iodine deficiency iodine deficiency iodine deficiency is a lack of the trace element iodine, an essential nutrient in the diet. it may result in metabolic problems such as goiter, sometimes as an endemic goiter as well as congenital iodine deficiency syndrome due to untreated congenital hypothyroidism, which results in developmental delays and other health problems. iodine deficiency is an important global health issue, especially for fertile and pregnant women. it is also a preventable cause of intellectual disability. iodine deficiencyspecialtyendocrinology iodine is an essential dietary mineral for neurodevelopment among children. the thyroid hormones thyroxine and triiodothyronine contain iodine. in areas where there is little iodine in the diet, typically remote inland areas where no marine foods are eaten, iodine deficiency is common. it is also common in mountainous regions of the world where food is grown in iodine-poor soil. prevention includes adding small amounts of iodine to table salt, a product known as iodized salt. iodine compounds have also been added to other foodstuffs, such as flour, water and milk, in areas of deficiency. seafood is also a well known source of iodine. in the u.s., the use of iodine has decreased over concerns of overdoses since mid-20th century, and the iodine antagonists bromine, perchlorate and fluoride have become more ubiquitous. in particular, around 1980 the practice of using potassium iodate as dough conditioner in bread and baked goods was gradually replaced by the use of other conditioning agents such as bromide. iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population). it resulted in 2700 deaths in 2013, up from 2100 deaths in 1990. signs and symptoms goiter main article: goiter a low amount of thyroxine (one of the two thyroid hormones) in the blood, due to lack of dietary iodine to make it, gives rise to high levels of thyroid stimulating hormone (tsh), which stimulates the thyroid gland to increase many biochemical processes; the cellular growth and proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland, or goiter. in mild iodine deficiency, levels of triiodothyronine (t3) may be elevated in the presence of low levels of levothyroxine, as the body converts more of the levothyroxine to triiodothyronine as a compensation. some such patients may have a goiter, without an elevated tsh. the introduction of iodized salt since the early 1900s has eliminated this condition in many affluent countries; however, in australia, new zealand, and several european countries, iodine deficiency is a significant public health problem. it is more common in developing countries. public health initiatives to lower the risk of cardiovascular disease have resulted in lower discretionary salt use at the table. additionally, there is a trend towards consuming more processed foods in western countries. the noniodized salt used in these foods means that people are less likely to obtain iodine from adding salt during cooking. goiter is said to be endemic when the prevalence in a population is > 5%, and in most cases goiter can be treated with iodine supplementation. if goiter is untreated for around five years, however, iodine supplementation or thyroxine treatment may not reduce the size of the thyroid gland because the thyroid is permanently damaged. congenital iodine deficiency syndrome main article: congenital iodine deficiency syndrome congenital iodine deficiency syndrome, previously known as cretinism, is a condition associated with iodine deficiency and goiter, commonly characterised by mental deficiency, deafness, squint, disorders of stance and gait and stunted growth due to hypothyroidism. paracelsus was the first to point out the relation between goitrous parents and their mentally disabled children. as a result of restricted diet, isolation, intermarriage, etc., as well as low iodine content in their food, children often had peculiar stunted bodies and retarded mental faculties, a condition later known to be associated with thyroid hormone deficiency. diderot, in his 1754 encyclopédie, described these patients as "crétins". in french, the term "crétin des alpes" also became current, since the condition was observed in remote valleys of the alps in particular. the word cretin appeared in english in 1779. while reporting recent progress towards overcoming iodine-deficiency disorders worldwide, the lancet noted: "according to world health organization, in 2007, nearly 2 billion individuals had insufficient iodine intake, a third being of school age." a conclusion was made that the single most preventable cause of intellectual disability is that of iodine deficiency. fibrocystic breast changes main article: fibrocystic breast changes there is preliminary evidence that iodine deficiency enhances the sensitivity of breast tissue to estrogen. in rats treated with estradiol, iodine deficiency has been shown to lead to changes similar to benign breast changes that are reversible by increased iodine in the diet. in a few studies, iodine supplementation had beneficial effects (such as reducing the presence of breast cyst, fibrous tissue plaques and breast pain) in women with fibrocystic breast changes. protective effects of iodine on breast cancer have been postulated from epidemiologic evidence and described in animal models. in view of the antiproliferative properties of iodine in breast tissue, molecular iodine supplementation has been suggested as an adjuvant in breast cancer therapy. risk factors following is a list of potential risk factors that may lead to iodine deficiency: low dietary iodine selenium deficiency pregnancy exposure to radiation increased intake/plasma levels of goitrogens, such as calcium sex (higher occurrence in women) smoking tobacco alcohol (reduced prevalence in users) oral contraceptives (reduced prevalence in users) perchlorates thiocyanates age (for different types of iodine deficiency at different ages) pathophysiology iodine accounts for 65% of the molecular weight of t4 and 59% of t3. there is a total of 15–20 mg of iodine in the human body, primarily concentrated in thyroid tissue and hormones. thirty percent of iodine is distributed in other tissues, including the mammary glands, eyes, gastric mucosa, choroid plexus, arterial walls, the cervix, and salivary glands. in the cells of these tissues, iodide enters directly by sodium-iodide symporter (nis). venturi s, guidi a, venturi m (1996). """. le basi razionali della terapia. 16: 267–275. pellerin p (1961). "la tecnique d'autoradiographie anatomique a la temperature de l'azote liquide". path biol. 232 (9): 233–252. diagnosis sequence of 123-iodide human scintiscans after an intravenous injection, (from left) after 30 minutes, 20 hours, and 48 hours. a high and rapid concentration of radio-iodide is evident in the periencephalic and cerebrospinal fluid (left), salivary glands, oral mucosa and the stomach. in the thyroid gland, i-concentration is more progressive, also in the reservoir (from 1% after 30 minutes, to 5.8% after 48 hours, of the total injected dose. the diagnostic workup of a suspected iodine deficiency includes signs and symptoms as well as possible risk factors mentioned above. a 24-hour urine iodine collection is a useful medical test, as approximately 90% of ingested iodine is excreted in the urine. for the standardized 24-hour test, a 50 mg iodine load is given first, and 90% of this load is expected to be recovered in the urine of the following 24 hours. recovery of less than 90% is taken to mean high retention, that is, iodine deficiency. the recovery may, however, be well less than 90% during pregnancy, and an intake of goitrogens can alter the test results. if a 24-hour urine collection is not practical, a random urine iodine-to-creatinine ratio can alternatively be used. however, the 24-hour test is found to be more reliable. a general idea of whether a deficiency exists can be determined through a functional iodine test in the form of an iodine skin test. in this test, the skin is painted with an iodine solution: if the iodine patch disappears quickly, this is taken as a sign of iodine deficiency. however, no accepted norms exist on the expected time interval for the patch to disappear, and in persons with dark skin color the disappearance of the patch may be difficult to assess. if a urine test is taken shortly after, the results may be altered due to the iodine absorbed previously in a skin test. treatment iodine supplements iodine deficiency is treated by ingestion of iodine salts, such as found in food supplements. mild cases may be treated by using iodized salt in daily food consumption, or drinking more milk, or eating egg yolks, and saltwater fish. for a salt and/or animal product restricted diet, sea vegetables (kelp, hijiki, dulse, nori (found in sushi)) may be incorporated regularly into a diet as a good source of iodine. the recommended daily intake of iodine for adult women is 150–300 µg for maintenance of normal thyroid function; for men, it is somewhat less at 150 µg. nonetheless, there is a lack of evidence on iodine fortification in foods, beverages, condiments, or seasonings other than salt in preventing goiter or improving physical development. on the other hand, such a measure may increase iodine concentration in urine. however, too high iodine intake, for example due to overdosage of iodine supplements, can have toxic side effects. it can lead to hyperthyroidism and consequently high blood levels of thyroid hormones (hyperthyroxinemia). in case of extremely high single-dose iodine intake, typically a short-term suppression of thyroid function (plummer effect and wolff–chaikoff effect) occurs. persons with pre-existing thyroid disease, elderly persons, fetuses and neonates, and patients with other risk factors are at a higher risk of experiencing iodine-induced thyroid abnormalities. in particular, in persons with goiter due to iodine deficiency or with altered thyroid function, a form of hyperthyroidism called jod-basedow phenomenon can be triggered even at small or single iodine dosages, for example as a side effect of administration of iodine-containing contrast agents. in some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (hashimoto's thyroiditis and graves' disease). different experts in nutrition advise different amounts of iodine supplementation. supplementation is typically in a product which contains roughly half iodine and half iodide (a popular product used and sold for decades is “iodoral®” which contains 5 mg of iodine and 7.5 mg of iodide). on low side there is kara fitzgerald recommending less than 1,100 mcg per day (except when treating some medical conditions), she considers long term dosage of 40,000 mcg per day “excessive”. in the middle we have dr. alan gaby who considers a “moderately high dose” to be 3,000 to 6,000 mcg per day. on the higher end we have dr. david brownstein, dr. jorge flechas, dr. guy abraham, dr. alan roby and dr. jonathan wright who recommend 6,000 mcg to 50,000 mcg per day. prognosis with iodine supplementation, goiters caused by iodine deficiency decrease in size in very young children and pregnant women. generally, however, long-standing goiters caused by iodine deficiency respond with only small amounts of shrinkage after iodine supplementation, and patients are at risk for developing hyperthyroidism. being pregnant while iodine-deficient additionally carries the risk of causing congenital iodine deficiency syndrome in the newborn. this disease can only be managed by lifelong administration of thyroxine (t4). epidemiology deaths due to iodine deficiency per million persons in 2012 0-0 1-1 2-3 4-18 disability-adjusted life year for iodine deficiency per 100,000 inhabitants in 2004. no data <50 50-100 100-150 150-200 200-250 250-300 300-350 350-400 400-450 450-500 500-750 >750 iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population). certain areas of the world, due to natural deficiency and unavailability of iodine, are severely affected by iodine deficiency, which affects approximately two billion people worldwide. it is particularly common in the western pacific, south-east asia and africa. among other nations affected by iodine deficiency, china and kazakhstan have begun taking action, while russia has not. successful campaigns for the adoption of the use of iodized salt require education of salt producers and sellers and a communication campaign directed at the public. the cost of adding iodine to salt is negligible—"only a few cents a ton." iodine deficiency has largely been confined to the developing world for several generations, but reductions in salt consumption and changes in dairy processing practices eliminating the use of iodine-based disinfectants have led to increasing prevalence of the condition in australia and new zealand in recent years. a proposal to mandate the use of iodized salt in most commercial breadmaking was adopted in australia in october 2009. in a study of the united kingdom published in 2011, almost 70% of test subjects were found