Selenium deficiency

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Selenium deficiency
Classification and external resources
Se-TableImage.png
ICD-10 E59
ICD-9 269.3
DiseasesDB 11941

Selenium deficiency is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.

Causes[edit]

It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also on advanced aged people (over 90).[1]

Alternatively, people dependent on food grown from selenium-deficient soil are also at risk.

For some time now in medical literature it has been noted the pattern of side-effects associated with cholesterol lowering drugs statins resembles the pathology of selenium deficiency.[2][3]

Reference ranges[edit]

In the USA, the Dietary Reference Intake for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma glutathione peroxidase. Selenoprotein P[4] is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.[5]

Presentation[edit]

Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes (along with iodine deficiency) to Kashin-Beck disease.[6] The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue.[7] Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.

Selenium is also necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart, triiodothyronine[6] , and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism and recurrent miscarriage.[8]

Epidemiology and prevention[edit]

These diseases are most common in certain parts of China where the intake is low[9] because the soil is extremely deficient in selenium. Studies in Jiangsu Province of China have indicated a reduction in the prevalence of these diseases by taking selenium supplements.[10] In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils.[11]

Selenium deficiency in non-human animals[edit]

In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and the southeastern US), selenium deficiency in some animal species is common unless supplementation is carried out.[12] Selenium deficiency is responsible (either alone or together with vitamin E deficiency) for many of the cases of WMD ("white muscle disease"), evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides.[13] Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible.[14] In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain.[15] Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep.[15] Because of selenium's role in certain peroxidases (converting hydroperoxides to alcohols) and because of the antioxidant role of vitamin E (preventing hydroperoxide formation), a low level of Se can be somewhat (but not wholly) compensated by a high level of vitamin E. (In the animal, localization of peroxidases and vitamin E differs, partly because of the fat-solubility of vitamin E.) Some studies have indicated that about 0.12 or 0.23 mg Se per kg of dry matter intake may be sufficient for avoiding Se deficiency in sheep in some circumstances.[12] However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed.[16] The cyanogenic glycosides in some white clover (Trifolium repens) varieties may influence the Se requirement,[15] presumably because of cyanide from the aglycone released by glucosidase activity in the rumen[17] and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the glutathione moiety.[18]

In areas where selenium deficiency in livestock is a concern, selenium (as selenite) may be supplemented in feed. In some countries, e.g. the US and Canada, such supplementation is regulated. Neonate ruminants at risk of WMD may be administered both Se and vitamin E by injection; some of the WMD myopathies respond only to Se, some only to vitamin E, and some to either.[19]

References[edit]

  1. ^ Ravaglia, Giovanni; Forti, Paola; Maioli, Fabiola; Bastagli, Luciana; Facchini, Andrea; Mariani, Erminia; Savarino, Lucia; Sassi, Simonetta et al. (2000). "Effect of micronutrient status on natural killer cell immune function in healthy free-living subjects aged ≥90 y". American Journal of Clinical Nutrition 71 (2): 590–8. PMID 10648276. [unreliable medical source?]
  2. ^ Moosmann, B; Behl, C (2004). "Selenoprotein synthesis and side-effects of statins". Lancet 363 (9412): 892–4. doi:10.1016/S0140-6736(04)15739-5. PMID 15031036. 
  3. ^ Moosmann, B; Behl, C (2004). "Selenoproteins, cholesterol-lowering drugs, and the consequences: Revisiting of the mevalonate pathway". Trends in Cardiovascular Medicine 14 (7): 273–81. doi:10.1016/j.tcm.2004.08.003. PMID 15542379. 
  4. ^ Papp, Laura Vanda; Lu, Jun; Holmgren, Arne; Khanna, Kum Kum (2007). "From Selenium to Selenoproteins: Synthesis, Identity, and Their Role in Human Health". Antioxidants & Redox Signaling 9 (7): 775–806. doi:10.1089/ars.2007.1528. PMID 17508906. 
  5. ^ Xia, Y; Hill, KE; Byrne, DW; Xu, J; Burk, RF (2005). "Effectiveness of selenium supplements in a low-selenium area of China". The American journal of clinical nutrition 81 (4): 829–34. PMID 15817859. 
  6. ^ a b http://www.atsdr.cdc.gov/toxprofiles/tp92-c3.pdf[full citation needed][unreliable medical source?]
  7. ^ Moreno-Reyes, Rodrigo; Suetens, Carl; Mathieu, Françoise; Begaux, Françoise; Zhu, Dun; Rivera, Maria T.; Boelaert, Marleen; Nève, Jean et al. (1998). "Kashin–Beck Osteoarthropathy in Rural Tibet in Relation to Selenium and Iodine Status". New England Journal of Medicine 339 (16): 1112–20. doi:10.1056/NEJM199810153391604. PMID 9770558. 
  8. ^ "Selenium: Dietary Supplement Fact Sheet". National Institutes of Health. Retrieved July 4th. 2013. 
  9. ^ "Selenium: Mineral Deficiency and Toxicity: Merck Manual Professional". Retrieved 2008-11-29. 
  10. ^ http://ods.od.nih.gov/factsheets/selenium.asp[full citation needed]
  11. ^ http://medicinefor.me/what-is-selenium/
  12. ^ a b Subcommittee On Sheep Nutrition. National Research Council (1985). Nutrient Requirements of Sheep. 
  13. ^ Kimberling, Cleon V (1988). Jensen and Swift's diseases of sheep. ISBN 9780812110999. 
  14. ^ Underwood, Eric John; Suttle, N. F (1999). The Mineral Nutrition of Livestock. ISBN 9780851991283. 
  15. ^ a b c National Research Council, Committee on Nutrient Requirements of Small Ruminants. 2007. Nutrient requirements of small ruminants. National Academies Press, Washington. 362 pp.
  16. ^ Whanger, P. D., P. H. Weswig, J. E. Oldfield, P. R. Cheeke and O. H. Muth. 1972. Factors influencing selenium and white muscle disease: forage types, salts, amino acids and dimethyl sulfoxide. Nutr. Rep. Int. 6; 21-37.
  17. ^ Coop, I. E. and R. L. Blakely. 1949. The metabolism and toxicity of cyanides and cyanogenic glycosides in sheep. N. Z. J. Sci. Technol. 30: 277-291.
  18. ^ Kraus, RJ; Prohaska, JR; Ganther, HE (1980). "Oxidized forms of ovine erythrocyte glutathione peroxidase. Cyanide inhibition of a 4-glutathione:4-selenoenzyme". Biochimica et Biophysica Acta 615 (1): 19–26. doi:10.1016/0005-2744(80)90004-2. PMID 7426660. 
  19. ^ Kahn, C. M. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.