Graves’ Disease: Causes, Symptoms, Diagnosis, and What It Means for Athletes
Table of Contents
Key Takeaways: Graves’ Disease
- Graves’ disease is the most common cause of hyperthyroidism and results from TSH-receptor antibodies that stimulate the thyroid independently of normal pituitary control.
- The symptoms are often nonspecific. Weight loss, fatigue, heat intolerance, tremor, palpitations, poor sleep, anxiety, and reduced performance can overlap with stress, work strain, overtraining, or low energy availability.
- Eye findings can be a major clinical clue. Characteristic Graves’ orbitopathy can make the diagnosis much more recognisable, although early eye changes may be subtle and can resemble an anxious or “wide-eyed” appearance.
- Diagnosis is primarily biochemical. A suppressed TSH with elevated thyroid hormones establishes hyperthyroidism, and positive TSH-receptor antibodies strongly support Graves’ disease as the underlying cause. Ultrasound and other imaging can provide additional information when needed.
- Patients usually cannot identify one clear reason why they developed Graves’ disease. Genetic susceptibility appears to play a major role, while environmental factors such as iodine exposure, smoking, infections, and possibly stress may contribute. In an individual patient, the exact trigger is often impossible to determine.
- Untreated hyperthyroidism can impair rather than improve athletic performance. Excess thyroid hormone can reduce exercise tolerance, muscle strength, lean body mass, and oxidative capacity despite increasing heart rate and cardiac output.
- Athletes do not need separate diagnostic criteria for Graves’ disease. They may simply notice subtle changes in resting heart rate, recovery, weight, or performance earlier and therefore seek assessment sooner.
- Do not assume declining performance is just overtraining. When symptoms such as persistent tachycardia, unexplained weight loss, heat intolerance, tremor, or eye changes accompany reduced performance, thyroid disease should remain in the differential diagnosis.
Introduction: Graves’ Disease
Graves’ disease is the most common cause of hyperthyroidism, and roughly 3% of women and 0.5% of men will develop it during their lifetime [1]. It is a diagnosis I encounter from time to time in clinical practice, although certainly not every day. Occasionally the eye findings are striking enough to immediately raise suspicion, but more often the presentation is less distinctive and the symptoms can point in several different directions.
For many patients, the first clues are symptoms such as unexplained weight loss, palpitations, tremor, heat intolerance, fatigue, or poor sleep. The difficulty is that none of these is unique to Graves’ disease. In practice, palpitations and insomnia may initially be attributed to stress, restlessness to work-related exhaustion, and weight loss may prompt concern about other systemic illness. Excessive sweating can also broaden the differential diagnosis considerably. In athletes, the picture can be even harder to interpret because unexplained weight loss, fatigue, disturbed sleep, and a rising resting heart rate can overlap with concerns such as overtraining or low energy availability. A report describing Graves’ disease in young athletes highlighted exactly this problem: some presentations can resemble ordinary sports-related concerns such as overtraining [2].
From a clinical perspective, thyroid disease is often uncovered because thyroid function tests are included early in the evaluation of otherwise unexplained systemic symptoms. This is one reason Graves’ disease can be identified through routine blood testing even when the initial clinical picture is nonspecific. In principle, the diagnosis should therefore not be especially difficult to reach once hyperthyroidism is considered, but in practice delays can still occur when the symptoms are initially interpreted through another, more familiar explanation.
This article explains what Graves’ disease is, what is known about its causes, how it is diagnosed and treated, and, in a dedicated section, what the condition means for training, performance, laboratory testing, and return to sport.
What Is Graves’ Disease?
Graves’ disease is an autoimmune disorder that mainly targets the thyroid gland. The immune system produces autoantibodies against the thyroid-stimulating hormone (TSH) receptor. Instead of blocking the receptor, these antibodies behave like agonists: they activate it and drive excessive thyroid hormone secretion, so the gland is no longer under normal pituitary control [3]. The same TSH-receptor antibodies also underlie the two characteristic features outside the thyroid, Graves’ orbitopathy and pretibial myxoedema [3].
This mechanism explains the typical laboratory picture. Normally, the pituitary lowers its TSH output when thyroid hormone levels rise. In Graves’ disease, the antibodies keep stimulating the gland regardless, so thyroid hormone levels climb while TSH is pushed down. How this feedback loop behaves in trained individuals is covered in more detail in thyroid function in athletes.
In clinical practice, Graves’ disease is something I encounter from time to time in primary care. Sometimes the suspicion arises from the patient’s symptoms, but in other cases the first clue comes from blood tests obtained for a broader reason, including routine laboratory work in occupational health care. A suppressed TSH or an elevated free T4 can be the finding that shifts the focus toward hyperthyroidism and prompts a more targeted evaluation. From a primary-care perspective, this is therefore not an especially exotic diagnosis, even though confirmation of the cause and decisions about treatment may involve specialist consultation.
Graves’ disease is the leading cause of hyperthyroidism in regions with adequate iodine intake. The 2018 European Thyroid Association (ETA) guideline puts its incidence at 20–30 new cases per 100,000 people per year, its population prevalence at 1–1.5%, and its peak incidence between the ages of 30 and 60 [4]. A 2016 review in the New England Journal of Medicine gives a wider incidence range of 20–50 cases per 100,000 per year, with a peak between 30 and 50 years of age, while emphasising that people of any age can be affected [1].
What Causes It? Genes, Smoking, and Stress
No single cause of Graves’ disease has been identified. The current understanding is that it develops through an interaction between genetic susceptibility and environmental factors [1].
Genetics. Twin studies from Denmark and Sweden show a concordance rate of 20–35% in identical twins compared with 2–3% in non-identical twins, a pattern consistent with genetic factors accounting for 60–80% of the risk of developing Graves’ disease [5].
Environmental factors. The factors most often cited are dietary iodine, tobacco smoke, infections, and emotional stress [1]. Iodine is a nuanced case. Long-term differences in iodine intake do not appear to change the risk of the disease, but a rapid increase in iodine intake can temporarily raise its incidence [1]. That observation comes from population-level iodine changes rather than from studies of individual supplement users, but it is one more reason not to take high-dose iodine or kelp products “just in case” — a point discussed further in iodine in athletes.
Stress. Stress is frequently mentioned as a trigger, and the question matters to athletes because hard training is itself a physiological stressor. A 2026 systematic review identified 13 eligible studies with at least 2,867 participants, including 1,134 with confirmed Graves’ disease [6]. Most of the retrospective case-control studies found that people with Graves’ disease reported a greater burden of negative life events in the year before diagnosis than controls. However, the limited prospective evidence did not support an association with new-onset disease, and the reviewers rated the overall certainty of the evidence as very low, mainly because of recall bias and the possibility of reverse causation [6]. Because these findings centre on negative life events rather than training load, they cannot be read as evidence that hard training triggers Graves’ disease.
From a clinical perspective, I would not usually frame Graves’ disease as something a patient has simply brought on themselves through their lifestyle. The working model is closer to an underlying susceptibility combined with environmental influences, while the exact event that ultimately triggers the disease in an individual patient is often impossible to identify. Patients sometimes ask whether something they did — their diet, stress level, training, or another aspect of their lifestyle — caused the disease. In many cases, there is no convincing way to make that connection. I think this distinction matters, because identifying a possible risk factor is not the same as being able to explain why a particular person developed Graves’ disease at a particular time.
Symptoms and Complications
How Graves’ disease presents depends on the patient’s age and on how severe and how long-standing the hyperthyroidism is [1]. The five most common symptoms, each reported by more than half of patients, are weight loss, fatigue, heat intolerance, tremor, and palpitations [1]. Other typical features include muscle weakness, breathlessness, increased sweating, more frequent bowel movements, anxiety, insomnia, menstrual disturbances in women, reduced libido, and a sense of fullness in the neck [1]. Not everyone loses weight: around 10% of patients gain weight instead [1].
One of the practical difficulties is that many of these symptoms are nonspecific. In both primary care and occupational health, I see plenty of patients with palpitations, poor sleep, restlessness, or a sense that they are under too much stress. Those symptoms can easily be interpreted through a psychological or workload-related lens. I try not to close the differential diagnosis too early. Even when stress seems like a plausible explanation, I still keep a somatic cause in mind until the clinical picture and basic investigations make that less likely.
In practice, this is where simple laboratory testing becomes useful. When symptoms are broad or difficult to explain, basic blood work often forms part of the initial assessment, and thyroid testing is commonly included. TSH is usually the first thyroid marker checked; free T4 may be added depending on the clinical situation or the laboratory panel being used. The important point is not that every patient with palpitations or insomnia has thyroid disease, but that Graves’ disease is easy to miss if these symptoms are assumed to be stress-related before a basic medical assessment has been completed.
Age changes the picture. A palpable goitre develops in most patients younger than 60, but in fewer than half of older patients, while weight loss, reduced appetite, and cardiac manifestations are more common in older people [1].
The heart. Atrial fibrillation is the arrhythmia most closely associated with hyperthyroidism. It is rare in patients younger than 60 but affects more than 10% of those aged 60 or older [1]. In a Danish registry of 40,628 patients with hyperthyroidism from any cause, 8.3% were diagnosed with atrial fibrillation or flutter within 30 days on either side of the hyperthyroidism diagnosis. The proportion was 12.1% in men and 7.6% in women, and the odds rose with male sex and with each additional decade of age [7].
Muscle. Neuromuscular involvement is common. In a prospective study of patients with newly diagnosed thyroid dysfunction, 67% of those with hyperthyroidism had neuromuscular symptoms and 62% had clinically detectable weakness in at least one muscle group. The degree of weakness correlated with free T4 concentrations but not with serum creatine kinase [8] — so a normal creatine kinase result alone should not be used to judge the presence or severity of hyperthyroid muscle weakness.
Bone. The ETA guideline lists weight loss, osteoporosis, fragility fractures, atrial fibrillation, embolic events, and cardiovascular dysfunction among the problems associated with hyperthyroidism [4]. In a study using high-resolution peripheral quantitative CT, women with hyperthyroidism had lower volumetric bone mineral density, lower estimated bone strength, and poorer cortical microarchitecture at the radius than healthy controls. After one year of restored euthyroidism, cortical area, cortical thickness, and total volumetric bone mineral density improved significantly; the change in estimated bone strength specifically was not confirmed to the same degree [9].
Quality of life. Beyond the physical symptoms, Graves’ disease affects quality of life through both somatic and psychiatric symptoms and through reduced ability to work, and it is associated with an increased risk of death [1].
Graves’ Orbitopathy: When the Eyes Are Involved
Graves’ orbitopathy, also called thyroid eye disease, is the most common and most serious manifestation outside the thyroid [1]. How often it is found depends heavily on how carefully it is looked for. A 2020 review concluded that orbitopathy of any grade affects between 25% and 40% of patients with Graves’ hyperthyroidism [10], and orbital imaging can show subtle abnormalities in 70% [1].
Clinically significant eye disease is much less common. In a prospective series of 346 patients with newly diagnosed Graves’ hyperthyroidism, 255 had no eye signs or symptoms, 70 had mild and inactive orbitopathy, 20 had moderate-to-severe active disease, and one had sight-threatening disease [11].
Bulging of the eyes (proptosis), swelling of the eyelids, and double vision are changes that may prompt a patient to see a doctor, and some first notice dry eyes, increased tearing, or eye discomfort [1].
The 2021 guidelines of the European Group on Graves’ Orbitopathy (EUGOGO) identify smoking, thyroid dysfunction, high TSH-receptor antibody levels, radioactive iodine treatment, and high cholesterol as risk factors. They recommend that every patient with Graves’ hyperthyroidism be urged to stop smoking, whether or not the eyes are affected [12]. For mild and active orbitopathy, controlling these risk factors, local eye treatments, and selenium supplementation in selenium-deficient areas are usually enough [12].
A skin manifestation, thyroid dermopathy (pretibial myxoedema), is rare. It affects 1–4% of patients and is almost always seen in those with severe eye disease [1].
From a clinical perspective, the eye manifestations are often among the clearest features of Graves’ disease. The systemic symptoms alone may already raise suspicion, but when symptoms such as palpitations, weight loss, tremor, or heat intolerance occur together with characteristic eye findings, the clinical picture becomes much more suggestive.
In practice, that combination is something that immediately catches a clinician’s attention. The systemic symptoms are relatively nonspecific and can have many possible explanations, whereas typical ocular findings make Graves’ disease much harder to overlook. That said, in my own clinical experience, very early eye changes are not always dramatic. A patient may simply look unusually wide-eyed or slightly worried, with the eyes appearing more open than expected. That appearance can resemble the facial expression of someone who is anxious or under significant stress, so the clue may be easy to dismiss if it is considered in isolation. For me, it becomes more meaningful when that visual impression appears alongside other features that fit hyperthyroidism.
At the same time, the absence of obvious eye involvement does not rule Graves’ disease out, so the diagnosis still has to be considered on the basis of the broader clinical picture.
How the Diagnosis Is Made
Diagnosis starts with blood tests. The usual first step is to measure TSH and free T4. A low TSH with a high free T4 indicates hyperthyroidism. A low TSH with a normal free T4 prompts measurement of free T3, which can reveal T3-predominant thyrotoxicosis or, if normal, subclinical hyperthyroidism [1].
This is a different picture from the one seen at group level in endurance athletes: in a 2024 study of 1,342 euthyroid Olympic athletes, those competing in endurance disciplines had lower mean TSH, free T3, and free T4 than athletes in other sporting disciplines, rather than showing the suppressed-TSH-with-elevated-hormone pattern of Graves’ disease [17]. That athlete-specific pattern is discussed further in low TSH in athletes.
Once hyperthyroidism is confirmed, the next question is its cause. The ETA guideline recommends measuring TSH-receptor antibodies (TRAb) as a sensitive and specific tool for a rapid and accurate diagnosis [4]. In a meta-analysis of second- and third-generation TRAb assays, all of the pooled sensitivity and specificity estimates fell between 97.1% and 99.2%, with little difference between assay types [13].
The ETA recommends thyroid ultrasound with colour-flow or power Doppler as the supporting imaging method [4]. According to the guideline, the diagnosis is straightforward when biochemically confirmed thyrotoxicosis is accompanied by positive TRAb, a hypervascular and hypoechoic gland on ultrasound, and orbitopathy [4]. When doubt remains, radionuclide scanning or radioiodine uptake can help separate the causes: homogeneous, increased uptake points to Graves’ disease; patchy uptake or a single hot nodule points to toxic nodular goitre; and low or absent uptake points to thyroiditis or excess thyroid hormone intake [1].
In a straightforward case, the combination of a suppressed TSH, elevated free T4, and positive TSH-receptor antibodies can make the diagnosis clinically quite clear. In my own practice, once that biochemical pattern is present, the next step is usually to involve specialist care rather than to delay the process while waiting for every additional investigation to be completed in primary care. Thyroid ultrasound can add useful information, but it is not always immediately available, and in practice it may be performed later as part of the specialist assessment.
The practical pathway also depends on where the patient enters the healthcare system. In occupational health care, for example, TSH and free T4 are usually easy to obtain, but TSH-receptor antibodies may not be included in every employer’s laboratory agreement. That can occasionally add an extra step before the diagnosis is fully clarified. More comprehensive occupational health coverage or private insurance can sometimes make the diagnostic pathway more direct simply because the necessary tests and consultations are easier to access.
The bottleneck can look different in public primary care. There, the delay may be less about which test is theoretically needed and more about ordinary resource constraints: appointment availability, laboratory access, and the time required to obtain specialist input. Specialist services themselves can also have waiting times. In my experience in Finland, treatment may sometimes be started after specialist consultation before the patient has attended the full specialist assessment, with the patient then seen later for more detailed evaluation and follow-up. From a clinical perspective, this is a useful reminder that the biology of Graves’ disease is only one part of the diagnostic process; access to testing and specialist care can also influence how quickly the diagnosis is completed.
Graves’ Disease in Athletes: What It Means for Training and Performance
The sources reviewed here do not include large studies of Graves’ disease specifically in competitive athletes. What follows therefore combines physiology studies, clinical cohorts, and sports medicine reasoning. Where a point is clinical synthesis rather than a direct research finding, it is labelled as such.
Why It Can Look Like Overtraining
The overlap with overtraining is easy to see when the two symptom lists are placed side by side. Fatigue, weight loss, disturbed sleep, anxiety, and declining performance can occur in both, and a rising resting heart rate is a common talking point in both settings (see resting heart rate changes in overtrained athletes and why is my performance declining). A report on Graves’ disease in young athletes made the same point: certain presentations can mimic overtraining [2].
Some features point more toward hyperthyroidism than toward training load. These include weight loss despite unchanged or increased food intake, new heat intolerance and sweating, a fine tremor, eye changes, a palpable goitre, and a resting heart rate that stays high through planned rest days. Several of these are described in the symptom profile of Graves’ disease [1]; using them together to distinguish thyroid disease from training load is clinical synthesis, not a tested diagnostic rule. None of them is diagnostic on its own, but together they justify a thyroid panel rather than another week of reduced training.
It is also worth keeping the testing threshold in perspective. From a clinical standpoint, I would not use fundamentally different criteria for thyroid testing simply because someone is an athlete. The same symptoms and basic medical reasoning still apply. What can differ in practice is the threshold for seeking care: athletes may notice relatively small changes in performance, recovery, or resting heart rate earlier because these variables matter to them and are often followed more closely. When an athlete presents because performance has declined without a clear explanation, basic laboratory testing, including thyroid function, often becomes relevant fairly early in the work-up. In that sense, sport does not place the patient in a separate diagnostic category, but it may make subtle physiological changes noticeable sooner.
Female athletes face an additional trap. Menstrual disturbances, including oligomenorrhoea and amenorrhoea, are part of the symptom profile of Graves’ disease [1], and menstrual dysfunction is also a well-recognised consequence and indicator of problematic low energy availability, which can occur with or without obvious weight loss [18].
Exercise Capacity: Why Hyperthyroid Athletes Get Slower, Not Faster
It is tempting to assume that more thyroid hormone, with its “faster metabolism”, would help performance. The evidence points the other way. A review of cardiovascular function in thyroid disease concluded that excess thyroid hormone can substantially reduce the strength of respiratory and skeletal muscles. Exercise testing in hyperthyroidism shows inefficient cardiopulmonary function with impaired heart rate, contractile, and vasodilatory reserves, and these abnormalities reverse once normal thyroid function is restored [14].
The clearest mechanistic data come from an experiment in which 18 healthy young adults (mean age 26) took 100 µg of T3 daily for two weeks [15]. Resting oxygen uptake, heart rate, and cardiac output increased, as did heart rate and cardiac output at the same submaximal workload. Yet maximal oxygen uptake fell from 3.08 to 2.94 L/min, even though heart rate and cardiac output at maximal exercise were higher. Blood lactate at an equivalent submaximal intensity was 25% higher. Muscle samples showed a 21–37% decline in the activity of oxidative and glycolytic enzymes and a 15% reduction in the cross-sectional area of type IIA muscle fibres, alongside reduced lean body mass and faster whole-body protein breakdown [15]. The authors attributed the impaired exercise tolerance to loss of muscle mass and oxidative capacity from accelerated protein breakdown, not to reduced cardiac pumping [15].
Two caveats apply. This was short-term, experimentally induced T3 excess in healthy volunteers rather than Graves’ disease, and the severity and duration of thyrotoxicosis in real patients vary widely. Still, the direction of the findings is consistent with the clinical data.
The good news is that weakness in hyperthyroidism appears to be largely functional and reversible. In the prospective neuromuscular study described above, weakness developed rapidly early in the disease and resolved completely during treatment, on average within 3.6 months [8].
Conclusion: Graves’ Disease
Graves’ disease is a common autoimmune cause of hyperthyroidism, but the diagnosis is not always obvious from the first symptom. Weight loss, palpitations, poor sleep, restlessness, fatigue, and declining performance can all be interpreted through other explanations, particularly stress, work strain, or training load. In my view, the practical challenge is therefore less about recognising a textbook case and more about remembering to keep thyroid disease in the differential diagnosis when otherwise common symptoms do not quite fit together.
Fortunately, once hyperthyroidism is suspected, the diagnostic pathway is usually much more straightforward. A suppressed TSH, elevated thyroid hormones, and positive TSH-receptor antibodies can make the underlying diagnosis quite clear, while imaging and specialist assessment help refine the picture when needed. The eye findings remain particularly useful clinically: obvious Graves’ orbitopathy can make the diagnosis immediately more recognisable, although subtle early changes may still resemble the wide-eyed or worried appearance of someone who is simply anxious or under stress.
For athletes, Graves’ disease does not require a separate diagnostic framework, but the context can make the condition easier to notice. Athletes may seek assessment sooner because changes in resting heart rate, recovery, weight, or performance matter to them and are often followed closely. At the same time, those same changes can easily be attributed to overtraining or low energy availability. The important distinction is that sport does not change the basic medical reasoning; it simply creates another set of plausible explanations that can compete with the correct one.
The broader lesson is that Graves’ disease is rarely something a patient can reasonably blame on a single lifestyle choice. Genetic susceptibility appears to play a major role, while environmental influences and possible triggers are much harder to pin down in an individual case. From a clinical perspective, the most useful approach is not to search for one simple cause, but to recognise the pattern, confirm the biochemical diagnosis, and move the patient into appropriate follow-up and treatment without unnecessary delay.
Bibliography
[1] https://doi.org/10.1056/NEJMra1510030
[2] https://doi.org/10.1080/00913847.1996.11948058
[3] https://doi.org/10.1038/s41572-020-0184-y
[4] https://doi.org/10.1159/000490384
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC10808215/
[6] https://doi.org/10.7759/cureus.113609
[7] https://doi.org/10.1001/archinte.164.15.1675
[8] https://doi.org/10.1136/jnnp.68.6.750
[9] https://doi.org/10.1089/thy.2020.0084
[10] https://doi.org/10.3389/fendo.2020.615993
[11] https://doi.org/10.1210/jc.2012-3873
[12] https://doi.org/10.1530/EJE-21-0479
[13] https://pubmed.ncbi.nlm.nih.gov/22776786/
[14] https://doi.org/10.1089/105072502760143845
[15] https://doi.org/10.1172/JCI115533
