Preemptive iodide treatment in the event of a nuclear disaster: The prepper's guide to the galaxy

IF 2.8 4区 医学 Q2 PHYSIOLOGY Experimental Physiology Pub Date : 2025-02-14 DOI:10.1113/EP092154
Per Karkov Cramon, Søren Holm, Ronan M. G. Berg
{"title":"Preemptive iodide treatment in the event of a nuclear disaster: The prepper's guide to the galaxy","authors":"Per Karkov Cramon,&nbsp;Søren Holm,&nbsp;Ronan M. G. Berg","doi":"10.1113/EP092154","DOIUrl":null,"url":null,"abstract":"<p>Over the past decades, the post-Cold War optimism that followed the dissolution of the Soviet Union, famously captured by American political scientist Francis Fukuyama, has gradually eroded. Fukuyama's assertion of the ‘ascendancy of Western liberal democracy’ as marking ‘the end of history as such’ no longer reflects the realities of our current era (Fukuyama, <span>1992</span>). Instead, we find ourselves in a time defined by political and ideological unrest, existential threats to humanity and civilisation, environmental catastrophes, and war. A distinct subculture of so-called survivalism has thus emerged, referred to as ‘preppers’. These individuals advocate for preparedness in anticipation of worst-case scenarios – a movement that has proliferated through newsletters, blogs and dedicated stores offering supplies and strategies for survival. Indeed, many European governments now recommend basic preparedness measures for their citizens, such as maintaining various emergency supplies. One pressing concern has been the resurgence of acts of war on the European continent following Russia's invasion of Ukraine in February 2022. Russia, which currently holds approximately 45% of the world's nuclear warheads (Kristensen et al., <span>2024</span>), has intensified anxieties, also because of targeted bombings near nuclear plants, including Chornobyl. For context, the atomic bombs dropped on Hiroshima and Nagasaki in 1945 had yields of approximately 15 and 21 kilotons of TNT, respectively. In contrast, many modern nuclear weapons are far more powerful, with yields often measured in megatons – thousands of times greater. The devastating consequences of such an event, combined with growing concerns over nuclear plant safety, have led to a renewed focus on protective measures in the event of radiation exposure. One widely discussed recommendation – popular within the prepper community but increasingly supported by some governments and the WHO – is the stockpiling of iodine tablets, often incorrectly referred to as an ‘antidote’ to nuclear radiation. This concern became particularly visible in March 2022, when <i>The Telegraph</i> reported a dramatic surge in demand for iodine tablets across the UK and the Oxford Health Company experienced a staggering 15,000% increase in page views for its iodine tablets over the course of a few months (Rees, <span>2022</span>). By October 2022, <i>Associated Press</i> noted that Finnish pharmacies had entirely run out of iodine tablets following recommendations from the country's health ministry that each household purchase a single dose (Associated Press, <span>2022</span>). Here, we aim to highlight the physical and physiological basis of whether – and how – preemptive iodine administration may offer protection in the event of a nuclear accident, a tale that turns out to be deeply entwined with conflict, weaponry and war.</p><p>Most iodine – its name derived from the Greek word ‘iodes’, meaning violet – was forged in the violent birth of the Solar System with the cataclysmic collision of two neutron stars, scattering material into space and creating an environment suitable for the formation of heavy elements (Bartos &amp; Marka, <span>2019</span>). In such extreme conditions, the so-called rapid neutron capture process (the r-process) may occur, in which free neutrons are absorbed into the nucleus of atoms where they are converted into protons (Côté et al., <span>2021</span>). As more neutrons are captured, heavier nuclei including iodine form – in a stepwise accumulation that forges even the heaviest elements of the periodic table. These newly synthesised elements were deposited into the pre-solar nebula more than 4.6 billion years ago. Over time, they became part of the molecular cloud that collapsed to form our solar system, including Earth. Looking at the authoritative source of nuclear information, NUDAT3 (NuDat 3, <span>2025</span>), the nuclear charts show a total of 42 isotopes of iodine (from <sup>106</sup>I to <sup>147</sup>I). Forty-two is a notable number. A curious and poetic coincidence, perhaps, given that the supercomputer Deep Thought famously determined 42 to be ‘the Answer to the Ultimate Question of Life, the Universe, and Everything’ in <i>The Hitchhiker's Guide to the Galaxy</i> (1979) by Douglas Adams (1952–2001) (Adams, <span>1979</span>). Hence, the subtitle of this editorial! Iodine today is present naturally on Earth solely as <sup>127</sup>I if we neglect the tiny amounts of radioactive <sup>129</sup>I (<i>T</i><sub>½</sub> = 16 million years) that is continuously produced in the atmosphere by cosmic radiation, but also present in larger man-made amounts from bomb testing fallout and nuclear accidents.</p><p>The history of iodine is tied to the Napoleonic Wars. By 1811, as the wars were drawing to a close, France faced a severe shortage of gunpowder, and the chemist Bernard Courtois (1777–1838) sought alternative ways to produce potassium nitrate by processing seaweed. During his experiments, Courtois extracted potassium chloride and, after crystallising it, added sulfuric acid to the remaining liquid. To his surprise, the resulting heating produced a striking purple vapour, which condensed into dark, lustrous crystals that he first named ‘substance X’. The word ‘iodine’ was coined 2 years later by the French chemist Joseph Louis Gay Lussac (1778–1850), based on the colour of the vapour. Soon after, a Swiss physician named Jean-François Coindet (1774–1834), who had previously used burnt sponge and seaweed to treat goitre, took interest in Courtois's discovery, because seaweed had been used for treating goitre as far back as 3600 <span>bc</span>, as recorded in Chinese medical writings, and was also noted in the works of the Greek physician Hippocrates. Coindet suspected that iodine might be the active ingredient responsible for the goitre-curing properties of seaweed, and subsequently he successfully tested a tincture of iodine on 150 patients, observing a notable reduction in the size of their goitre within 1 week (Coindet, <span>1820</span>). Already then, the clear link between iodine and thyroid function was thus evident – a link that also renders the gland particularly susceptible in the event of a nuclear disaster.</p><p>The thyroid gland is a butterfly-shaped endocrine organ located anteriorly in the neck, and like iodine, it has war-related connotations. The English physician and anatomist Thomas Wharton apparently coined the name of the gland in his medical work <i>Adenographia</i> of 1656 (Wharton, <span>1656</span>). The term ‘thyroid’ is likely derived from the Greek word <i>thyreos</i>, referring to a large oblong shield often used by Hellenistic armies (Connelly et al., <span>2022</span>). The principal function of the thyroid is to produce and secrete the thyroid hormones, thyroxine (T<sub>4</sub>) and triiodothyronine (T<sub>3</sub>). These iodine-containing hormones are essential for development, growth and metabolic homeostasis (Leung et al., <span>2010</span>). The basic principles of iodide transport in thyroid follicular cells (thyrocytes), including synthesis, storage and secretion, are outlined in Figure 1. Ingested iodine is reduced to iodide and absorbed primarily in the stomach and duodenum. It is then transported through the circulation to the thyroid gland. Varying amounts (5–100%) of the absorbed iodine are taken up by the thyroid, depending on thyroid function and iodine status. Under normal conditions, intrathyroidal iodide concentrations are 20–50 times higher than those in plasma due to the action of the sodium–iodide symporter (NIS), which enables iodide uptake against a steep concentration gradient (Pearce et al., <span>2004</span>). The remaining iodine is predominantly excreted via the kidneys, with smaller quantities eliminated in stool and sweat (Leung et al., <span>2010</span>). During nuclear disasters involving fission, such as nuclear power plant accidents or atomic bomb detonations, large quantities of radioactive isotopes are released into the atmosphere. When heavy nuclei like <sup>235</sup>U or <sup>239</sup>Pu undergo fission – splitting them into two parts, these resulting nuclei are inevitably highly radioactive (Figure 2, top). A large number of iodine isotopes are created and released in this process (Figure 2, bottom). In nuclear power plant accidents, the volatility of iodine also contributes to the high fractional release. For instance, the Fukushima accident in 2011 resulted in the release of approximately 73 radioactive isotopes (135 when including their radioactive progeny) (Evangeliou et al., <span>2014</span>). Amongst these are several radioactive isotopes of iodine, notably <sup>131</sup>I, <sup>132</sup>I, <sup>133</sup>I and <sup>135</sup>I, with half-lives ranging from approximately 2 h to 8 days. Given that they have identical chemical properties, NIS cannot distinguish them from <sup>127</sup>I, causing radioactive iodine to accumulate in the thyroid gland alongside stable iodine.</p><p>In the following, we focus entirely on <sup>131</sup>I, as this isotope is the main radioactive iodine isotope posing health concerns following nuclear disasters for several reasons. First, <sup>131</sup>I is a major fission product of plutonium and uranium, and therefore, large quantities are released into the environment. It is estimated that ∼1760 PBq <sup>131</sup>I was released in the Chornobyl accident, considered the worst nuclear plant disaster in history. This is enough to treat the entire present human population with 200 MBq radioactive iodine; that is a low standard dose for the treatment of hyperthyroidism (Saenko &amp; Mitsutake, <span>2024</span>). Second, the half-life of <sup>131</sup>I is 8 days; in the event of a nuclear disaster, this is long enough for the isotope to be distributed widely geographically and then ingested and accumulated in the thyroid gland. In contrast, most other iodine fission products have much shorter half-lives and therefore undergo radioactive decay before they can reach a human body. The thyroid takes up and accumulates <sup>131</sup>I in the follicular colloid according to the plasma concentration of the radioisotope and thyroid function (see Figure 1). It is well documented that the thyroid is one of the most radiosensitive organs, particularly in children, with the two main risk factors being radiation dose and age of exposure (Iglesias et al., <span>2017</span>). The increase in thyroid cancer following the Chornobyl accident speaks for itself, as it has been estimated that the number of thyroid cancers attributable to the consequent radiation exposure will exceed 15,000 by the year 2065 (Cardis et al., <span>2006</span>). The rise in thyroid cancer incidence in relation to the Chornobyl accident has predominantly been observed amongst those exposed as children and adolescents, while there is little evidence of an increased risk for thyroid cancer amongst those exposed as adults (Saenko &amp; Mitsutake, <span>2024</span>). Accordingly, WHO states that ‘The groups most likely to benefit from iodine thyroid blocking are children, adolescents, pregnant and breastfeeding women, whereas individuals over 40 years of age are less likely to benefit from iodine thyroid blocking’ (WHO, <span>2017</span>).</p><p>Prevention of <sup>131</sup>I intake following a nuclear disaster requires the routes of exposure to be considered. During a nuclear accident, radioactivity is released into the atmosphere as radioactive plumes, and these are spread geographically according to wind direction and speed. The plumes contain <sup>131</sup>I in both gaseous and particulate forms, and when inhaled, the blood absorption is high (Crocker, <span>1984</span>). Inhalation of <sup>131</sup>I may be the primary exposure pathway for some (Verger et al., <span>2001</span>), while deposition of radioactive fallout will result in another route of exposure. The latter will cause <sup>131</sup>I contamination of drinking water, freshwater foods and most importantly plants. Accordingly, the main exposure pathway following the Chornobyl accident was ingestion of fresh milk from cows grazing on contaminated grass. In contrast to a much earlier nuclear accident (Windscale, UK, 1957) where this was acknowledged very early on, no adequate measures were taken in the Chornobyl area. Consequently, children received high thyroid radiation doses, which were also higher than adults because their milk consumption was higher (Saenko &amp; Mitsutake, <span>2024</span>). Moreover, <sup>131</sup>I also accumulates in breast milk leading to exposure of newborns. This is likely the reason for the observed rise in thyroid cancer incidence amongst infants after the Chornobyl accident (Unno et al., <span>2012</span>). Based on the routes of exposure, there are several means to prevent ingestion of <sup>131</sup>I, such as sheltering (go inside and close windows and doors), evacuation (leave the contaminated areas), and avoidance (of foods that likely contain high amounts of radioisotopes). It may not be possible to avoid inhalation or ingestion of <sup>131</sup>I, but uptake and accumulation in the thyroid can be minimised with oral administration of stable iodine, so-called iodine thyroid blocking, usually administered as potassium iodide (KI) tablets (Verger et al., <span>2001</span>).</p><p>For obvious reasons, no randomised clinical trials have been conducted to evaluate the effect of iodine thyroid blocking during nuclear disasters. However, clinical studies have proven that high doses of KI can minimise thyroid uptake of radioactive iodine. The efficacy depends on the KI dose, and it seems that a dose of around 130 mg (∼100 mg iodine) as recommended by WHO is optimal (WHO, <span>2017</span>). The efficacy of KI administration for thyroid blocking is often reported as the averted dose, defined by the equation: averted thyroid dose = (thyroid dose without blocking − thyroid dose with blocking) / thyroid dose without blocking. When 100 mg or 200 mg KI was administered simultaneously with the radioactive iodine tracer, the dose averted to the thyroid, 24 h after ingestion, exceeded 95% for most study subjects (Blum &amp; Eisenbud, <span>1967</span>). Increasing the KI dose above this level did not improve the averted <sup>131</sup>I dose (Koutras &amp; Livadas, <span>1965</span>). The timing of KI administration is also important. Hence, 100 mg KI has been found to block 98% of thyroid <sup>131</sup>I uptake when taken simultaneously with the radiotracer, but only 60% was blocked when KI was taken 3 h later, and this blocking effect does decrease steadily. Seventy-two hours after administration of a single 100 mg KI tablet, only 24% of thyroid <sup>131</sup>I uptake was blocked (Blum &amp; Eisenbud, <span>1967</span>). An averted dose above 90% can be maintained by repeated daily administration of 15 mg sodium iodide (∼16.5 mg KI) after initial administration of a single dose of 100 mg sodium iodide (∼111 mg KI) (Sternthal et al., <span>1980</span>).</p><p>So, what is the mechanism of iodine thyroid blocking at the cellular level? There are several possible mechanisms of action. One principal mechanism is often referred to as ‘thyroid saturation’. When plasma iodide suddenly rises to a high concentration, the thyrocytes will take up a high amount resulting in high intrathyroidal iodide concentrations, followed by thyroid uptake blockade (Verger et al., <span>2001</span>). The blockade is, at least partly, caused by a fast downregulation of the NIS proteins at the basolateral membrane of the thyrocytes (see Figure 1). When rats were acutely exposed to a single intraperitoneal administration of high dose iodide, NIS mRNA was decreased at 6–24 h, whereas NIS protein was decreased only at 24 h (Eng et al., <span>1999</span>). This downregulation will effectively minimise <sup>131</sup>I uptake since NIS activity is the major determinant of thyroid iodide uptake rate. Another principal mechanism is isotopic dilution. When stable iodide, that is, <sup>127</sup>I, is present in plasma in high concentrations, most iodide (including <sup>131</sup>I) will be excreted via the kidneys rather than taken up in the thyroid. And when the thyroid does take up iodine, it will most likely be in the stable non-radioactive form. High plasma iodide levels inhibit the organic binding of iodide within the colloid and thus inhibit thyroid hormone synthesis. This phenomenon, known as the Wolff–Chaikoff effect (Eng et al., <span>1999</span>), may prevent the storage of organified <sup>131</sup>I in the thyroid colloid and thereby reduce thyroid radiation. Nonetheless, the Wolff–Chaikoff effect could lead to prolonged biological half-life of <sup>131</sup>I in the thyroid, and thus increased thyroid radiation, if KI tablets are taken after exposure rather than before. The inhibitory effect is transient. In adults without thyroid disease, thyroid hormone synthesis resumes after 26–50 h (referred to as ‘escape’), even if the iodine overload persists (Wolff &amp; Chaikoff, <span>1949</span>). Patients with Graves’ disease are more sensitive to the Wolff–Chaikoff effect, and hence, the effect on thyroid hormone synthesis lasts much longer (Burch &amp; Cooper, <span>2015</span>). Similarly, a recent study demonstrated that high dose stable iodine (∼80 mg KI) given daily for 10 days improved thyroid function in patients with toxic nodular goitre (Hedberg et al., <span>2024</span>). However, it is a concern that escape from the Wolff–Chaikoff effect can result in severe hyperthyroidism in patients with pre-existing Graves’ disease or nodular goitre. Lastly, high dose iodine administered daily for 3–14 days to patients with Graves’ disease decreases thyroid vascularity and blood flow (Tsai et al., <span>2019</span>). This may represent a complementary protective role, since less <sup>131</sup>I will reach the thyrocytes. It remains to be determined whether iodine thyroid blocking decreases thyroid vascularity and blood flow in individuals without thyroid disease.</p><p>Based on the abovementioned kinetic and clinical studies, WHO recommends a single tablet of 130 mg KI in the event of a nuclear disaster. The tablet should be ingested less than 24 h before exposure and not later than 8 h after exposure and is mostly effective in individuals younger than 40 years of age. In case of prolonged exposure, repeated administration of stable iodine may be necessary (WHO, <span>2017</span>). Some people mistakenly believe that stable iodine is a universal radiation antidote. It is important to stress that stable iodine only protects exposed individuals from radiation-induced thyroid cancer. It has no effect on other health-hazardous radioisotopes (such as <sup>90</sup>Sr, <sup>134</sup>Cs and <sup>137</sup>Cs) produced in nuclear disasters.</p><p>So, the take-home message is this: preemptive iodine is not a universal antidote for radiation exposure. It provides protection only against radiation from radioactive iodine isotopes, which are only a subset of the isotopes hazardous to health that are released during a nuclear event. The primary risk to the general population arises from ingesting iodine-containing foods contaminated with radioactive isotopes, leading to an increased long-term risk of thyroid cancer. Preemptive iodine should be ingested as a single dose immediately before or at the time of exposure and is particularly relevant for individuals under 40 years of age. It is not for us to determine the relevance of preppers’ strategies to keep iodine tablets stored at home, as long as governmental instructions are followed. Yet, when reflecting on the violent history of iodine – from its cosmic creation to its discovery and now to its therapeutic use for nuclear preparedness – perhaps the message to us all is clear, to resonate the words of John Lennon (1940–1980) and Yoko Ono (b. 1933) when the Cold War was at its height in 1969: Give peace a chance!</p><p>Per Karkov Cramon: conception, first draft, revisions. Søren Holm: first draft, revisions. Ronan M. G. Berg: conception, first draft, revisions. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed.</p><p>The authors have no conflict of interest to declare.</p><p>The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390, ID 20045, ID 125132, and ID 177225). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":"110 12","pages":"1771-1776"},"PeriodicalIF":2.8000,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://physoc.onlinelibrary.wiley.com/doi/epdf/10.1113/EP092154","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP092154","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
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Abstract

Over the past decades, the post-Cold War optimism that followed the dissolution of the Soviet Union, famously captured by American political scientist Francis Fukuyama, has gradually eroded. Fukuyama's assertion of the ‘ascendancy of Western liberal democracy’ as marking ‘the end of history as such’ no longer reflects the realities of our current era (Fukuyama, 1992). Instead, we find ourselves in a time defined by political and ideological unrest, existential threats to humanity and civilisation, environmental catastrophes, and war. A distinct subculture of so-called survivalism has thus emerged, referred to as ‘preppers’. These individuals advocate for preparedness in anticipation of worst-case scenarios – a movement that has proliferated through newsletters, blogs and dedicated stores offering supplies and strategies for survival. Indeed, many European governments now recommend basic preparedness measures for their citizens, such as maintaining various emergency supplies. One pressing concern has been the resurgence of acts of war on the European continent following Russia's invasion of Ukraine in February 2022. Russia, which currently holds approximately 45% of the world's nuclear warheads (Kristensen et al., 2024), has intensified anxieties, also because of targeted bombings near nuclear plants, including Chornobyl. For context, the atomic bombs dropped on Hiroshima and Nagasaki in 1945 had yields of approximately 15 and 21 kilotons of TNT, respectively. In contrast, many modern nuclear weapons are far more powerful, with yields often measured in megatons – thousands of times greater. The devastating consequences of such an event, combined with growing concerns over nuclear plant safety, have led to a renewed focus on protective measures in the event of radiation exposure. One widely discussed recommendation – popular within the prepper community but increasingly supported by some governments and the WHO – is the stockpiling of iodine tablets, often incorrectly referred to as an ‘antidote’ to nuclear radiation. This concern became particularly visible in March 2022, when The Telegraph reported a dramatic surge in demand for iodine tablets across the UK and the Oxford Health Company experienced a staggering 15,000% increase in page views for its iodine tablets over the course of a few months (Rees, 2022). By October 2022, Associated Press noted that Finnish pharmacies had entirely run out of iodine tablets following recommendations from the country's health ministry that each household purchase a single dose (Associated Press, 2022). Here, we aim to highlight the physical and physiological basis of whether – and how – preemptive iodine administration may offer protection in the event of a nuclear accident, a tale that turns out to be deeply entwined with conflict, weaponry and war.

Most iodine – its name derived from the Greek word ‘iodes’, meaning violet – was forged in the violent birth of the Solar System with the cataclysmic collision of two neutron stars, scattering material into space and creating an environment suitable for the formation of heavy elements (Bartos & Marka, 2019). In such extreme conditions, the so-called rapid neutron capture process (the r-process) may occur, in which free neutrons are absorbed into the nucleus of atoms where they are converted into protons (Côté et al., 2021). As more neutrons are captured, heavier nuclei including iodine form – in a stepwise accumulation that forges even the heaviest elements of the periodic table. These newly synthesised elements were deposited into the pre-solar nebula more than 4.6 billion years ago. Over time, they became part of the molecular cloud that collapsed to form our solar system, including Earth. Looking at the authoritative source of nuclear information, NUDAT3 (NuDat 3, 2025), the nuclear charts show a total of 42 isotopes of iodine (from 106I to 147I). Forty-two is a notable number. A curious and poetic coincidence, perhaps, given that the supercomputer Deep Thought famously determined 42 to be ‘the Answer to the Ultimate Question of Life, the Universe, and Everything’ in The Hitchhiker's Guide to the Galaxy (1979) by Douglas Adams (1952–2001) (Adams, 1979). Hence, the subtitle of this editorial! Iodine today is present naturally on Earth solely as 127I if we neglect the tiny amounts of radioactive 129I (T½ = 16 million years) that is continuously produced in the atmosphere by cosmic radiation, but also present in larger man-made amounts from bomb testing fallout and nuclear accidents.

The history of iodine is tied to the Napoleonic Wars. By 1811, as the wars were drawing to a close, France faced a severe shortage of gunpowder, and the chemist Bernard Courtois (1777–1838) sought alternative ways to produce potassium nitrate by processing seaweed. During his experiments, Courtois extracted potassium chloride and, after crystallising it, added sulfuric acid to the remaining liquid. To his surprise, the resulting heating produced a striking purple vapour, which condensed into dark, lustrous crystals that he first named ‘substance X’. The word ‘iodine’ was coined 2 years later by the French chemist Joseph Louis Gay Lussac (1778–1850), based on the colour of the vapour. Soon after, a Swiss physician named Jean-François Coindet (1774–1834), who had previously used burnt sponge and seaweed to treat goitre, took interest in Courtois's discovery, because seaweed had been used for treating goitre as far back as 3600 bc, as recorded in Chinese medical writings, and was also noted in the works of the Greek physician Hippocrates. Coindet suspected that iodine might be the active ingredient responsible for the goitre-curing properties of seaweed, and subsequently he successfully tested a tincture of iodine on 150 patients, observing a notable reduction in the size of their goitre within 1 week (Coindet, 1820). Already then, the clear link between iodine and thyroid function was thus evident – a link that also renders the gland particularly susceptible in the event of a nuclear disaster.

The thyroid gland is a butterfly-shaped endocrine organ located anteriorly in the neck, and like iodine, it has war-related connotations. The English physician and anatomist Thomas Wharton apparently coined the name of the gland in his medical work Adenographia of 1656 (Wharton, 1656). The term ‘thyroid’ is likely derived from the Greek word thyreos, referring to a large oblong shield often used by Hellenistic armies (Connelly et al., 2022). The principal function of the thyroid is to produce and secrete the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). These iodine-containing hormones are essential for development, growth and metabolic homeostasis (Leung et al., 2010). The basic principles of iodide transport in thyroid follicular cells (thyrocytes), including synthesis, storage and secretion, are outlined in Figure 1. Ingested iodine is reduced to iodide and absorbed primarily in the stomach and duodenum. It is then transported through the circulation to the thyroid gland. Varying amounts (5–100%) of the absorbed iodine are taken up by the thyroid, depending on thyroid function and iodine status. Under normal conditions, intrathyroidal iodide concentrations are 20–50 times higher than those in plasma due to the action of the sodium–iodide symporter (NIS), which enables iodide uptake against a steep concentration gradient (Pearce et al., 2004). The remaining iodine is predominantly excreted via the kidneys, with smaller quantities eliminated in stool and sweat (Leung et al., 2010). During nuclear disasters involving fission, such as nuclear power plant accidents or atomic bomb detonations, large quantities of radioactive isotopes are released into the atmosphere. When heavy nuclei like 235U or 239Pu undergo fission – splitting them into two parts, these resulting nuclei are inevitably highly radioactive (Figure 2, top). A large number of iodine isotopes are created and released in this process (Figure 2, bottom). In nuclear power plant accidents, the volatility of iodine also contributes to the high fractional release. For instance, the Fukushima accident in 2011 resulted in the release of approximately 73 radioactive isotopes (135 when including their radioactive progeny) (Evangeliou et al., 2014). Amongst these are several radioactive isotopes of iodine, notably 131I, 132I, 133I and 135I, with half-lives ranging from approximately 2 h to 8 days. Given that they have identical chemical properties, NIS cannot distinguish them from 127I, causing radioactive iodine to accumulate in the thyroid gland alongside stable iodine.

In the following, we focus entirely on 131I, as this isotope is the main radioactive iodine isotope posing health concerns following nuclear disasters for several reasons. First, 131I is a major fission product of plutonium and uranium, and therefore, large quantities are released into the environment. It is estimated that ∼1760 PBq 131I was released in the Chornobyl accident, considered the worst nuclear plant disaster in history. This is enough to treat the entire present human population with 200 MBq radioactive iodine; that is a low standard dose for the treatment of hyperthyroidism (Saenko & Mitsutake, 2024). Second, the half-life of 131I is 8 days; in the event of a nuclear disaster, this is long enough for the isotope to be distributed widely geographically and then ingested and accumulated in the thyroid gland. In contrast, most other iodine fission products have much shorter half-lives and therefore undergo radioactive decay before they can reach a human body. The thyroid takes up and accumulates 131I in the follicular colloid according to the plasma concentration of the radioisotope and thyroid function (see Figure 1). It is well documented that the thyroid is one of the most radiosensitive organs, particularly in children, with the two main risk factors being radiation dose and age of exposure (Iglesias et al., 2017). The increase in thyroid cancer following the Chornobyl accident speaks for itself, as it has been estimated that the number of thyroid cancers attributable to the consequent radiation exposure will exceed 15,000 by the year 2065 (Cardis et al., 2006). The rise in thyroid cancer incidence in relation to the Chornobyl accident has predominantly been observed amongst those exposed as children and adolescents, while there is little evidence of an increased risk for thyroid cancer amongst those exposed as adults (Saenko & Mitsutake, 2024). Accordingly, WHO states that ‘The groups most likely to benefit from iodine thyroid blocking are children, adolescents, pregnant and breastfeeding women, whereas individuals over 40 years of age are less likely to benefit from iodine thyroid blocking’ (WHO, 2017).

Prevention of 131I intake following a nuclear disaster requires the routes of exposure to be considered. During a nuclear accident, radioactivity is released into the atmosphere as radioactive plumes, and these are spread geographically according to wind direction and speed. The plumes contain 131I in both gaseous and particulate forms, and when inhaled, the blood absorption is high (Crocker, 1984). Inhalation of 131I may be the primary exposure pathway for some (Verger et al., 2001), while deposition of radioactive fallout will result in another route of exposure. The latter will cause 131I contamination of drinking water, freshwater foods and most importantly plants. Accordingly, the main exposure pathway following the Chornobyl accident was ingestion of fresh milk from cows grazing on contaminated grass. In contrast to a much earlier nuclear accident (Windscale, UK, 1957) where this was acknowledged very early on, no adequate measures were taken in the Chornobyl area. Consequently, children received high thyroid radiation doses, which were also higher than adults because their milk consumption was higher (Saenko & Mitsutake, 2024). Moreover, 131I also accumulates in breast milk leading to exposure of newborns. This is likely the reason for the observed rise in thyroid cancer incidence amongst infants after the Chornobyl accident (Unno et al., 2012). Based on the routes of exposure, there are several means to prevent ingestion of 131I, such as sheltering (go inside and close windows and doors), evacuation (leave the contaminated areas), and avoidance (of foods that likely contain high amounts of radioisotopes). It may not be possible to avoid inhalation or ingestion of 131I, but uptake and accumulation in the thyroid can be minimised with oral administration of stable iodine, so-called iodine thyroid blocking, usually administered as potassium iodide (KI) tablets (Verger et al., 2001).

For obvious reasons, no randomised clinical trials have been conducted to evaluate the effect of iodine thyroid blocking during nuclear disasters. However, clinical studies have proven that high doses of KI can minimise thyroid uptake of radioactive iodine. The efficacy depends on the KI dose, and it seems that a dose of around 130 mg (∼100 mg iodine) as recommended by WHO is optimal (WHO, 2017). The efficacy of KI administration for thyroid blocking is often reported as the averted dose, defined by the equation: averted thyroid dose = (thyroid dose without blocking − thyroid dose with blocking) / thyroid dose without blocking. When 100 mg or 200 mg KI was administered simultaneously with the radioactive iodine tracer, the dose averted to the thyroid, 24 h after ingestion, exceeded 95% for most study subjects (Blum & Eisenbud, 1967). Increasing the KI dose above this level did not improve the averted 131I dose (Koutras & Livadas, 1965). The timing of KI administration is also important. Hence, 100 mg KI has been found to block 98% of thyroid 131I uptake when taken simultaneously with the radiotracer, but only 60% was blocked when KI was taken 3 h later, and this blocking effect does decrease steadily. Seventy-two hours after administration of a single 100 mg KI tablet, only 24% of thyroid 131I uptake was blocked (Blum & Eisenbud, 1967). An averted dose above 90% can be maintained by repeated daily administration of 15 mg sodium iodide (∼16.5 mg KI) after initial administration of a single dose of 100 mg sodium iodide (∼111 mg KI) (Sternthal et al., 1980).

So, what is the mechanism of iodine thyroid blocking at the cellular level? There are several possible mechanisms of action. One principal mechanism is often referred to as ‘thyroid saturation’. When plasma iodide suddenly rises to a high concentration, the thyrocytes will take up a high amount resulting in high intrathyroidal iodide concentrations, followed by thyroid uptake blockade (Verger et al., 2001). The blockade is, at least partly, caused by a fast downregulation of the NIS proteins at the basolateral membrane of the thyrocytes (see Figure 1). When rats were acutely exposed to a single intraperitoneal administration of high dose iodide, NIS mRNA was decreased at 6–24 h, whereas NIS protein was decreased only at 24 h (Eng et al., 1999). This downregulation will effectively minimise 131I uptake since NIS activity is the major determinant of thyroid iodide uptake rate. Another principal mechanism is isotopic dilution. When stable iodide, that is, 127I, is present in plasma in high concentrations, most iodide (including 131I) will be excreted via the kidneys rather than taken up in the thyroid. And when the thyroid does take up iodine, it will most likely be in the stable non-radioactive form. High plasma iodide levels inhibit the organic binding of iodide within the colloid and thus inhibit thyroid hormone synthesis. This phenomenon, known as the Wolff–Chaikoff effect (Eng et al., 1999), may prevent the storage of organified 131I in the thyroid colloid and thereby reduce thyroid radiation. Nonetheless, the Wolff–Chaikoff effect could lead to prolonged biological half-life of 131I in the thyroid, and thus increased thyroid radiation, if KI tablets are taken after exposure rather than before. The inhibitory effect is transient. In adults without thyroid disease, thyroid hormone synthesis resumes after 26–50 h (referred to as ‘escape’), even if the iodine overload persists (Wolff & Chaikoff, 1949). Patients with Graves’ disease are more sensitive to the Wolff–Chaikoff effect, and hence, the effect on thyroid hormone synthesis lasts much longer (Burch & Cooper, 2015). Similarly, a recent study demonstrated that high dose stable iodine (∼80 mg KI) given daily for 10 days improved thyroid function in patients with toxic nodular goitre (Hedberg et al., 2024). However, it is a concern that escape from the Wolff–Chaikoff effect can result in severe hyperthyroidism in patients with pre-existing Graves’ disease or nodular goitre. Lastly, high dose iodine administered daily for 3–14 days to patients with Graves’ disease decreases thyroid vascularity and blood flow (Tsai et al., 2019). This may represent a complementary protective role, since less 131I will reach the thyrocytes. It remains to be determined whether iodine thyroid blocking decreases thyroid vascularity and blood flow in individuals without thyroid disease.

Based on the abovementioned kinetic and clinical studies, WHO recommends a single tablet of 130 mg KI in the event of a nuclear disaster. The tablet should be ingested less than 24 h before exposure and not later than 8 h after exposure and is mostly effective in individuals younger than 40 years of age. In case of prolonged exposure, repeated administration of stable iodine may be necessary (WHO, 2017). Some people mistakenly believe that stable iodine is a universal radiation antidote. It is important to stress that stable iodine only protects exposed individuals from radiation-induced thyroid cancer. It has no effect on other health-hazardous radioisotopes (such as 90Sr, 134Cs and 137Cs) produced in nuclear disasters.

So, the take-home message is this: preemptive iodine is not a universal antidote for radiation exposure. It provides protection only against radiation from radioactive iodine isotopes, which are only a subset of the isotopes hazardous to health that are released during a nuclear event. The primary risk to the general population arises from ingesting iodine-containing foods contaminated with radioactive isotopes, leading to an increased long-term risk of thyroid cancer. Preemptive iodine should be ingested as a single dose immediately before or at the time of exposure and is particularly relevant for individuals under 40 years of age. It is not for us to determine the relevance of preppers’ strategies to keep iodine tablets stored at home, as long as governmental instructions are followed. Yet, when reflecting on the violent history of iodine – from its cosmic creation to its discovery and now to its therapeutic use for nuclear preparedness – perhaps the message to us all is clear, to resonate the words of John Lennon (1940–1980) and Yoko Ono (b. 1933) when the Cold War was at its height in 1969: Give peace a chance!

Per Karkov Cramon: conception, first draft, revisions. Søren Holm: first draft, revisions. Ronan M. G. Berg: conception, first draft, revisions. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed.

The authors have no conflict of interest to declare.

The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390, ID 20045, ID 125132, and ID 177225). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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核灾难发生时先发制人的碘化物治疗:银河系的预备指南。
在过去的几十年里,美国政治学家弗朗西斯·福山(Francis Fukuyama)捕捉到的苏联解体后的后冷战乐观主义,已经逐渐消退。福山关于“西方自由民主的优势”标志着“历史的终结”的断言不再反映我们当前时代的现实(Fukuyama, 1992)。相反,我们发现自己处在一个政治和意识形态动荡、人类和文明面临生存威胁、环境灾难和战争的时代。因此,一种独特的所谓生存主义亚文化出现了,被称为“准备者”。这些人提倡在最坏的情况下做好准备——这一运动已经通过新闻通讯、博客和专门提供生存用品和策略的商店激增。事实上,许多欧洲国家的政府现在建议其公民采取基本的防范措施,例如维持各种应急物资供应。一个紧迫的问题是,在俄罗斯于2022年2月入侵乌克兰之后,欧洲大陆上的战争行为重新抬头。俄罗斯目前拥有世界上大约45%的核弹头(Kristensen et al., 2024),它加剧了焦虑,这也是因为在包括切尔诺贝利在内的核电站附近进行了有针对性的轰炸。作为背景,1945年投在广岛和长崎的原子弹分别产生了大约15千吨和21千吨TNT当量。相比之下,许多现代核武器的威力要大得多,其当量通常以兆吨计,是前者的数千倍。这种事件的破坏性后果,加上对核电站安全的日益关注,导致人们重新关注辐射暴露时的保护措施。一个广泛讨论的建议——在准备者群体中很流行,但越来越多地得到一些政府和世界卫生组织的支持——是储存碘片,碘片经常被错误地称为核辐射的“解毒剂”。这种担忧在2022年3月变得尤为明显,当时《每日电讯报》报道称,全英国对碘片的需求急剧增加,牛津健康公司的碘片页面浏览量在几个月内惊人地增长了15,000% (Rees, 2022)。到2022年10月,美联社注意到,芬兰卫生部建议每户购买一剂碘片,芬兰药房的碘片已经完全售罄(美联社,2022)。在这里,我们的目标是强调在发生核事故时,先发制人的碘管理是否以及如何提供保护的物理和生理基础,这个故事被证明与冲突,武器和战争深深交织在一起。大多数碘——它的名字来源于希腊语“iodes”,意思是紫色——是在太阳系的剧烈诞生中形成的,当时两颗中子星发生了灾难性的碰撞,将物质散射到太空中,创造了一个适合重元素形成的环境(Bartos & Marka, 2019)。在这种极端条件下,可能会发生所谓的快中子捕获过程(r过程),自由中子被吸收到原子核中,在原子核中转化为质子(Côté et al., 2021)。随着更多的中子被捕获,包括碘在内的更重的原子核就形成了——在一个逐步积累的过程中,甚至可以锻造出元素周期表中最重的元素。这些新合成的元素在46亿年前沉积在前太阳星云中。随着时间的推移,它们成为分子云的一部分,分子云坍塌形成了我们的太阳系,包括地球。参考权威的核信息来源NUDAT3 (NUDAT3, 2025),核图显示了碘的42种同位素(从106I到147I)。42是个值得注意的数字。考虑到超级计算机“深思”(Deep Thought)在道格拉斯·亚当斯(Douglas Adams, 1952-2001)的《银河系漫游指南》(the Hitchhiker’s Guide to the Galaxy, 1979)中被公认为“生命、宇宙和一切终极问题的答案”,这也许是一个奇怪而诗意的巧合。因此,这篇社论的副标题!如果我们忽略宇宙辐射在大气中不断产生的微量放射性碘(1½= 1600万年),那么今天在地球上自然存在的碘仅以127I的形式存在,但在原子弹试验和核事故中,人造碘也以更大的数量存在。碘的历史与拿破仑战争有关。到1811年,随着战争接近尾声,法国面临着严重的火药短缺,化学家伯纳德·库尔图瓦(Bernard Courtois, 1777-1838)寻求通过加工海藻来生产硝酸钾的替代方法。在他的实验中,库尔图瓦提取了氯化钾,将其结晶后,在剩余的液体中加入硫酸。 令他惊讶的是,由此产生的加热产生了一种引人注目的紫色蒸汽,这些蒸汽凝结成黑暗而有光泽的晶体,他首先将其命名为“物质X”。两年后,法国化学家约瑟夫·路易斯·盖伊·吕萨克(1778-1850)根据这种蒸汽的颜色创造了“碘”这个词。不久之后,一位名叫jean - franois Coindet(1774-1834)的瑞士医生对库尔图瓦的发现产生了兴趣,因为根据中国医学著作的记载,早在公元前3600年,海藻就被用于治疗甲状腺肿,希腊医生希波克拉底的著作也提到了这一点。Coindet怀疑碘可能是海藻治疗甲状腺肿特性的有效成分,随后他成功地在150名患者身上测试了碘酊剂,观察到他们的甲状腺在一周内显着缩小(Coindet, 1820)。那时,碘和甲状腺功能之间的明确联系就已经很明显了——这种联系也使甲状腺在发生核灾难时特别容易受到影响。甲状腺是一个蝴蝶状的内分泌器官,位于颈部的前部,和碘一样,它有与战争有关的含义。英国内科医生和解剖学家托马斯·沃顿显然是在他1656年的医学著作《腺图》(Wharton, 1656)中创造了腺的名字。“甲状腺”一词可能来源于希腊语thyreos,指的是希腊化军队经常使用的大型长方形盾牌(Connelly et al., 2022)。甲状腺的主要功能是产生和分泌甲状腺激素甲状腺素(T4)和三碘甲状腺原氨酸(T3)。这些含碘激素对发育、生长和代谢稳态至关重要(Leung et al., 2010)。碘在甲状腺滤泡细胞(甲状腺细胞)中运输的基本原理,包括合成、储存和分泌,如图1所示。摄入的碘被还原为碘化物,并主要在胃和十二指肠被吸收。然后通过循环输送到甲状腺。不同数量(5-100%)的碘被甲状腺吸收,取决于甲状腺功能和碘状态。在正常情况下,由于碘化钠同调体(NIS)的作用,甲状腺内碘浓度比血浆中的碘浓度高20-50倍,这使得碘吸收能够抵抗陡峭的浓度梯度(Pearce et al., 2004)。剩余的碘主要通过肾脏排出,少量通过粪便和汗液排出(Leung et al., 2010)。在涉及裂变的核灾难中,如核电站事故或原子弹爆炸,大量的放射性同位素被释放到大气中。当像235U或239Pu这样的重核发生裂变——将它们分裂成两部分时,这些产生的核不可避免地具有高放射性(图2,顶部)。在这个过程中产生并释放了大量的碘同位素(图2,底部)。在核电站事故中,碘的挥发性也是造成高分数释放的原因之一。例如,2011年的福岛事故导致大约73种放射性同位素的释放(包括其放射性后代时为135种)(Evangeliou et al., 2014)。其中有几种碘的放射性同位素,特别是131I、132I、133I和135I,半衰期从大约2小时到8天不等。由于它们具有相同的化学性质,NIS无法将它们与127I区分开来,导致放射性碘与稳定碘一起积聚在甲状腺中。在下面,我们完全关注131I,因为这种同位素是核灾难后造成健康问题的主要放射性碘同位素,原因有几个。首先,131I是钚和铀的主要裂变产物,因此,大量的131I被释放到环境中。据估计,在被认为是历史上最严重的核电站灾难的切尔诺贝利事故中释放了~ 1760 PBq 131I。这足以用200mbq的放射性碘治疗目前的整个人口;这是治疗甲状腺机能亢进的低标准剂量(Saenko & Mitsutake, 2024)。第二,131I的半衰期为8天;在发生核灾难的情况下,这段时间足以让同位素在地理上广泛分布,然后被摄入并积聚在甲状腺中。相比之下,大多数其他碘裂变产物的半衰期要短得多,因此在到达人体之前会经历放射性衰变。根据血浆放射性同位素浓度和甲状腺功能,甲状腺对131I在滤泡胶体中的吸收和积累(见图1)。 有充分的证据表明,甲状腺是对辐射最敏感的器官之一,特别是在儿童中,两个主要的危险因素是辐射剂量和暴露年龄(Iglesias et al., 2017)。切尔诺贝利事故后甲状腺癌的增加本身就说明了这一点,因为据估计,到2065年,由于随后的辐射暴露而导致的甲状腺癌人数将超过15,000人(Cardis et al., 2006)。与切尔诺贝利事故相关的甲状腺癌发病率的上升主要发生在儿童和青少年暴露者中,而几乎没有证据表明成年暴露者患甲状腺癌的风险增加(Saenko & Mitsutake, 2024)。因此,世卫组织指出,“最有可能从碘甲状腺阻断中受益的群体是儿童、青少年、孕妇和哺乳期妇女,而40岁以上的人不太可能从碘甲状腺阻断中受益”(世卫组织,2017年)。核灾难发生后预防131 - i的摄入需要考虑暴露途径。在核事故中,放射性物质以放射性羽状物的形式释放到大气中,这些羽状物根据风向和风速在地理上扩散。烟雾中含有气态和颗粒形式的131I,当吸入时,血液吸收率很高(Crocker, 1984)。吸入131I可能是一些人的主要暴露途径(Verger et al., 2001),而放射性沉降物的沉积将导致另一种暴露途径。后者会造成饮用水、淡水食品、最重要的是植物的污染。因此,切尔诺贝利事故后的主要暴露途径是摄入了在受污染草地上放牧的奶牛所产的鲜奶。与早得多的核事故(Windscale, UK, 1957)相比,切尔诺贝利地区没有采取足够的措施。因此,儿童接受了高甲状腺辐射剂量,这也高于成人,因为他们的牛奶摄入量更高(Saenko & Mitsutake, 2024)。此外,131 - i也会在母乳中积累,导致新生儿接触。这可能是切尔诺贝利事故后婴儿甲状腺癌发病率上升的原因(Unno et al., 2012)。根据接触途径,有几种方法可以防止摄入131I,例如躲避(进入室内并关闭门窗)、疏散(离开污染区域)和避免(可能含有大量放射性同位素的食物)。可能不可能避免吸入或摄入131I,但口服稳定碘,即所谓的碘甲状腺阻断剂,通常以碘化钾(KI)片剂的形式给药,可以最大限度地减少其在甲状腺中的吸收和积聚(Verger等人,2001年)。由于显而易见的原因,没有进行随机临床试验来评估核灾难期间碘甲状腺阻断的效果。然而,临床研究已经证明,高剂量的碘化钾可以减少甲状腺对放射性碘的吸收。效果取决于KI剂量,世卫组织建议的约130毫克(~ 100毫克碘)的剂量似乎是最佳的(世卫组织,2017年)。KI给药对甲状腺阻断的疗效通常被报道为避免剂量,由公式定义:避免甲状腺剂量=(无阻断的甲状腺剂量-有阻断的甲状腺剂量)/无阻断的甲状腺剂量。当100mg或200mg碘化钾与放射性碘示踪剂同时服用时,对大多数研究对象来说,摄入24小时后避免给甲状腺的剂量超过95% (Blum & Eisenbud, 1967)。将KI剂量增加到这个水平以上并不能改善可避免的131I剂量(Koutras & Livadas, 1965)。KI管理的时机也很重要。因此,100 mg碘化钾与放射性示踪剂同时服用时,可阻断98%的甲状腺131I摄取,但在3小时后服用碘化钾时,仅阻断60%,而且这种阻断作用确实稳步下降。服用100毫克碘化钾片剂72小时后,只有24%的甲状腺碘吸收被阻断(Blum & Eisenbud, 1967)。在最初单次给药100 mg碘化钠(~ 111 mg碘化钠)后,通过每天重复给药15 mg碘化钠(~ 16.5 mg碘化钾),可以保持90%以上的避免剂量(Sternthal et al., 1980)。那么,碘在细胞水平上阻断甲状腺的机制是什么呢?有几种可能的作用机制。一种主要机制通常被称为“甲状腺饱和”。当血浆碘突然升高到高浓度时,甲状腺细胞大量摄取,导致甲状腺内碘浓度升高,进而发生甲状腺摄取阻断(Verger et al., 2001)。 这种阻断至少部分是由甲状腺细胞基底外膜上NIS蛋白的快速下调引起的(见图1)。当大鼠急性暴露于高剂量碘的单次腹腔注射时,NIS mRNA在6-24小时内减少,而NIS蛋白仅在24小时内减少(Eng等,1999)。这种下调将有效地减少131I的摄取,因为NIS活性是甲状腺碘摄取率的主要决定因素。另一个主要机制是同位素稀释。当血浆中存在高浓度的稳定碘,即127I时,大多数碘(包括131I)将通过肾脏排出体外,而不是被甲状腺吸收。当甲状腺吸收碘时,它很可能会以稳定的非放射性形式存在。高血浆碘水平抑制胶体内碘的有机结合,从而抑制甲状腺激素的合成。这种现象被称为Wolff-Chaikoff效应(Eng et al., 1999),可能会阻止有组织的131I在甲状腺胶体中的储存,从而减少甲状腺辐射。然而,如果碘化钾片在暴露后服用,而不是在暴露前服用,那么沃尔夫-柴可夫效应可能导致131I在甲状腺中的生物半衰期延长,从而增加甲状腺辐射。抑制作用是短暂的。在没有甲状腺疾病的成年人中,即使碘超载仍然存在,甲状腺激素的合成也会在26-50小时后恢复(称为“逃逸”)(Wolff & Chaikoff, 1949)。Graves病患者对Wolff-Chaikoff效应更敏感,因此对甲状腺激素合成的影响持续时间更长(Burch & Cooper, 2015)。同样,最近的一项研究表明,每天服用高剂量稳定碘(~ 80 mg KI),持续10天,可改善中毒性甲状腺结节患者的甲状腺功能(Hedberg et al, 2024)。然而,逃避Wolff-Chaikoff效应可能导致已有Graves病或结节性甲状腺肿的患者出现严重的甲状腺功能亢进,这是一个值得关注的问题。最后,Graves病患者每天服用高剂量碘,持续3-14天,可降低甲状腺血管和血流量(Tsai et al., 2019)。这可能是一种补充性的保护作用,因为较少的131 - i到达甲状腺细胞。在没有甲状腺疾病的个体中,碘甲状腺阻断是否会降低甲状腺血管和血流量仍有待确定。根据上述动力学和临床研究,世卫组织建议在发生核灾难时服用一片130毫克碘化钾。该片剂应在接触前24小时内服用,不迟于接触后8小时,对40岁以下的人最有效。在长期暴露的情况下,可能需要反复服用稳定碘(世卫组织,2017年)。有些人错误地认为稳定的碘是万能的辐射解毒剂。需要强调的是,稳定碘只能保护受照射者免受辐射诱发的甲状腺癌。它对核灾难中产生的其他危害健康的放射性同位素(如90Sr、134Cs和137Cs)没有影响。所以,关键的信息是:先发制人的碘并不是辐射暴露的万能解药。它只提供针对放射性碘同位素辐射的保护,而放射性碘同位素只是核事件期间释放的对健康有害的同位素的一个子集。一般人群的主要风险来自于摄入受放射性同位素污染的含碘食品,导致患甲状腺癌的长期风险增加。预防性碘应在接触前或接触时立即单剂量摄入,尤其适用于40岁以下的人。只要遵守政府的指示,准备者将碘片储存在家里的策略的相关性就不应由我们来确定。然而,当我们回顾碘的暴力历史时——从它的宇宙创造到它的发现,再到现在它在核准备中的治疗用途——也许它给我们所有人的信息是明确的,可以引起约翰·列侬(1940-1980)和小野洋子(1933年出生)在1969年冷战达到顶峰时所说的话的共鸣:给和平一个机会!Per Karkov Cramon:构思,初稿,修改。Søren Holm:初稿,修改。罗南·m·g·伯格:构思,初稿,修改。所有作者都已阅读并批准了此手稿的最终版本,并同意对工作的各个方面负责,以确保与工作任何部分的准确性或完整性相关的问题得到适当的调查和解决。所有被指定为作者的人都有资格获得作者身份,所有有资格获得作者身份的人都被列出。作者无利益冲突需要声明。 体育活动研究中心(CFAS)由TrygFonden资助(资助ID 101390, ID 20045, ID 125132和ID 177225)。资助者在研究设计、数据收集和分析、发表决定或手稿准备方面没有任何作用。
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来源期刊
Experimental Physiology
Experimental Physiology 医学-生理学
CiteScore
5.10
自引率
3.70%
发文量
262
审稿时长
1 months
期刊介绍: Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged. Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.
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Myths and methodologies: Optimising experimental rigour in heat adaptation research: Menstrual status classification and scheduling approaches. Bed rest decreases resting skeletal muscle O2 uptake and resting energy expenditure in young and elderly subjects. Effects of reducing sedentary behaviour on heart rate variability and cardio-metabolic biomarkers in desk workers with untreated high blood pressure. Noradrenergic regulation of skeletal muscle oxygen pressures: Impact of heart failure with preserved ejection fraction and heat therapy. Hypogravity simulation using the Variable Gravity Suspension System: A technical report.
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