Iodine deficiency

Iodine deficiency
Classification and external resources
ICD-10 E00E02
DiseasesDB 6933
eMedicine med/1187

Iodine is an essential trace element; the thyroid hormones thyroxine and triiodotyronine contain iodine. In areas where there is little iodine in the diet—typically remote inland areas where no marine foods are eaten—iodine deficiency gives rise to goiter (so-called endemic goiter), as well as cretinism, which results in developmental delays and other health problems. While noting recent progress, The Lancet noted, "According to WHO, in 2007, nearly 2 billion individuals had insufficient iodine intake, a third being of school age. ... Thus iodine deficiency, as the single greatest preventable cause of mental retardation, is an important public-health problem."[1]

In some such areas, this is now combatted by the addition of small amounts of iodine to table salt in form of sodium iodide, potassium iodide, and/or potassium iodate—this product is known as iodized salt. Iodine compounds have also been added to other foodstuffs, such as flour, water and milk in areas of deficiency.[2] Seafood is also a well known source of iodine.[3] Thus, iodine deficiency is more common in mountainous regions of the world where food is grown in soil poor in iodine.

Contents

Signs and symptoms

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 triiodiothyronine (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.[4] It is more common in third-world nations. Public health initiatives to lower the risk of cardiovascular disease have resulted in lower discretionary salt use at the table, and with a trend towards consuming more processed foods. The noniodized salt used in these foods also 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.

Cretinism

Iodine deficiency is one of the leading causes of preventable mental handicaps worldwide, producing typical reductions in IQ of 10 to 15 IQ points. It has been speculated that deficiency of iodine and other micronutrients may be a possible factor in observed differences in IQ between ethnic groups: see race and intelligence for a further discussion of this controversial issue.

Cretinism is a condition associated with iodine deficiency and goiter, commonly characterised by mental deficiency, deaf-mutism, squint, disorders of stance and gait, stunted growth and hypothyroidism. Paracelsus was the first to point out the relation between goitrous parents and mentally retarded children.[5] 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 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.

Deficiency

In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten, iodine deficiency gives rise to hypothyroidism, symptoms of which are extreme fatigue, goiter, mental slowing, depression, weight gain, and low basal body temperatures.[6]

Iodine deficiency is the leading cause of preventable mental retardation, a result which occurs primarily when babies or small children are rendered hypothyroidic by a lack of the element. The addition of iodine to table salt has largely eliminated this problem in the wealthier nations, but as of March 2006, iodine deficiency remained a serious public health problem in the developing world.[7] Iodine deficiency is also a problem in certain areas of Europe. In Germany it has been estimated to cause a billion dollars in health care costs per year.[8]

Iodine may also help prevent diseases of the oral and salivary glands.[9]

Extrathyroidal iodine

Iodine accounts for 65% of the molecular weight of T4 and 59% of the T3. 15–20 mg of iodine is concentrated in thyroid tissue and hormones, but 70% of the body's iodine is distributed in other tissues, including mammary glands, eyes, gastric mucosa, the cervix, and salivary glands. In the cells of these tissues iodide enters directly by sodium-iodide symporter (NIS). Its role in mammary tissue is related to fetal and neonatal development, but its role in the other tissues is unknown.[8][10].[11] It has been shown to act as an antioxidant in these tissues.The US Food and Nutrition Board and Institute of Medicine recommended daily allowance of iodine ranges from 150 micrograms /day for adult humans to 290 micrograms /day for lactating mothers. However, the thyroid gland needs no more than 70 micrograms /day to synthesize the requisite daily amounts of T4 and T3. These higher recommended daily allowance levels of iodine seem necessary for optimal function of a number of body systems, including lactating breast, gastric mucosa, salivary glands, oral mucosa, thymus, epidermis, choroid plexus, etc.[12][13][14] Moreover, iodine can add to double bonds of docosahexaenoic acid and arachidonic acid of cellular membranes, making them less reactive to free oxygen radicals.[15]

Iodine deficiency and cancer risk

Epidemiology

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.

India is the most outstanding, with 100 million suffering from deficiency, 4 million from goiter, and 0.5 million from cretinism.[25]

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."[25]

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 is expected to be adopted in 2009.[26][27] In a study of the United Kingdom published in 2011, almost 70% of test subjects were found to be iodine deficient.[28] The study's authors suggested an investigation regarding "evidence-based recommendations for iodine supplementation".[28]

Risk factors

Following is a list of potential risk factors that may lead to iodine deficiency:[29]

  1. Low dietary iodine
  2. Selenium deficiency
  3. Pregnancy
  4. Exposure to radiation
  5. Increased intake/plasma levels of goitrogens, such as calcium
  6. Gender (higher occurrence in women)
  7. Smoking tobacco
  8. Alcohol (reduced prevalence in users)
  9. Oral contraceptives (reduced prevalence in users)
  10. Perchlorates
  11. Thiocyanates
  12. Age (for different types of iodine deficiency at different ages)

Diagnosis

The diagnostic workup of a suspected iodine deficiency includes signs and symptoms as well as possible risk factors mentioned above.

In addition, a 24-hour urine iodine collection is a useful medical test, as approximately 90% of ingested iodine is excreted in the urine. If a 24-hour urine collection is not practical, a random urine iodine-to-creatinine ratio can alternatively be used.[30]

Treatment

Iodine deficiency is treated by ingestion of iodine, such as found in food supplements. Mild cases may be treated by using iodized salt in daily food consumption, or eating more of milk, egg yolks, and saltwater fish. Iodized salt offers sufficient amounts of iodine. For a salt-restricted diet, try incorporating sea vegetables (kelp, hijiki, dulse, nori (found in sushi)) into your diet for an excellent source of iodine. [30]

In an adult, 150 µg/d is sufficient for normal thyroid function. However, because of the additional requirements of women, it is recommended that higher intake levels of 150-300 µg/d should be taken daily. [30]

Prognosis

With iodine supplementation, goiters caused by iodine deficiency decrease in size of 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.[30]

See also

References

  1. ^ The Lancet (12 July 2008). "Iodine deficiency—way to go yet". The Lancet 372 (9633): 88. doi:10.1016/S0140-6736(08)61009-0. PMID 18620930. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)61009-0/fulltext. Retrieved 2008-12-05. 
  2. ^ François Delange, Basil Hetzel. "The Iodine Deficiency Disorders". Thyroid Disease Manager. http://www.thyroidmanager.org/Chapter20/20-frame.htm. 
  3. ^ Iodine in Seaweed
  4. ^ Andersson M, Takkouche B, Egli I, Allen HE, de Benoist B (2005). "Current global iodine status and progress over the last decade towards the elimination of iodine deficiency". Bull. World Health Organ. 83 (7): 518–25. PMC 2626287. PMID 16175826. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2626287. 
  5. ^ T. E. C. Jr. M.D. (August 1, 1974). "Paracelsus on What the Physician Should Know". Pediatrics (American Academy of Pediatrics) 54 (2): 141. http://pediatrics.aappublications.org/cgi/content/abstract/54/2/141. Retrieved 2008-12-05. 
  6. ^ Felig, Philip; Frohman, Lawrence A. (2001). "Endemic Goiter". Endocrinology & metabolism. McGraw-Hill Professional. ISBN 9780070220010. http://books.google.com/?id=AZUUGrp6yUgC&pg=RA1-PA351. 
  7. ^ "Micronutrients — Iodine, Iron and Vitamin A". UNICEF. http://www.unicef.org/nutrition/index_iodine.html. 
  8. ^ a b Patrick L (2008). "Iodine: deficiency and therapeutic considerations". Altern Med Rev 13 (2): 116. PMID 18590348. http://www.thorne.com/altmedrev/.fulltext/13/2/116.pdf. 
  9. ^ Venturi, S; Venturi, M (2009). "Iodine in evolution of salivary glands and in oral health". Nutrition and health (Berkhamsted, Hertfordshire) 20 (2): 119–34. PMID 19835108.  edit
  10. ^ Venturi S, Venturi M (2007). "Evolution of Dietary Antioxidant Defences". European Epi-Marker 11 (3): 1–12. http://www.icb-asbl.com/en/pdf/epimarker/epimarker_3_07.pdf. 
  11. ^ Venturi, S; Donati, FM; Venturi, A; Venturi, M (2000). "Environmental iodine deficiency: A challenge to the evolution of terrestrial life?". Thyroid : official journal of the American Thyroid Association 10 (8): 727–9. doi:10.1089/10507250050137851. PMID 11014322. 
  12. ^ Brown-Grant, K. (1961). "Extrathyroidal iodide concentrating mechanisms". Physiol Rev. 41 (1): 189. http://physrev.physiology.org/cgi/reprint/41/1/189.pdf. 
  13. ^ Spitzweg, C., Joba, W., Eisenmenger, W. and Heufelder, A.E. (1998). "Analysis of human sodium iodide symporter gene expression in extrathyroidal tissues and cloning of its complementary deoxyribonucleic acid from salivary gland, mammary gland, and gastric mucosa". J Clin Endocrinol Metab. 83 (5): 1746. doi:10.1210/jc.83.5.1746. PMID 9589686. 
  14. ^ Banerjee, R.K., Bose, A.K., Chakraborty, t.K., de, S.K. and datta, A.G. (1985). "Peroxidase catalysed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues". J Endocrinol. 2: 159. 
  15. ^ Cocchi, M. and Venturi, S. Iodide, antioxidant function and Omega-6 and Omega-3 fatty acids: a new hypothesis of a biochemical cooperation? Progress in Nutrition, 2000, 2, 15-19
  16. ^ Venturi, S. (2001). "Is there a role for iodine in breast diseases?". The Breast 10 (5): 379–382. doi:10.1054/brst.2000.0267. PMID 14965610.  edit
  17. ^ a b Stoddard II, F. R.; Brooks, A. D.; Eskin, B. A.; Johannes, G. J. (2008). "Iodine Alters Gene Expression in the MCF7 Breast Cancer Cell Line: Evidence for an Anti-Estrogen Effect of Iodine". International Journal of Medical Science 5 (4): 189. PMC 2452979. PMID 18645607. http://www.medsci.org/v05p0189.htm. 
  18. ^ Eskin, B. A.; Grotkowski, C. E.; Connolly, C. P.; Ghent W. R.; (1995). "Different tissue responses for iodine and iodide in rat thyroid and mammary glands". Bioligal Trace Elements Research 49 (5): 9. doi:10.1007/BF02788999. PMID 7577324. 
  19. ^ Venturi, S.; Grotkowski, CE; Connolly, CP; Ghent, WR (2001). "Is there a role for iodine in breast diseases?". The Breast 10 (1): 379. doi:10.1054/brst.2000.0267. PMID 14965610. 
  20. ^ Josefssson, M.; Ekblad, E. (2009). "Sodium Iodide Symporter (NIS) in Gastric Mucosa: Gastric Iodide Secretion". In Preedy, Victor R.; Burrow, Gerard N.; Watson, Ronald. Comprehensive Handbook of Iodine: Nutritional, Biochemical, Pathological and Therapeutic Aspects 
  21. ^ Abnet CC, Fan JH, Kamangar F, Sun XD, Taylor PR, Ren JS, Mark SD, Zhao P, Fraumeni JF Jr, Qiao YL, Dawsey SM (2006). "Self-reported goiter is associated with a significantly increased risk of gastric noncardia adenocarcinoma in a large population-based Chinese cohort". International Journal of Cancer 119 (6): 1508–1510. doi:10.1002/ijc.21993. PMID 16642482. 
  22. ^ Behrouzian, R.; Aghdami, N. (2004). "Urinary iodine/creatinine ratio in patients with stomach cancer in Urmia, Islamic Republic of Iran". East Mediterr Health J. 10 (6): 921–924. PMID 16335780 .
  23. ^ Golkowski F, Szybinski Z, Rachtan J, Sokolowski A, Buziak-Bereza M, Trofimiuk M, Hubalewska-Dydejczyk A, Przybylik-Mazurek E, Huszno B. (2007). "Iodine prophylaxis--the protective factor against stomach cancer in iodine deficient areas". Eur J Nutr. 46 (5): 251. doi:10.1007/s00394-007-0657-8. PMID 17497074. 
  24. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. http://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls. 
  25. ^ a b "In Raising the World’s I.Q., the Secret's in the Salt", article by Donald G. McNeil, Jr., The New York Times, December 16, 2006.
  26. ^ "Iodine plan no help for mums-to-be", article appearing on April 23, 2008, from Herald Sun.
  27. ^ "Nutritionist supports switch to iodised bread, article by Rebecca Gardiner, April 3, 2008, Howick and Pakuranga Times
  28. ^ a b "Iodine status of UK schoolgirls: a cross-sectional survey". The Lancet. 11 June 2011. PMID 21640375. 
  29. ^ Knudsen N, Laurberg P, Perrild H, Bülow I, Ovesen L, Jørgensen T (October 2002). "Risk factors for goiter and thyroid nodules". Thyroid : Official Journal of the American Thyroid Association 12 (10): 879–88. doi:10.1089/105072502761016502. PMID 12487770. 
  30. ^ a b c d medscape > Iodine Deficiency Authors and editors: Stephanie L Lee and George T Griffing. Updated: Apr 22, 2009

External links