Iodine in Athletes: The Mineral Undermining Thyroid Function and Performance
Table of Contents
Key takeaways: Iodine in Athletes
- Iodine is essential for thyroid hormone synthesis, but it should not be treated as a universal performance supplement for athletes.
- In routine clinical practice, especially in Finland, clinically meaningful iodine deficiency appears relatively uncommon when people eat a varied diet and use iodized salt.
- Athlete status alone is usually not enough to suspect iodine deficiency. The more relevant factors are diet, thyroid-related symptoms, laboratory findings, and the broader clinical context.
- Sweat can contain iodine, and high sweat losses may matter over time, but iodine is not an acute electrolyte issue like sodium or potassium. Its relevance is more chronic and nutritional.
- Endurance athletes may show lower thyroid hormone markers, but this should not automatically be interpreted as iodine deficiency. Energy availability, training load, recovery, and overall nutrition often matter more.
- Vegan and plant-based athletes may be at higher risk of low iodine intake, especially if they avoid dairy, seafood, eggs, and iodized salt.
- In many cases, low iodine intake can be addressed through simple dietary choices, such as using iodized salt when salt is already being used, rather than immediately turning to supplements.
- Urinary iodine is mainly useful for iodine status assessment, but in Finnish primary care it is not usually measured routinely. Thyroid function tests are typically the first-line clinical tests.
- Iodine supplements should not be used casually “just in case.” Excess iodine can disturb thyroid function, especially in people with underlying autoimmune thyroid disease.
- The practical clinical message is balance: iodine is worth remembering in selected athletes, but it should not be overdiagnosed or placed ahead of more common issues such as low energy intake, iron deficiency, vitamin B12 deficiency, vitamin D status, hydration, and electrolyte balance.
Introduction: Iodine in Athletes
Scan a typical athlete’s supplement cabinet and you’ll find protein powder, creatine, vitamin D, magnesium — all the expected players. What you almost certainly won’t find is iodine. Yet iodine is the raw material the body uses to build thyroid hormones, and thyroid hormones regulate metabolism, energy production, and protein synthesis — functions central to aerobic capacity, muscle recovery, and cardiac adaptation. Without adequate iodine over time, the substrate needed for normal thyroid hormone synthesis becomes limited.
Despite widespread salt iodization programs in many countries, 30% of the world’s population is still at risk of iodine deficiency [1]. In athletes — particularly those with high sweat losses, low intake of iodized salt, dairy, seafood, or eggs, or restrictive dietary patterns — iodine status may warrant closer attention. The problem is especially insidious because iodine deficiency does not usually announce itself clearly. Fatigue, slow recovery, weight changes, cold intolerance, and low-normal thyroid markers can easily be interpreted only through the lens of training stress, recovery debt, or under-fueling.
At the same time, iodine deficiency is not something I would overstate in routine clinical practice. In the setting where I work in Finland, clinically relevant iodine deficiency appears relatively uncommon, and iodine supplementation is not usually a central part of everyday patient care. That observation is partly shaped by the Finnish nutrition context, where iodized salt is widely used and iodine is added to many table salts. For most people eating a varied diet, iodine intake is generally adequate. This is also why iodine deficiency is not often at the center of clinical decision-making in athletes, even though iodine remains physiologically important.
From a clinical perspective, iodine is an interesting paradox. Many people are more familiar with iodine tablets used in radiation emergencies than with iodine as an everyday nutrient involved in thyroid function. In routine clinical conversations, it often stays almost invisible unless there is a specific dietary risk, thyroid-related concern, or unusual exposure context. For athletes, this means iodine is not a nutrient to panic about, but it is one worth considering when the broader picture includes restrictive eating, low use of iodized salt, vegan diets, high sweat losses, or unexplained symptoms that overlap with thyroid dysfunction.
This article reviews the physiology of iodine and thyroid hormone synthesis, examines how exercise and diet can create specific iodine-related vulnerabilities in athletes, and outlines practical assessment and intervention strategies without treating iodine deficiency as a universal explanation for poor performance.
Iodine in Athletes: A Practical Perspective on Thyroid Function
Iodine is a trace element and an essential component of thyroid hormones thyroxine (T4) and triiodothyronine (T3), which are critical for liver, kidney, muscle, brain and central nervous system function [1]. Adequate dietary iodine availability is required to sustain normal T3 and T4 synthesis over time — there is no substitute mineral that can perform this role [7].
The cascade is straightforward: adequate dietary iodine → sufficient T3 and T4 synthesis → optimal metabolism, aerobic capacity, thermoregulation, protein synthesis, and recovery. When iodine intake remains inadequate over time, thyroid hormone synthesis can become constrained, with potential downstream consequences for metabolism and training adaptation. This is why iodine in athletes deserves the same systematic attention as iron, vitamin D, or magnesium.
The World Health Organization (WHO) defines adequate iodine status in a non-pregnant population as a median urinary iodine concentration (UIC) of 100–199 µg/L, with severe iodine deficiency defined as UIC concentrations < 20 µg/L [1]. The daily recommended dietary allowance (RDA) established by the Institute of Medicine is 150 µg for adults ages 14 and older, rising to 220 µg for pregnant women and 290 µg for lactating women [1].
Despite these established thresholds, iodine deficiency remains widely prevalent. In the U.S. in 2011–2012, 38% of population UIC measurements fell below 100 µg/L — a threshold the review authors used to characterize iodine deficiency at the group level [1]. These are not numbers from a developing country — this is a modern, industrialized population in which iodized salt has been available for nearly a century. For athletes who salt their food less, follow specialty diets, or train in conditions that drive high sweat losses, iodine intake may warrant additional scrutiny.
Although iodine deficiency remains a real public health issue globally, I would be careful not to overstate how often it becomes clinically relevant in everyday practice, at least in Finland. In the Finnish setting, it is relatively uncommon to see clear cases where a patient’s thyroid function or general health appears to be meaningfully impaired because of iodine deficiency alone.
Part of this is likely explained by the local nutrition context. In Finland, iodized salt has long been part of public nutrition strategy, and many people still consume more salt than is ideal from a cardiovascular perspective. That is not a reason to encourage higher salt intake, but it does mean that iodine intake is often indirectly protected through ordinary dietary habits. The situation is not the same everywhere in the world, and athletes with restrictive diets or low use of iodized salt may still deserve individual attention. But in Finnish athletic populations, iodine deficiency is rarely the first issue I would place at the center of clinical reasoning.
Exercise and Iodine in Athletes — Why the Vulnerability Is Unique
The Sweat Loss Problem
Most discussions of micronutrient losses in exercise focus on sodium, potassium, and magnesium. Iodine rarely comes up — yet athletes or those participating in vigorous exercise can lose a considerable amount of iodine in sweat, depending on environmental factors such as temperature and humidity [5]. Unlike electrolyte losses, iodine losses in sweat receive almost no routine attention in sports nutrition practice.
Athletes or those participating in vigorous exercise can lose a considerable amount of iodine in sweat, depending on environmental factors such as temperature and humidity [5]. Sweat iodine concentrations have been reported around 35–40 µg/L, and calculations suggest that losses with 4–5 liters of sweat could approach the daily RDA of ~150 µg [5]. When added to urinary iodine excretion, such losses would result in a significant diminution in the body’s iodine stores [5].
When discussing nutrient losses through sweat, it is important to keep iodine in the right clinical perspective. In practice, iodine deficiency is not usually an acute safety issue in the way that fluid balance and major electrolytes can be. Sodium and potassium tend to receive more clinical attention for a good reason: disturbances such as exercise-associated hyponatremia or clinically significant potassium abnormalities can, in some situations, become acute medical problems that require rapid assessment and treatment.
Iodine is different. It is not usually a “same-day” electrolyte problem after a hard training session. Its relevance is more likely to emerge over time, as part of a chronic nutritional and thyroid-related picture, especially if high sweat losses occur alongside low iodine intake. In my clinical setting in Finland, this risk is often partly buffered by ordinary dietary patterns and the use of iodized salt, so iodine deficiency is not usually the first explanation I would reach for in an athlete with fatigue or poor recovery. Still, the point is not that iodine should replace sodium, potassium, or hydration as priorities. Rather, it can become relevant in selected athletes when the broader context includes restrictive eating, low use of iodized salt, vegan diets, high sweat losses, or thyroid-related symptoms.
Exercise-Induced Thyroid Hormone Changes
Exercise itself alters thyroid hormone dynamics, and these changes are more pronounced in endurance athletes than in any other athletic group. A large study evaluating 1342 Olympic athletes across power, skill, endurance, and mixed sports found that endurance athletes presented the lowest TSH (p < 0.0001), fT3 (p = 0.007), and fT4 (p < 0.0001) in comparison to the remaining disciplines [3].
Chronic aerobic training is associated with lower thyroid hormone levels in cross-sectional data, a finding that may reflect an adaptive response to sustained training load [3]. Whether this pattern is fully reversible with changes in training or nutrition is not established from this cross-sectional study alone. From a clinical perspective, when this pattern coexists with inadequate iodine intake, interpretation of thyroid markers becomes more complex — because substrate limitation and training-related adaptation can produce overlapping findings. This is precisely why standard thyroid function in athletes testing should be paired with dietary review and urinary iodine assessment when relevant.
Thyroid dysfunction can be brought on by nutritional factors, including insufficient energy intake and iodine, selenium, iron, and vitamin D deficiency [4]. Among these, iodine is often the least systematically reviewed in athletic nutrition assessments — a gap that this article aims to address. The interaction with selenium is worth noting specifically: selenium is required for the deiodinase enzymes that convert T4 into the active T3, meaning iodine and selenium deficiency can act in concert to suppress thyroid hormone output — a distinction explored further in copper in athletes, which covers the broader network of trace elements affecting mitochondrial and hormonal function.
It is important to separate exercise-related changes in thyroid markers from true iodine deficiency. In clinical reasoning, I would not usually assume that lower thyroid hormone values in an athlete are caused by iodine deficiency unless the dietary history or iodine status points in that direction. These are related topics, but they are not the same mechanism.
In practice, many thyroid hormone changes seen in athletes are more closely connected to energy availability than to iodine itself. When energy intake is low relative to energy expenditure, the body may downshift thyroid hormone activity as part of a broader adaptation to limited energy availability. This can happen in athletes, but the underlying issue is not necessarily exercise itself. A similar pattern could theoretically occur without sport if a person were in a sustained energy deficit. From a clinical perspective, this is why I would interpret low-normal thyroid markers in an athlete alongside training load, diet, weight changes, recovery, menstrual status when relevant, and overall energy balance — not as automatic evidence of iodine deficiency.
At-Risk Athletic Populations — Iodine Deficiency in Athletes Who Look Healthy
Vegan and Plant-Based Athletes
The convergence of athletic culture and plant-based eating has created a population with disproportionate iodine vulnerability. In this systematic review and meta-analysis, vegan diets had the poorest iodine intake (17.3 µg/d) and were strongly associated with lower iodine intake (P < 0.001) compared with omnivorous diets [2]. For context, 17.3 µg/day is approximately 11% of the adult RDA of 150 µg/day — a shortfall of a magnitude that is often invisible in standard blood panels.
In the same review, the vegan group with the lowest reported status had a median urinary iodine concentration (mUIC) of 12.2 µg/L [2], which falls in the range of severe iodine deficiency according to WHO population-level criteria (< 20 µg/L). Across the entire review, none of the dietary groups had mUIC within the optimal range for iodine status (100–200 µg/L) according to WHO criteria [2].
The mechanistic explanation is simple: dairy products and seafood — the primary dietary iodine sources in most Western countries — are excluded from vegan diets. Plant foods are naturally low in iodine unless grown in iodine-rich soil or biofortified. Plant-based milk alternatives, increasingly common in the sports nutrition community, are rarely fortified with iodine despite being fortified with calcium, vitamin B12, and vitamin D. Female athletes following plant-based diets face a compounded risk, as discussed in female athlete bloodwork, where multiple micronutrient deficiencies — iron, vitamin B12, and now iodine — often coexist.
If iodine intake is low in a plant-based athlete, the solution is not always complicated. In Finland, for example, simply choosing iodized salt instead of non-iodized specialty salt can often improve iodine intake, as long as total salt use remains medically appropriate. This is not a reason to increase salt indiscriminately, but it is a practical detail that is easy to miss. In clinical discussions with plant-based athletes, iodine is rarely the first concern; still, if the athlete avoids dairy, seafood, and iodized salt, iodine becomes a simple but relevant question to ask.
Energy Restriction and RED-S
Another contributor to thyroid suppression in athletes is chronic energy restriction. As noted by Larson-Meyer, insufficient energy intake is one nutritional factor that can impair thyroid function, and low energy availability often coexists with marginal micronutrient status, including iodine [4]. An athlete in chronic low energy availability who also has marginal iodine intake may face both substrate limitation and energy-related thyroid suppression simultaneously. The resulting low fT3 with non-elevated TSH can resemble other patterns seen in RED-S blood work, which is why distinguishing energy-deficiency thyroid changes from nutritional iodine insufficiency requires a complete clinical picture including dietary history, energy intake assessment, and urinary iodine testing when indicated.
The symptom overlap is also significant: fatigue, mood changes, impaired recovery, and cold intolerance characterize both iodine deficiency and the hormonal dysregulation detailed in cortisol and overtraining. In practice, evaluating both together — rather than sequentially — avoids missing a treatable nutritional contribution to what looks like a pure training-load problem.
In most cases, however, RED-S-related changes in thyroid hormones should not be interpreted as direct evidence of iodine deficiency. Low energy availability can reduce overall nutrient intake, so an athlete who is under-fueling may also consume less iodine simply because they are eating less food. However, the thyroid hormone pattern seen in RED-S is usually more closely related to energy availability itself than to iodine as the primary mechanism. From a clinical perspective, this distinction matters: low-normal thyroid markers in an under-fueled athlete should prompt a broader assessment of energy intake, training load, recovery, and diet rather than being treated automatically as an iodine problem.
Assessing Iodine in Athletes — Understanding the Biomarkers
Standard blood panels rarely include iodine status assessment. The most practical biomarkers available are:
Urinary iodine concentration (UIC): The gold standard for population-level assessment. Over 90% of ingested iodine is excreted in the urine [5], making UIC a sensitive marker of recent dietary intake. For individual assessment, spot urine UIC is less reliable due to day-to-day variation; multiple collections or a 24-hour urine capture is more accurate. WHO thresholds: adequate = 100–199 µg/L; mild deficiency = 50–99 µg/L; moderate deficiency = 20–49 µg/L; severe deficiency = < 20 µg/L [1].
Thyroid-stimulating hormone (TSH): The best clinical marker of thyroid function, but not a sensitive indicator of iodine status in adults except in cases of overt or severe deficiency [1]. Importantly, serum T3 and T4 concentrations often remain in the normal range despite meaningful iodine deficiency in adults [1], meaning a normal thyroid panel does not exclude suboptimal iodine status.
Free T3 and free T4: Useful for assessing thyroid hormone output, particularly relevant in athletes given the documented tendency of endurance training to be associated with lower values for these markers [3]. If fT3 or fT4 are in the lower range of normal alongside borderline TSH, iodine insufficiency is worth considering. A more complete picture of how to interpret these markers in athletic context — including when to extend beyond TSH — is covered in thyroid function in athletes.
Thyroglobulin (Tg): An emerging biomarker of thyroid stimulation. Serum thyroglobulin reflects thyroid gland activity and increases when iodine supply is restricted. Currently, no validated individual-level threshold is established for adults, but it is increasingly used in research contexts as a complement to UIC [1].
In clinical practice, athlete status alone is usually not enough to make me suspect iodine deficiency. The diagnostic reasoning is largely the same as it would be for a non-athlete: the question becomes relevant when the diet, thyroid-related symptoms, laboratory findings, or broader clinical context point in that direction. I would not usually assume that training, sweating, or being an athlete by itself creates a clinically meaningful iodine deficiency.
This is also reflected in everyday testing. At least in Finnish primary care, iodine status is not something that is commonly measured directly. In practice, clinicians usually start with thyroid function tests rather than urinary iodine. If there is a genuine clinical suspicion of iodine deficiency — which, in the Finnish context, would be relatively uncommon — more specific iodine assessment, such as urinary iodine testing, is typically something that belongs more naturally in endocrinology or specialist care rather than routine primary care screening.
That does not mean sweat losses are irrelevant, but they need to be interpreted in context. If an athlete has high training volume, avoids iodized salt, eats little dairy or seafood, follows a vegan or highly restrictive diet, or has unexplained thyroid-related symptoms, iodine status may become worth considering. In my view, the more important driver is usually nutrition rather than athlete status itself. Sport can add to the picture, but it is rarely the whole explanation.
Evidence-Based Solutions for Iodine in Athletes
Dietary Iodine First
The most reliable dietary iodine sources are iodized salt, dairy products, seafood, and eggs. For athletes who consume these foods regularly, meeting the 150 µg/day RDA is achievable through diet alone [6]. The practical guidance is straightforward: use iodized table salt (confirming it is actually iodized), include dairy or seafood regularly, and be aware that sea salt, Himalayan salt, and restaurant/processed food salt typically contain no iodine [6].
For athletes following plant-based diets, seaweed can serve as a natural source of iodine. However, iodine content in seaweed varies widely depending on species, origin, and processing method. Brown seaweeds such as kelp generally contain higher amounts than red seaweeds such as nori. Because of this variability, kelp supplements in particular can deliver very high doses of iodine. Excessive iodine intake from supplements or large amounts of seaweed has been associated with adverse effects in some populations, and the tolerable upper intake level (UL) for adults is 1100 µg/day [1]. Therefore, athletes using seaweed or kelp products should do so with awareness of total iodine intake and consider monitoring if intake is high or prolonged.
For most patients in everyday clinical practice, iodine intake is usually adequate when they eat a varied mixed diet and use ordinary iodized table salt. In that setting, I rarely find a need to discuss iodine supplementation unless there is a specific dietary reason to do so, such as a vegan diet, very low salt intake, avoidance of dairy and seafood, or use of non-iodized specialty salts. Clinically, this is the main point: iodine is worth remembering, but in most people it does not require a separate supplement if the basic dietary pattern already provides reliable iodine sources.
Supplementation
For athletes who cannot reliably meet iodine needs through diet — particularly vegans, those in iodine-poor regions, and those with consistently high sweat losses — supplementation is a practical and effective strategy. Standard potassium iodide supplements provide 75–150 µg/day and are generally well-tolerated.
In practice, iodine supplementation is usually best understood as a targeted option rather than something to be used universally; the decision depends on dietary context, thyroid history, and the broader clinical picture. Fortunately, long-term iodine supplementation is not something I often encounter in everyday clinical practice. In most cases, there is no reason to take more iodine than the thyroid gland needs for normal hormone synthesis. More is not necessarily better: excessive iodine intake can disturb thyroid function, and people with underlying autoimmune thyroid disease may be more sensitive to iodine intakes that are otherwise tolerated by the general population [1][6].
For that reason, I would not frame iodine as a “just in case” supplement. Separate iodine supplementation is usually most relevant when there is a clear reason to suspect low intake, such as a restrictive diet, very low use of iodized salt, avoidance of dairy and seafood, or a thyroid-related concern. In my view, iodine tablets are best used after medical consultation rather than started casually without a specific indication.
Conclusion: Iodine in Athletes
Iodine is essential for thyroid hormone synthesis, but in athletes it should be understood in the right clinical proportion. It is not usually an acute electrolyte issue like sodium or potassium, and athlete status alone is rarely enough to make iodine deficiency the first explanation for fatigue, poor recovery, or low-normal thyroid markers. In practice, the more relevant question is usually the broader nutritional context: whether the athlete eats a varied diet, uses iodized salt, consumes dairy, seafood, or eggs, follows a vegan or restrictive diet, or has thyroid-related symptoms that make iodine status worth considering.
For many athletes, especially in countries such as Finland where iodized salt is commonly used, iodine needs are usually met through ordinary dietary habits. The risk becomes more relevant when several factors overlap: low iodine intake, high sweat losses, plant-based eating, energy restriction, or avoidance of key iodine sources. Even then, iodine should not be treated as a universal performance supplement. The first step is usually dietary review, not automatic supplementation.
The practical message is simple: iodine is worth remembering, but not overdiagnosing. It belongs in the conversation when the clinical picture points toward it, particularly in athletes with restrictive diets or thyroid-related concerns. Used thoughtfully, this perspective helps avoid two opposite mistakes: ignoring iodine completely, or turning it into another unnecessary “just in case” supplement.
Bibliography
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC9459956/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC10551477/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC11274392/
[4] https://pubmed.ncbi.nlm.nih.gov/32028353/
[5] https://pubmed.ncbi.nlm.nih.gov/16175493/
[6] https://ods.od.nih.gov/factsheets/Iodine-HealthProfessional/
