypothyroidism: TSH above the reference range, with free T4 still within it.
A much rarer form, central hypothyroidism, originates in the pituitary or hypothalamus. Its key feature is a low free T4 without the expected rise in TSH, which is why measuring free T4 alongside TSH protects against missing it [1]. Central and peripheral forms together account for less than 1% of hypothyroidism worldwide [1].
How Common Is Hypothyroidism?
In iodine-sufficient countries, overt hypothyroidism affects approximately 1–2% of the population, and hypothyroidism (subclinical and overt combined) is around ten times more common in women than in men [1]. In older people, the prevalence is as high as 7% in those aged 85–89 when age-related reference ranges are not used [1].
Antibodies to thyroid peroxidase (TPO-Ab), the defining laboratory feature of Hashimoto’s thyroiditis, are found in roughly 11% of the general population [1]. The antibodies become particularly relevant in subclinical hypothyroidism, as discussed below.
What Causes Hypothyroidism?
Globally, iodine intake is a key determinant of thyroid disease risk, alongside factors such as ageing, smoking, genetic susceptibility, and ethnicity [2]. In practice, the main causes are:
Hashimoto’s thyroiditis. Chronic autoimmune thyroiditis is the most common cause of hypothyroidism in iodine-sufficient countries [1]. Lymphocytes infiltrate the gland and gradually destroy it, so thyroid function usually fails slowly [1]. The condition is thought to arise from genetic susceptibility combined with environmental factors, and twin studies estimate that about 65% of the variance is genetic [1].
Iodine deficiency. Historically, severe iodine deficiency was the most common cause worldwide. Only severe, not mild-to-moderate, deficiency results in hypothyroidism. The prevalence of iodine deficiency has declined dramatically since the early 1990s, and 88% of the global population now has access to iodised salt [1]. At the other extreme, a sudden large iodine load, for example from iodinated contrast media, can temporarily suppress hormone production; this is usually mild and transient [1].
Treatment of other thyroid disease. A total thyroidectomy creates an immediate need for thyroid hormone replacement, and hypothyroidism can also follow radioactive-iodine treatment for an overactive thyroid [1].
In my clinical experience, hypothyroidism occasionally develops as a consequence of treating hyperthyroidism. Patients who have had their thyroid removed or have received radioactive-iodine therapy may be left with permanent hypothyroidism and then need levothyroxine.
Medicines. Amiodarone and lithium are long-recognised causes, and immune checkpoint inhibitors used in cancer treatment have more recently been added to the list [1].
Symptoms of Hypothyroidism
The classic symptoms are fatigue, lethargy, weight gain, and cold intolerance, and hoarse voice and dry skin are also among the most common [1]. Hypothyroidism affects the cardiovascular system as well: it slows the heart rate, lowers cardiac output, increases vascular resistance, can raise diastolic blood pressure, and is associated with higher total and LDL cholesterol [1]. That last point is worth remembering when LDL cholesterol is unexpectedly high.
The problem is that none of these symptoms is specific. A population-based case-control study compared 140 people newly diagnosed with overt autoimmune hypothyroidism with 560 matched controls. Of 34 symptoms examined, 13 were more common in the hypothyroid group, most often tiredness (81%), dry skin (63%), and shortness of breath (51%), yet none of the individual symptoms had high likelihood ratios or diagnostic odds ratios for distinguishing patients from controls [3].
At the severe end, untreated hypothyroidism can rarely progress to myxoedema coma, an endocrine emergency with a reported mortality of 25–70%, although widespread thyroid testing and a low threshold for treatment have made it uncommon [1].
Because hypothyroidism can cause fatigue, feeling cold, and exhaustion, it is an important differential diagnosis to consider and rule out in conditions such as depression, exhaustion, and work-related burnout. In my view, the same applies to the work-up of suspected overtraining. In my clinical experience, many presentations closely resemble hypothyroidism, and it is worth remembering that a patient can also have hypothyroidism together with depression, burnout, or overtraining at the same time. That is why the differential diagnosis matters, and why, in my practice, thyroid tests are usually included in fatigue and anaemia panels as well as in the laboratory work-up for insomnia.
How Hypothyroidism Is Diagnosed
TSH is the preferred first test, with a typical reference range of about 0.4–4.0 mIU/L [1]; the TSH normal range article covers its interpretation in more detail. Several practical points help avoid misdiagnosis [1]:
- Repeat a raised TSH before diagnosing hypothyroidism. Marginally raised TSH values return to the reference range without treatment in up to half of cases.
- Measure free T4. It separates overt from subclinical hypothyroidism and prevents central hypothyroidism from being missed.
- Avoid testing during acute illness unless thyroid disease is the suspected cause. Unwell people often have temporarily abnormal results, typically low free thyroid hormones, and TSH can rise transiently, sometimes above 10 mIU/L, during recovery.
- Mention biotin. Biotin-containing supplements can interfere with some laboratory assays and produce misleading results.
- Account for age. In people over 65, the TSH reference range shifts towards higher values; in healthy older people, the 97.5th percentile is around 7.5 mIU/L, so older adults risk being started on levothyroxine unnecessarily.
- TPO antibodies add context. They are the defining feature of Hashimoto’s thyroiditis, and in subclinical hypothyroidism a positive result is an important risk factor for progression to overt disease.
In my practice, the starting point is usually TSH and free T4, and sometimes free T3. TSH is generally a sensitive marker, so when it is abnormal, free T4 is usually the first-line follow-up test to see where things stand. If the results are abnormal or point towards hypothyroidism, TPO antibodies are often checked at that stage, as they can help confirm an autoimmune cause.
Patients often ask when and how thyroid tests should be taken. TSH shows circadian variation, with higher concentrations towards the evening [1]. In the laboratories where I work, patients are usually instructed to have the sample taken in the morning or early afternoon, at least before 4 pm. For patients already on levothyroxine, I advise them not to take their dose on the morning of the test, as it may affect the result. Sampling instructions vary between laboratories, so it is worth following the local laboratory’s guidance.
Subclinical Hypothyroidism: To Treat or Not to Treat?
Most of the debate around hypothyroidism concerns the subclinical form. The main randomised evidence and the guidance built on it:
- A meta-analysis of 21 randomised trials including 2,192 adults found that thyroid hormone therapy was not associated with improvements in general quality of life or thyroid-related symptoms [4].
- In the TRUST trial, 737 adults aged 65 or older with persistent subclinical hypothyroidism (TSH 4.60–19.99 mIU/L) received either levothyroxine or placebo. At one year, there was no difference in the two primary outcomes, the hypothyroid symptoms and tiredness scores, and the authors concluded that levothyroxine provided no apparent benefit [5].
- Drawing on a systematic review of randomised trials, a BMJ Rapid Recommendations panel issued a strong recommendation against thyroid hormones for adults with subclinical hypothyroidism, concluding that almost all would not benefit and that clinicians should instead monitor whether the abnormality progresses or resolves. The recommendation does not apply to women trying to become pregnant or to people with TSH above 20 mIU/L, and it may not apply to people with severe symptoms or to young adults, such as those aged 30 or younger [6].
Some guidelines remain more permissive. European Thyroid Association, American Thyroid Association, and NICE guidance suggests that levothyroxine can be considered when TSH is 10 mIU/L or higher on two occasions three months apart, and the European and NICE guidance also allows a treatment trial in symptomatic people under 65 with a mildly raised TSH, to be stopped if symptoms persist once TSH has normalised [1]. A definitive trial showing benefit of levothyroxine for subclinical hypothyroidism in younger people is still missing [1]. People planning pregnancy or undergoing fertility treatment are managed according to separate guidance [1].
In practice, these situations are individual. Some patients have early hypothyroidism, and many are at the subclinical stage, in which TSH starts to rise above the reference range while free T4 remains within it. How I proceed depends on how high the values are and whether the patient has specific symptoms, but in many cases I tend to follow the patient and repeat thyroid tests at regular intervals, for example every few months. TPO antibodies can also help: if they are positive, gradual progression towards overt hypothyroidism is more likely. As long as the patient remains at the subclinical level, however, starting medication is not always necessary.
Treatment of Hypothyroidism: Levothyroxine
Overt hypothyroidism should be treated, although specific situations, such as resolving thyroiditis, can be managed expectantly [1]. Levothyroxine remains the standard of care [7]. The practical essentials [1]:
- Dose. The usual full daily dose in overt hypothyroidism is 1.5–1.8 µg per kilogram of body weight. Younger people without significant comorbidities can generally start on the full dose, whereas adults aged 65 or older and people with cardiovascular disease are usually started at 25–50 µg a day and titrated upwards.
- Timing. Absorption is best on an empty stomach and is reduced by many foods and drinks, particularly caffeine and milk. The usual advice is to take levothyroxine with water at least an hour before a meal; taking it at bedtime, or consistently 30 minutes before breakfast, are alternatives when that is impractical.
- Interactions. Calcium and iron preparations, antacids, and proton-pump inhibitors can reduce absorption.
- Monitoring. In adults taking levothyroxine for primary hypothyroidism, TSH is typically checked about every three months until it is stable, then once a year. In central hypothyroidism, treatment is monitored with free T4 rather than TSH.
- Pregnancy. Thyroid hormone requirements rise early in pregnancy, and guidelines recommend increasing the levothyroxine dose as soon as pregnancy is confirmed.
Interactions are worth discussing with patients. Some widely used medicines can affect the absorption of levothyroxine, and proton-pump inhibitors are a good example, because they are such a common drug group. In my clinical practice, I make a point of telling patients about this.
Even with a normal TSH, roughly 10–15% of treated patients remain dissatisfied because of persistent symptoms [1]. Combination therapy with levothyroxine and liothyronine (T3) has been tested in 18 randomised trials, and systematic reviews have not found a clear benefit over levothyroxine alone, although the trials had important limitations [1].
Getting the Levothyroxine Dose Right
Real-world control is often imperfect: the 2024 Lancet Seminar notes that 25–40% of people on long-term levothyroxine have a TSH outside the reference range [1].
That matters. A retrospective UK primary-care cohort study followed 162,369 patients with hypothyroidism. Outcomes were similar across the whole recommended TSH range, but compared with a TSH of 2–2.5 mIU/L, mortality was higher at TSH below 0.1 mIU/L (hazard ratio 1.18), 4–10 mIU/L (1.29), and above 10 mIU/L (2.21) [8]. A TSH above 10 mIU/L was also associated with more ischaemic heart disease, heart failure, and fragility fractures [8]. In older adults, overtreatment increases the risk of atrial fibrillation and osteoporosis [1].
When levothyroxine is first being adjusted, many patients need laboratory tests more often, and in my practice the interval at the start can range from weeks to months. Once the dose settles, less frequent testing is usually enough, often once a year. In my view, however, treatment is best not left unmonitored altogether: for my own patients, I check the values at least once a year, because in some patients thyroid levels may start to drift over the years if they are not followed. That said, many patients recognise their own symptoms, and this often prompts them to seek testing.
Hypothyroidism in Athletes: What It Means for Training and Performance
Among the studies reviewed here, research specifically on hypothyroidism in competitive athletes is limited, so this section combines patient studies, physiology research, and anti-doping data. Where a point is clinical synthesis rather than a direct research finding, it is labelled as such.
From a clinical perspective, hypothyroidism in athletes is treated in the same way as in sedentary people. In my view, being an athlete is not in itself a reason to deviate from standard treatment protocols, nor is it an indication for additional measurements. In my clinical experience, however, athletes may have a lower threshold for seeking testing, because they often notice when their performance starts to decline, whereas a sedentary person may not notice a drop in performance as easily. Otherwise, treatment and follow-up are the same as for anyone else.
Exercise Intolerance — and Why It Can Persist on Treatment
A systematic review concluded that exercise intolerance in untreated hypothyroidism has several causes acting together, involving cardiovascular, cardiopulmonary, musculoskeletal, neuromuscular, and cellular metabolic systems, and that it is not always reversed by adequate hormone replacement [9]. Only two of the included studies examined a physical training programme, and they showed inconsistent effects on performance capacity in untreated subclinical hypothyroidism [9].
In a Dutch case-control survey of 1,724 women treated for primary hypothyroidism and 1,802 controls, two-thirds of the patients reported that hypothyroidism limited their physical activity, and the limitation was more pronounced in those with autoimmune thyroiditis (odds ratio 1.93) [10]. The patients were less likely than controls to meet the moderate-intensity activity guideline (odds ratio 0.70) but more likely to take part in sports (odds ratio 1.40) [10].
Clinical synthesis: a normal TSH on treatment does not guarantee normal exercise capacity. If performance stays limited after thyroid levels have normalised, it is reasonable to look beyond the thyroid rather than simply increasing the dose; the broader differential is covered in why is my performance declining.
Low T3 From Energy Deficiency Is Not Hypothyroidism
Low energy availability can lower thyroid hormone levels without any thyroid disease. In a controlled study of 46 healthy, regularly menstruating sedentary women, four days of low energy availability (8 vs. 30 kcal per kg body weight per day) reduced T3 by 15% and free T3 by 18%, whereas the amount and intensity of exercise did not affect any thyroid hormone, and increasing dietary energy intake prevented the change [11]. In a separate study of women athletes, those with amenorrhoea had substantially reduced T4, T3, free T4, free T3, and reverse T3 despite normal TSH, while regularly menstruating athletes showed only a reduction in T4 [12].
This pattern, low thyroid hormones without a raised TSH, differs from primary hypothyroidism, in which TSH rises [1]. Clinical synthesis: in an athlete with low or low-normal free T3 and a normal TSH, low energy availability is one important explanation worth assessing before the finding is attributed to thyroid disease. The topic is covered in more depth in thyroid function in athletes and female athlete bloodwork.
In athletes, I sometimes see a different and somewhat unusual pattern in which both TSH and free T4 are low. In my clinical experience, this pattern has sometimes been seen in the context of energy deficiency. Athletes may be more prone to energy deficiency because of their high energy expenditure, and some need to diet to make a lower weight class, while in sports such as figure skating and gymnastics a low body weight can simply be an advantage. I may also see low TSH and free T4 together in patients with eating disorders, such as anorexia nervosa. In my view, such findings are not ordinary primary hypothyroidism, but they do need careful interpretation. Low free T4 with a non-elevated TSH is also the pattern of central hypothyroidism, which is rare but important not to miss [1], and the energy-deficiency research above mainly shows a fall in T3: in the controlled study, free T4 did not change [11].
Levothyroxine, Anti-Doping Rules, and Misuse
At the time of a 2023 study, thyroid hormone was not prohibited under the World Anti-Doping Code [13], so athletes with diagnosed hypothyroidism can generally be treated in the usual way; as with any medicine, it is still worth checking the current Prohibited List. In the Australian anti-doping programme that study examined, athletes declared all drugs used in the week before a test on a mandatory doping control form [13].
Misuse is a separate issue. Sports medicine doctors receive anecdotal reports of non-prescribed thyroid hormone use, particularly in weight-class sports such as weightlifting and combat sports, to make weight before a weigh-in [13]. Among Australian athletes undergoing anti-doping tests, biochemical thyrotoxicosis was found in 4 per 1000 in serum samples from 498 athletes, and in a separate sample, 2 of 509 doping control forms declared T4 use; the authors concluded that there was minimal evidence of thyroid hormone abuse in that group [13]. Abuse can nevertheless cause severe, dangerous thyrotoxicosis [13]; safer approaches are covered in weight cutting in combat sports.
Conclusion: Hypothyroidism
Hypothyroidism is common and its symptoms are vague, so the diagnosis is made with blood tests. Primary hypothyroidism, by far the most common form, shows a raised TSH, confirmed on repeat testing and read together with free T4; the rare central form is different and can show a low free T4 without a raised TSH. Overt primary hypothyroidism should generally be treated with levothyroxine, taken consistently on an empty stomach and adjusted to keep TSH within the reference range; in central hypothyroidism, treatment is instead monitored with free T4 rather than TSH [1]. Subclinical hypothyroidism is different: randomised trials have not shown that treating it improves how most people feel, so careful monitoring is often the better choice.
From a clinical perspective, thyroid tests are worth keeping in mind whenever fatigue, exhaustion, or a drop in performance is being investigated, because hypothyroidism can resemble, and coexist with, depression, burnout, and overtraining. In my practice, a mildly raised TSH is often followed with repeat testing rather than treated straight away, and once treatment has started, I check thyroid levels at least once a year, because they can drift over time.
For athletes, the main messages are practical. Hypothyroidism is treated in the same way as in anyone else, being an athlete is not in itself an indication for extra testing, and thyroid hormone was not prohibited under the World Anti-Doping Code at the time of the anti-doping study cited above. In my clinical experience, athletes may notice the problem sooner, because a drop in performance is easier for them to detect. Exercise capacity may not fully recover even when blood tests normalise, and low energy availability can lower T3 without thyroid disease, although a low free T4 with a non-elevated TSH still needs evaluation for central hypothyroidism. Using thyroid hormone without a diagnosis, for example to make weight, risks dangerous thyrotoxicosis.
Bibliography
[1] https://doi.org/10.1016/S0140-6736(24)01614-3
[2] https://doi.org/10.1038/nrendo.2018.18
[3] https://doi.org/10.1530/EJE-14-0481
[4] https://doi.org/10.1001/jama.2018.13770
[5] https://doi.org/10.1056/NEJMoa1603825
[6] https://doi.org/10.1136/bmj.l2006
[7] https://doi.org/10.1089/thy.2014.0028
[8] https://doi.org/10.1136/bmj.l4892
[9] https://doi.org/10.1080/02701367.2014.930405
[10] https://doi.org/10.1080/02640414.2021.1940696
[11] https://doi.org/10.1152/ajpregu.1993.264.5.R924
