Selenium deficiency

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Selenium deficiency
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Selenium
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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.

Contents

Signs and symptoms

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 the 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

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.[ 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 the medical literature that a pattern of side effects possibly associated with cholesterol-lowering drugs (e.g., 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 selenium levels in croplands and diet. [9] The worldwide prevalence of selenium deficiency is however predicted to rise under climate change due to the loss of selenium from croplands. [9] 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

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 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 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. [14] However, a somewhat higher Se intake may be required to avoid 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. Certain countries, e.g., the US and Canada, regulate such supplementation. 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]

Related Research Articles

Antioxidants are compounds that inhibit oxidation, a chemical reaction that can produce free radicals. Autoxidation leads to degradation of organic compounds, including living matter. Antioxidants are frequently added to industrial products, such as polymers, fuels, and lubricants, to extend their usable lifetimes. Foods are also treated with antioxidants to forestall spoilage, in particular the rancidification of oils and fats. In cells, antioxidants such as glutathione, mycothiol, or bacillithiol, and enzyme systems like superoxide dismutase, can prevent damage from oxidative stress.

<span class="mw-page-title-main">Selenium</span> Chemical element with atomic number 34 (Se)

Selenium is a chemical element; it has the symbol Se and atomic number 34. It has various physical appearances, including a brick-red powder, a vitreous black solid, and a grey metallic-looking form. It seldom occurs in this elemental state or as pure ore compounds in Earth's crust. Selenium was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium.

<span class="mw-page-title-main">Vitamin A</span> Essential nutrient

Vitamin A is a fat-soluble vitamin that is an essential nutrient. The term "vitamin A" encompasses a group of chemically related organic compounds that includes retinol, retinyl esters, and several provitamin (precursor) carotenoids, most notably β-carotene (beta-carotene). Vitamin A has multiple functions: growth during embryo development, maintaining the immune system, and healthy vision. For aiding vision specifically, it combines with the protein opsin to form rhodopsin, the light-absorbing molecule necessary for both low-light and color vision.

<span class="mw-page-title-main">Folate</span> Vitamin B9; nutrient essential for DNA synthesis

Folate, also known as vitamin B9 and folacin, is one of the B vitamins. Manufactured folic acid, which is converted into folate by the body, is used as a dietary supplement and in food fortification as it is more stable during processing and storage. Folate is required for the body to make DNA and RNA and metabolise amino acids necessary for cell division and maturation of blood cells. As the human body cannot make folate, it is required in the diet, making it an essential nutrient. It occurs naturally in many foods. The recommended adult daily intake of folate in the U.S. is 400 micrograms from foods or dietary supplements.

A nutrient is a substance used by an organism to survive, grow and reproduce. The requirement for dietary nutrient intake applies to animals, plants, fungi and protists. Nutrients can be incorporated into cells for metabolic purposes or excreted by cells to create non-cellular structures such as hair, scales, feathers, or exoskeletons. Some nutrients can be metabolically converted into smaller molecules in the process of releasing energy such as for carbohydrates, lipids, proteins and fermentation products leading to end-products of water and carbon dioxide. All organisms require water. Essential nutrients for animals are the energy sources, some of the amino acids that are combined to create proteins, a subset of fatty acids, vitamins and certain minerals. Plants require more diverse minerals absorbed through roots, plus carbon dioxide and oxygen absorbed through leaves. Fungi live on dead or living organic matter and meet nutrient needs from their host.

Vitamin deficiency is the condition of a long-term lack of a vitamin. When caused by not enough vitamin intake it is classified as a primary deficiency, whereas when due to an underlying disorder such as malabsorption it is called a secondary deficiency. An underlying disorder can have 2 main causes:

<span class="mw-page-title-main">Dietary supplement</span> Product providing additional nutrients

A dietary supplement is a manufactured product intended to supplement a person's diet by taking a pill, capsule, tablet, powder, or liquid. A supplement can provide nutrients either extracted from food sources, or that are synthetic. The classes of nutrient compounds in supplements include vitamins, minerals, fiber, fatty acids, and amino acids. Dietary supplements can also contain substances that have not been confirmed as being essential to life, and so are not nutrients per se, but are marketed as having a beneficial biological effect, such as plant pigments or polyphenols. Animals can also be a source of supplement ingredients, such as collagen from chickens or fish for example. These are also sold individually and in combination, and may be combined with nutrient ingredients. The European Commission has also established harmonized rules to help insure that food supplements are safe and appropriately labeled.

<span class="mw-page-title-main">Glutathione peroxidase</span> Enzyme family protecting the organism from oxidative damages

Glutathione peroxidase (GPx) is the general name of an enzyme family with peroxidase activity whose main biological role is to protect the organism from oxidative damage. The biochemical function of glutathione peroxidase is to reduce lipid hydroperoxides to their corresponding alcohols and to reduce free hydrogen peroxide to water.

<span class="mw-page-title-main">Mineral (nutrient)</span> Chemical element required by organisms for life functions

In the context of nutrition, a mineral is a chemical element. Some "minerals" are essential for life, but most are not. Minerals are one of the four groups of essential nutrients; the others are vitamins, essential fatty acids, and essential amino acids. The five major minerals in the human body are calcium, phosphorus, potassium, sodium, and magnesium. The remaining minerals are called "trace elements". The generally accepted trace elements are iron, chlorine, cobalt, copper, zinc, manganese, molybdenum, iodine, selenium, and bromine; there is some evidence that there may be more.

In molecular biology a selenoprotein is any protein that includes a selenocysteine amino acid residue. Among functionally characterized selenoproteins are five glutathione peroxidases (GPX) and three thioredoxin reductases, (TrxR/TXNRD) which both contain only one Sec. Selenoprotein P is the most common selenoprotein found in the plasma. It is unusual because in humans it contains 10 Sec residues, which are split into two domains, a longer N-terminal domain that contains 1 Sec, and a shorter C-terminal domain that contains 9 Sec. The longer N-terminal domain is likely an enzymatic domain, and the shorter C-terminal domain is likely a means of safely transporting the very reactive selenium atom throughout the body.

<span class="mw-page-title-main">Cholecalciferol</span> Vitamin D3, a chemical compound

Cholecalciferol, also known as vitamin D3 or colecalciferol, is a type of vitamin D that is produced by the skin when exposed to UVB light; it is found in certain foods and can be taken as a dietary supplement.

<span class="mw-page-title-main">Nutrition and pregnancy</span> Nutrient intake and dietary planning undertaken before, during and after pregnancy

Nutrition and pregnancy refers to the nutrient intake, and dietary planning that is undertaken before, during and after pregnancy. Nutrition of the fetus begins at conception. For this reason, the nutrition of the mother is important from before conception as well as throughout pregnancy and breastfeeding. An ever-increasing number of studies have shown that the nutrition of the mother will have an effect on the child, up to and including the risk for cancer, cardiovascular disease, hypertension and diabetes throughout life.

Keshan disease is a congestive cardiomyopathy caused by a combination of dietary deficiency of selenium and the presence of a mutated strain of Coxsackievirus, named after Keshan County of Heilongjiang province, Northeast China, where symptoms were first noted. These symptoms were later found prevalent in a wide belt extending from northeast to southwest China, all due to selenium-deficient soil. The disease peaked in 1960–1970, killing thousands of people.

<span class="mw-page-title-main">Glutathione peroxidase 4</span> Mammalian protein found in Homo sapiens

Glutathione peroxidase 4, also known as GPX4, is an enzyme that in humans is encoded by the GPX4 gene. GPX4 is a phospholipid hydroperoxidase that protects cells against membrane lipid peroxidation.

Vitamin B<sub><small>12</small></sub> Vitamin used in animal cell metabolism

Vitamin B12, also known as cobalamin, is a water-soluble vitamin involved in metabolism. It is one of eight B vitamins. It is required by animals, which use it as a cofactor in DNA synthesis, and in both fatty acid and amino acid metabolism. It is important in the normal functioning of the nervous system via its role in the synthesis of myelin, and in the circulatory system in the maturation of red blood cells in the bone marrow. Plants do not need cobalamin and carry out the reactions with enzymes that are not dependent on it.

<span class="mw-page-title-main">Vitamin D</span> Group of fat-soluble secosteroids

Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, along with numerous other biological functions. In humans, the most significant compounds within this group are vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol).

<span class="mw-page-title-main">Nutritional muscular dystrophy</span>

Nutritional Muscular Dystrophy is a disease caused by a deficiency of selenium and vitamin E in dietary intake. Soils that contains low levels of selenium produce forages and grains that are deficient in selenium. Similarly, if the forage is of low quality or is not stored properly it may be deficient in vitamin E. If an animal consumes this type of diet without additional supplementation they become susceptible to this disease. This condition often affects young ruminants, such as calves and lambs.

Relatively speaking, the brain consumes an immense amount of energy in comparison to the rest of the body. The mechanisms involved in the transfer of energy from foods to neurons are likely to be fundamental to the control of brain function. Human bodily processes, including the brain, all require both macronutrients, as well as micronutrients.

<span class="mw-page-title-main">Selenium in biology</span> Use of Selenium by organisms

Selenium is an essential micronutrient for animals, though it is toxic in large doses. In plants, it sometimes occurs in toxic amounts as forage, e.g. locoweed. Selenium is a component of the amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase. Selenium-containing proteins are produced from inorganic selenium via the intermediacy of selenophosphate (PSeO33−).

<span class="mw-page-title-main">Christine Thomson</span> Emerita professor of human nutrition in New Zealand

Christine Dumont Thomson is a New Zealand nutritionist and academic, and is professor emerita at the University of Otago. Before her retirement in 2010 she researched iodine and selenium dietary deficiencies.

References

  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): 1298. doi: 10.3390/molecules24071298 . PMC   6480557 . PMID   30987088.
  3. 1 2 "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". New England Journal of Medicine. 339 (16): 1112–20. doi: 10.1056/NEJM199810153391604 . PMID   9770558. S2CID   2485235.
  5. 1 2 "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. ↑ 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.
  8. ↑ 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.
  9. 1 2 3 Razaghi, Ali; Poorebrahim, Mansour; Sarhan, Dhifaf; Björnstedt, Mikael (2021-09-01). "Selenium stimulates the antitumour immunity: Insights to future research". European Journal of Cancer. 155: 256–267. doi: 10.1016/j.ejca.2021.07.013 . ISSN   0959-8049. PMID   34392068.
  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. S2CID   38176932. Archived from the original (PDF) on 2019-02-28.
  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. 1 2 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. 1 2 3 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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