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Def. "any inorganic element that is essential to nutrition"[1] is called a mineral.

Chromium[edit | edit source]

"Chromium is a trace mineral that helps to regulate blood sugar and lipid levels. Typical nutritional levels range from 50 mcg to 200 mcg in well nourished people. However, in diabetic patients, high doses of chromium, which are extremely safe, can significantly reduce blood sugar and enhance insulin sensitivity (Anderson et al 1997). When 1000 mcg of chromium were administered to type II diabetics, 90% of them were able to eliminate the need for medication to control blood sugar levels (Anderson 1997). Chromium supplements also lower total cholesterol and increase high density lipoprotein levels."[2]

Copper[edit | edit source]

In humans, copper is found mainly in the liver, muscle, and bone.[3] The adult body contains between 1.4 and 2.1 mg of copper per kilogram of body weight.[4]

Copper is an essential trace element in plants and animals, but not all microorganisms. The human body contains copper at a level of about 1.4 to 2.1 mg per kg of body mass.[5]

Copper is absorbed in the gut, then transported to the liver bound to albumin.[6] After processing in the liver, copper is distributed to other tissues in a second phase, which involves the protein ceruloplasmin, carrying the majority of copper in blood. Ceruloplasmin also carries the copper that is excreted in milk, and is particularly well-absorbed as a copper source.[7] Copper in the body normally undergoes enterohepatic circulation (about 5 mg a day, vs. about 1 mg per day absorbed in the diet and excreted from the body), and the body is able to excrete some excess copper, if needed, via bile, which carries some copper out of the liver that is not then reabsorbed by the intestine.[8][9]

Manganese[edit | edit source]

Manganese is an essential human dietary element, important in macronutrient metabolism, bone formation, and free radical defense systems. It is a critical component in dozens of proteins and enzymes.[10] It is found mostly in the bones, but also the liver, kidneys, and brain.[11] In the human brain, the manganese is bound to manganese metalloproteins, most notably glutamine synthetase in astrocytes.

Selenium[edit | edit source]

In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase.[12] Selenium-containing proteins are produced from inorganic selenium via the intermediacy of selenophosphate (PSeO33−).

Twenty-five selenoproteins are encoded in the human genome.[13]

Glutathione peroxidase functions as a catalyst for the destruction of hydrogen peroxide.[14]

A related selenium-containing enzyme in some plants and in animals (thioredoxin reductase) generates reduced thioredoxin, a dithiol that serves as an electron source for peroxidases and also the important reducing enzyme ribonucleotide reductase that makes DNA precursors from RNA precursors.[15]

Selenium also plays a role in the functioning of the thyroid gland by participating as a cofactor for the three thyroid hormone deiodinases, where these enzymes activate and then deactivate various thyroid hormones and their metabolites.[16] It may inhibit Hashimoto's thyroiditis, or Hashimotos's disease, an auto-immune disease in which the body's own thyroid cells are attacked by the immune system: A reduction of 21% on TPO antibodies was reported with the dietary intake of 0.2 mg of selenium.[17]

Zinc[edit | edit source]

Zinc is an essential mineral (a micronutrient), including to prenatal and postnatal development.[18] Zinc deficiency affects about two billion people in the developing world and is associated with many diseases.[19] In children, deficiency causes growth retardation, delayed sexual maturation, infection susceptibility, and diarrhea.[18] Enzymes with a zinc atom in the prosthetic group, reactive center, are widespread in biochemistry, such as alcohol dehydrogenase in humans.[20]

The World Health Organization advocates zinc supplementation for severe malnutrition and diarrhea.[21] Zinc supplements help prevent disease and reduce mortality, especially among children with low birth weight or stunted growth.[21] However, zinc supplements should not be administered alone, because many in the developing world have several deficiencies, and zinc interacts with other micronutrients.[22] While zinc deficiency is usually due to insufficient dietary intake, it can be associated with malabsorption, acrodermatitis enteropathica, chronic liver disease, chronic renal disease, sickle cell disease, diabetes, malignancy, and other chronic illnesses.[19]

Symptoms of mild zinc deficiency are diverse.[23] Clinical outcomes include depressed growth, diarrhea, impotence and delayed sexual maturation, alopecia, eye and skin lesions, impaired appetite, altered cognition, impaired immune functions, defects in carbohydrate utilization, and reproductive teratogenesis.[23] Zinc deficiency depresses immunity,[24] but excessive zinc does also.[25]

Despite some concerns,[26] western vegetarians and vegans do not suffer any more from overt zinc deficiency than meat-eaters.[27] Major plant sources of zinc include cooked dried beans, sea vegetables, fortified cereals, soy foods, nuts, peas, and seeds.[26] However, phytates in many whole-grains and fibers may interfere with zinc absorption and marginal zinc intake has poorly understood effects. The zinc chelator phytate, found in seeds and cereal bran, can contribute to zinc malabsorption.[19] Some evidence suggests that more than the US RDA (8 mg/day for adult women; 11 mg/day for adult men) may be needed in those whose diet is high in phytates, such as some vegetarians.[26] The European Food Safety Authority (EFSA) guidelines attempt to compensate for this by recommending higher zinc intake when dietary phytate intake is greater.[28] These considerations must be balanced against the paucity of adequate zinc biomarkers, and the most widely used indicator, plasma zinc, has poor sensitivity and specificity.[29]

See also[edit | edit source]

References[edit | edit source]

  1. SemperBlotto (12 April 2006). "mineral". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 2013-08-30. {{cite web}}: |author= has generic name (help)
  2. Michael Janson (September 2006). "Orthomolecular medicine: the therapeutic use of dietary supplements for anti-aging". Clinical Interventions in Aging 1 (3): 261-5. PMID 18046879. Retrieved 25 September 2018. 
  3. Johnson, MD PhD, Larry E., ed. (2008). "Copper". Merck Manual Home Health Handbook. Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc. Retrieved 7 April 2013.
  4. "Copper in human health".
  5. "Amount of copper in the normal human body, and other nutritional copper facts". Retrieved 3 April 2009.
  6. Adelstein, S. J.; Vallee, B. L. (1961). "Copper metabolism in man". New England Journal of Medicine 265 (18): 892–897. doi:10.1056/NEJM196111022651806. PMID 13859394. 
  7. M.C. Linder; Wooten, L.; Cerveza, P.; Cotton, S.; Shulze, R.; Lomeli, N. (1 May 1998). "Copper transport". The American Journal of Clinical Nutrition 67 (5): 965S–971S. doi:10.1093/ajcn/67.5.965S. PMID 9587137. 
  8. Frieden, E.; Hsieh, H.S. (1976). Ceruloplasmin: The copper transport protein with essential oxidase activity. Advances in Enzymology – and Related Areas of Molecular Biology. 44. pp. 187–236. doi:10.1002/9780470122891.ch6. ISBN 978-0-470-12289-1. 
  9. S.S. Percival; Harris, E.D. (1 January 1990). "Copper transport from ceruloplasmin: Characterization of the cellular uptake mechanism". American Journal of Physiology. Cell Physiology 258 (1): C140–C146. doi:10.1152/ajpcell.1990.258.1.c140. PMID 2301561. 
  10. Erikson, Keith M.; Ascher, Michael (2019). "Chapter 10. Manganese: Its Role in Disease and Health". In Sigel, Astrid; Freisinger, Eva; Sigel, Roland K. O. et al.. Essential Metals in Medicine:Therapeutic Use and Toxicity of Metal Ions in the Clinic. 19. Berlin: de Gruyter GmbH. 253–266. doi:10.1515/9783110527872-016. ISBN 978-3-11-052691-2. 
  11. Emsley, John (2001). "Manganese". Nature's Building Blocks: An A-Z Guide to the Elements. Oxford, UK: Oxford University Press. pp. 249–253. ISBN 978-0-19-850340-8. 
  12. S. J. Lippard, J. M. Berg "Principles of Bioinorganic Chemistry" University Science Books: Mill Valley, CA; 1994. ISBN 0-935702-73-3.
  13. Kurokawa, Suguru; Berry, Marla J. (2013). "Selenium. Role of the Essential Metalloid in Health". In Astrid Sigel, Helmut Sigel and Roland K. O. Sigel. Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences. 13. Springer. pp. 499–534 Selenium. Role of the Essential Metalloid in Health. doi:10.1007/978-94-007-7500-8_16. ISBN 978-94-007-7499-5. 
  14. Bhabak Krishna P., Mugesh Govindasamy; Mugesh (2010). "Functional Mimics of Glutathione Peroxidase: Bioinspired Synthetic Antioxidants". Acc. Chem. Res. 43 (11): 1408–1419. doi:10.1021/ar100059g. PMID 20690615. 
  15. Stadtman TC (1996). "Selenocysteine". Annual Review of Biochemistry 65: 83–100. doi:10.1146/ PMID 8811175. 
  16. "Selenium". Linus Pauling Institute at Oregon State University. 2014-04-23. Retrieved 2009-01-05.
  17. Mazokopakis, EE; Papadakis, JA; Papadomanolaki, MG; Batistakis, AG; Giannakopoulos, TG; Protopapadakis, EE; Ganotakis, ES (2007). "Effects of 12 months treatment with L-selenomethionine on serum anti-TPO Levels in Patients with Hashimoto's thyroiditis". Thyroid 17 (7): 609–12. doi:10.1089/thy.2007.0040. PMID 17696828. 
  18. 18.0 18.1 Hambidge, K. M.; Krebs, N. F. (2007). "Zinc deficiency: a special challenge". J. Nutr. 137 (4): 1101–5. doi:10.1093/jn/137.4.1101. PMID 17374687. 
  19. 19.0 19.1 19.2 Prasad, AS (2003). "Zinc deficiency : Has been known of for 40 years but ignored by global health organisations". British Medical Journal 326 (7386): 409–410. doi:10.1136/bmj.326.7386.409. PMID 12595353. PMC 1125304. // 
  20. Maret, Wolfgang (2013). "Chapter 14 Zinc and the Zinc Proteome". In Banci, Lucia. Metallomics and the Cell. Metal Ions in Life Sciences. 12. Springer. pp. 479–501. doi:10.1007/978-94-007-5561-1_14. ISBN 978-94-007-5561-1. 
  21. 21.0 21.1 WHO contributors (2007). "The impact of zinc supplementation on childhood mortality and severe morbidity". World Health Organization. Archived from the original on March 2, 2009. {{cite web}}: |author= has generic name (help)
  22. Shrimpton, R; Gross R; Darnton-Hill I; Young M (2005). "Zinc deficiency: what are the most appropriate interventions?". British Medical Journal 330 (7487): 347–349. doi:10.1136/bmj.330.7487.347. PMID 15705693. PMC 548733. // 
  23. 23.0 23.1 Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. National Academy Press. 2001. pp. 442–501. Retrieved September 19, 2017. 
  24. Ibs, KH; Rink L (2003). "Zinc-altered immune function". Journal of Nutrition 133 (5 Suppl 1): 1452S–1456S. doi:10.1093/jn/133.5.1452S. PMID 12730441. 
  25. Rink, L.; Gabriel P. (2000). "Zinc and the immune system". Proc Nutr Soc 59 (4): 541–52. doi:10.1017/S0029665100000781. PMID 11115789. 
  26. 26.0 26.1 26.2 American Dietetic Association (2003). "Position of the American Dietetic Association and Dietitians of Canada: Vegetarian diets". Journal of the American Dietetic Association 103 (6): 748–765. doi:10.1053/jada.2003.50142. PMID 12778049. 
  27. Freeland-Graves JH; Bodzy PW; Epright MA (1980). "Zinc status of vegetarians". Journal of the American Dietetic Association 77 (6): 655–661. PMID 7440860. 
  28. "Overview on Dietary Reference Values for the EU population as derived by the EFSA Panel on Dietetic Products, Nutrition and Allergies" (PDF). 2017.
  29. Hambidge, M (2003). "Biomarkers of trace mineral intake and status". Journal of Nutrition. 133 133 (3): 948S–955S. doi:10.1093/jn/133.3.948S. PMID 12612181. 

Further reading[edit | edit source]

External links[edit | edit source]