Selenium deficiency

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Selenium deficiency
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Selenium
SpecialtyEndocrinology Edit this on Wikidata
Causescompromised intestinal function

Selenium deficiency occurs when an organism lacks the required levels of selenium, a critical nutrient in many species. Deficiency, although relatively rare in healthy well-nourished individuals,[1] can have significant negative results,[2] affecting the health of the heart and the nervous system; contributing to depression, anxiety, and dementia; and interfering with reproduction and gestation.

Signs and symptoms[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.[3] 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.[4] 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 (T3),[3] and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.[5]

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 in persons of advanced age (i.e., over 90).[6]

People dependent on food grown from selenium-deficient soil may be at risk for deficiency.[7][citation needed] Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as deficient.[citation needed]

For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs (e.g., statins) may resemble the pathology of selenium deficiency.[8][9]

Diagnosis[edit]

Reference ranges[edit]

In the US, 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[10] is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.[11]

Epidemiology and prevention[edit]

These diseases are most common in certain parts of China where the intake is low[12] 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.[5] In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils.[13] Dietary supplements may utilize sodium selenite, L-selenomethionine or selenium-enriched yeast.

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.[14] 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.[15] Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible.[16] In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain.[17] Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep.[17] 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.[14] However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed.[18] The cyanogenic glycosides in some white clover (Trifolium repens) varieties may influence the Se requirement,[17] presumably because of cyanide from the aglycone released by glucosidase activity in the rumen[19] and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the glutathione moiety.[20]

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.[21]

References[edit]

  1. ^ Weeks, Benjamin S.; Hanna, Mirna S.; Cooperstein, Deborah (2012). "Dietary selenium and selenoprotein function". Medical Science Monitor. 18 (8): RA127–RA132. doi:10.12659/msm.883258. PMC 3560698. PMID 22847213.
  2. ^ Kieliszek, Marek (3 April 2019). "Selenium–Fascinating Microelement, Properties and Sources in Food". Molecules. 24 (7). doi:10.3390/molecules24071298. PMC 6480557. PMID 30987088.
  3. ^ a b "Toxicological Profile for Selenium" (PDF). Agency for Toxic Substances and Disease Registry. U.S. Department of Health and Human Services. September 2003. Retrieved 7 Sep 2015.
  4. ^ 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" (PDF). New England Journal of Medicine. 339 (16): 1112–20. doi:10.1056/NEJM199810153391604. PMID 9770558. S2CID 2485235.
  5. ^ a b "Selenium". Office of Dietary Supplements.
  6. ^ 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. doi:10.1093/ajcn/71.2.590. PMID 10648276.
  7. ^ "Selenium Deficiency". Healthline. Retrieved 10 May 2020.
  8. ^ 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. S2CID 43675310.
  9. ^ 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.
  10. ^ Papp, Laura Vanda; Lu, Jun; Holmgren, Arne; Khanna, Kum Kum (2007). "From Selenium to Selenoproteins: Synthesis, Identity, and Their Role in Human Health" (PDF). Antioxidants & Redox Signaling. 9 (7): 775–806. doi:10.1089/ars.2007.1528. PMID 17508906.
  11. ^ Xia, Yiming; Hill, Kristina E; Byrne, Daniel W; Xu, Jiayuan; Burk, Raymond F (1 April 2005). "Effectiveness of selenium supplements in a low-selenium area of China". The American Journal of Clinical Nutrition. 81 (4): 829–834. doi:10.1093/ajcn/81.4.829. PMID 15817859.
  12. ^ Johnson, Larry E. (May 2020). "Selenium Deficiency". Merck Manuals Professional Edition.
  13. ^ Varo, P; Alfthan, G; Ekholm, P; Aro, A; Koivistoinen, P (1 August 1988). "Selenium intake and serum selenium in Finland: effects of soil fertilization with selenium". The American Journal of Clinical Nutrition. 48 (2): 324–329. doi:10.1093/ajcn/48.2.324. PMID 2841842.
  14. ^ a b Nutrient Requirements of Sheep (6th ed.). National Academies Press. 1985. ISBN 978-0-309-03596-5.
  15. ^ Jensen, Rue; Swift, Brinton L.; Kimberling, Cleon V. (1988). Jensen and Swift's Diseases of Sheep. Lea & Febiger. ISBN 978-0-8121-1099-9.[page needed]
  16. ^ Underwood, Eric John (1999). The Mineral Nutrition of Livestock. CABI. ISBN 978-0-85199-128-3.[page needed]
  17. ^ a b c Committee on the Nutrient Requirements of Small Ruminants (2007). Nutrient Requirements of Small Ruminants: Sheep, Goats, Cervids, and New World Camelids. National Academies Press. ISBN 978-0-309-10213-1.[page needed]
  18. ^ Whanger, P. D.; Weswig, P. H.; Oldfield, J. E.; Cheeke, P. R.; Muth, O. H. (1972). "Factors influencing selenium and white muscle disease: forage types, salts, amino acids and dimethyl sulfoxide". Nutr. Rep. Int. 6: 21–37.
  19. ^ Coop, I. E.; Blakely, R. L. (1949). "The metabolism and toxicity of cyanides and cyanogenic glycosides in sheep". N. Z. J. Sci. Technol. 30: 277–291.
  20. ^ Kraus, Richard J.; Prohaska, Joseph R.; Ganther, Howard E. (September 1980). "Oxidized forms of ovine erythrocyte glutathione peroxidase cyanide inhibition of a 4-glutathione:4-selenoenzyme". Biochimica et Biophysica Acta (BBA) - Enzymology. 615 (1): 19–26. doi:10.1016/0005-2744(80)90004-2. PMID 7426660.
  21. ^ Kahn, Cynthia M., ed. (2005). The Merck Veterinary Manual (9th ed.). Wiley. ISBN 978-0-911910-50-6.[page needed]

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