Selenium deficiency

Source: Wikipedia, the free encyclopedia.
Selenium deficiency
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

Selenium deficiency in combination with

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

Causes

It can occur in patients with severely compromised

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.[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

statins) may resemble the pathology of selenium deficiency.[7][8]

Diagnosis

Reference ranges

The European Food Safety Authority (EFSA) recommends a dietary allowance of 70 μg per day selenium intake for adults.[9] 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. The 55 µg/day recommendation is based on the 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

Selenium deficiency is uncommon, but regions in China, Europe, Russia, and New Zealand have low levels of selenium 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

In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and 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 the 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, a 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

  1. PMID 22847213
    .
  2. .
  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. S2CID 2485235
    .
  5. ^ a b "Selenium". Office of Dietary Supplements.
  6. PMID 10648276
    .
  7. .
  8. .
  9. ^ .
  10. S2CID 38176932. Archived from the original
    (PDF) on 2019-02-28.
  11. .
  12. ^ Johnson, Larry E. (May 2020). "Selenium Deficiency". Merck Manuals Professional Edition.
  13. PMID 2841842
    .
  14. ^ .
  15. ]
  16. ]
  17. ^ ]
  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. PMID 7426660
    .
  21. ]

External links