Zinc deficiency

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Zinc Deficiency
Classification and external resources
Zn-TableImage.png
Zinc
ICD-10 E60
ICD-9 269.3
DiseasesDB 14272

Zinc deficiency can occur in soils, plants, and animals. In animals, including humans, it is defined either qualitatively as insufficient zinc to meet the needs of the body and thereby causing clinical manifestations, or quantitatively as a serum zinc level below the normal range. Normal values for soils and plants, especially crops, have also been defined.

Zinc deficiency in humans results from reduced dietary intake, inadequate absorption, increased loss, or increased use. The most common cause is reduced dietary intake, with as much as 25% of the world's population is at risk. Increasing the amount of zinc in the soil and thus in crops is an effective preventative measure. A lack of zinc has numerous clinical manifestations; the most common of which are an increased incidence of diarrhea, pneumonia, and malaria.

Classification[edit]

Zinc deficiency can be classified as acute, as may occur during prolonged inappropriate zinc-free total parenteral nutrition; or chronic, as may occur in dietary deficiency or inadequate absorption.[1] Zinc deficiency can also be considered as mild, as typically accompanies dietary deficiency; or severe, as typically accompanies congenital defective absorption.[2]

Signs and symptoms[edit]

Skin, nails and hair[edit]

Zinc deficiency may manifest as acne,[3] eczema,[2] xerosis (dry, scaling skin),[2] seborrheic dermatitis,[2] or alopecia (thin and sparse hair).[2][4] There may also be impaired wound healing.[4]

Mouth[edit]

Zinc deficiency can manifest as non-specific oral ulceration, stomatitis, or white tongue coating.[2] Rarely it can cause angular cheilitis (sores at the corners of the mouth)[5] and burning mouth syndrome.[6]

Vision, smell and taste[edit]

Severe zinc deficiency may disturb the sense of smell[4] and taste.[7][8][9][10][11][12] Night blindness may be a feature of severe zinc deficiency,[4] however most reports of night blindness and abnormal dark adaptation in humans with zinc deficiency have occurred in combination with other nutritional deficiencies (e.g. vitamin A).[13]

Immune system[edit]

Impaired immune function in children with zinc deficiency can lead to the development of respiratory infections especially pneumonia.[4][14][15]

Diarrhea[edit]

Zinc deficiency contributes to an increased incidence and severity of diarrhea.[14][15]

Hunger[edit]

Zinc levels may increase or decrease hunger depending on the status of other nutrients, the developmental stage of the animal, and percentage body fat. There is evidence zinc deficiency decreases hunger, and, in contrast, evidence that zinc supplementation can also decrease hunger, by increasing leptin levels.

Zinc deficiency may lead to anorexia and anorexia nervosa.[16] Appetite disorders can,in turn, cause malnutrition and inadequate zinc intake, leading to a vicious cycle. {citation needed}] The use of zinc in the treatment of anorexia has been advocated since 1979 by Bakan. At least 15 clinical trials have shown that zinc improved weight gain in anorexia. A 1994 trial showed that zinc doubled the rate of body mass increase in the treatment of anorexia nervosa. Deficiency of other nutrients such as tyrosine, tryptophan and thiamine could contribute to this phenomenon of "malnutrition-induced malnutrition".[17]


The way zinc influences hunger may depend on the sodium/osmotic status of the organism, with low sodium/low zinc levels increasing hunger and conversely.[citation needed] An organism with a low level of zinc has an increased susceptibility to hypoosmotic stress and cell rupture. Zinc is known to affect osmolality by increasing sodium retention.[citation needed] In rats, the first visible sign of zinc deficiency is decreased food seeking behaviour.[18]

Cognitive and motor function[edit]

Cognitive and motor function may be impaired in zinc deficient children. Zinc deficiency can interfere with many metabolic processes when it occurs during infancy and childhood, a time of rapid growth and development when nutritional needs are high.[19] Low maternal zinc status has been associated with less attention during the neonatal period and worse motor functioning.[20] In some studies, supplementation has been associated with motor development in very low birth weight infants and more vigorous and functional activity in infants and toddlers.[20]

Psychological disorders[edit]

Plasma zinc levels have been alleged to be associated with many psychological disorders. An increasing amount of evidence suggests that zinc deficiency could play a role depression.[21][22] Zinc may be an effective treatment.[23]

Growth[edit]

Zinc deficiency in children can cause delayed growth.[2] It is thought to be responsible for about one third of the world's population not reaching their optimal height.[1]

During pregnancy[edit]

Zinc deficiency during pregnancy can negatively affect both the mother and fetus. Animal studies indicate that maternal zinc deficiency can upset both the sequencing and efficiency of the birth process. An increased incidence of difficult and prolonged labor, hemorrhage, uterine dystocia and placental abruption has been documented in zinc deficient animals.[24] These effects may be mediated by the defective functioning of estrogen via the estrogen receptor, which contains a zinc finger protein.[24] A review of pregnancy outcomes in women with acrodermatitis enteropathica, reported that out of every seven pregnancies, there was one abortion and two malfunctions, suggesting the human fetus is also susceptible to the teratogenic effects of severe zinc deficiency. However, a review on zinc supplementation trials during pregnancy did not report a significant effect of zinc supplementation on neonatal survival.[24]

Testosterone production[edit]

Zinc is required to produce testosterone. Thus, zinc deficiency can lead to reduced circulating testosterone, hypogonadism,[2] and delayed puberty.[2]

Causes[edit]

Dietary deficiency[edit]

A diet which is high in phytate containing whole grains, high in foods grown in zinc deficient soil, or high in zinc poor processed foods can result in zinc deficiency.[25][26] Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency.[27]

Inadequate absorption[edit]

Acrodermatitis enteropathica is an inherited disorder causing severe zinc absorption.[4] It presents as growth retardation, severe diarrhea, hair loss, skin rash (most often around the genitalia and mouth) and opportunistic candidiasis and bacterial infections.[4]

Numerous small bowel diseases causing generalized malabsorption result in zinc deficiency.[citation needed]

Increased loss[edit]

Exercizing, high alcohol intake, and diarrhea all increase loss of zinc from the body[28] Diarrhea particularly is a common cause of zinc deficiency.[2] Changes in intestinal tract absorbability and permeability due, in part, to viral, protozoal, and bacteria pathogens may also encourage fecal losses of zinc.[29]

Increased utilization[edit]

Exercising, childhood growth, and pregnancy[30] all increase utilization.[clarification needed]

Chronic disease[edit]

The mechanism of zinc deficiency in some diseases has not been well defined; it may be multifactorial.

Wilson's disease, sickle cell disease, chronic kidney disease, chronic liver disease have all been associated with zinc deficiency.[31][32] It can also occur after bariatric surgery, mercury exposure[33][34] and tartrazine.[citation needed]

Although marginal zinc deficiency is often found in depression, low zinc levels could either be a cause or a consequence of mental disorders and their symptoms.[21]

Mechanism[edit]

The mechanism for the clinical manifestations of zinc deficiency is the fact that zinc is a cofactor for hundreds of enzymes and transcription factors, most related to nucleic acid, protein, lipid and carbohydrate metabolism.[2][4] Zinc deficiency results in disruption of hundreds of metabolic pathways, causing numerous clinical manifestations, including impaired growth and development, and disruption of reproductive and immune function.[2]

Prevention[edit]

Four interventional strategies can be used:

  • Oral repletion via tablets (e.g. zinc gluconate) or liquid (e.g. zinc acetate)
  • Adding zinc to food, called fortification
  • Adding zinc rich foods to diet
  • Adding zinc to soil, called agronomic biofortification, which both increases crop yields and provides more dietary zinc

Oral zinc supplementation in healthy infants more than six months old has been shown to reduce the duration of any subsequent diarrheal episodes by about 10 hours.[35]

The foods with the highest concentration of zinc are animal meats, the highest being oysters.[2] Although whole grains and cereals are high in zinc, they also contain chelating phytates which bind zinc and reduce its bioavailability.[2]

Epidemiology[edit]

Severe zinc deficiency is rare, and is mainly seen in persons with severe congenital defective zinc absorption.[2] Mild zinc deficiency due to reduced dietary intake is common.[2] Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency.[27] Zinc deficiency is thought to be a leading cause of infant mortality.[citation needed]

Providing micronutrients, including zinc, to humans is one of the four solutions to major global problems identified in the Copenhagen Consensus from an international panel of economists.[36]

History[edit]

Significant historical events related to zinc deficiency began in 1869 when zinc was first discovered to be essential to the growth of an organism (Aspergillus Niger). In 1929 Lutz measured zinc in numerous human tissues using the dithizone technique and estimated total body zinc in a 70 kg man to be 2.2 grams. Zinc was found to be essential to the growth of rats in 1933. In 1939 beriberi patients in China were noted to have decreased zinc levels in skin and nails. In 1940 zinc levels in a series of autopsies found it to be present in all tissues examined. In 1942 a study showed most zinc excretion was via the feces. In 1950 a normal serum zinc level was first defined, and found to be 17.3 - 22.1 micromoles/liter. In 1956 cirrhotic patients were found to have low serum zinc levels. In 1963 zinc was determined to be essential to human growth, three enzymes requiring zinc as a cofactor were described, and a report was published of a 21 year old Iranian man with stunted growth, infantile genitalia, and anemia which were all reversed by zinc supplementation. In 1972 fifteen Iranian rejected army inductees with symptoms of zinc deficiency were reported: all responded to zinc. In 1973 the first case of acrodermatitis enteropathica due to severe zinc deficiency was described. In 1974 the National Academy of Sciences declared zinc to be an essential element for humans and established a recommended daily allowance. In 1978 the Food and Drug Administration required zinc to be in total parenteral nutrition fluids. In the 1990s there was increasing attention on the role of zinc deficiency in childhood morbidity and mortality in developing countries.[37] In 2002 the zinc transporter protein ZIP4 was first identified as the mechanism for absorption of zinc in the gut across the enterocyte. By 2014 over 300 zinc containing enzymes have been identified, as well as over 1000 zinc containing transcription factors.[citation needed]

Soils and crops[edit]

Soil zinc is an essential micronutrient for crops. Almost half of the world’s cereal crops are deficient in zinc, leading to poor crop yields.[38] Many agricultural countries around the world are affected by zinc deficiencies. In China, zinc deficiency occurs on around half of the agricultural soils, affecting mainly rice and maize. Areas with zinc deficient soils are often regions with widespread zinc deficiency in humans. A basic knowledge of the dynamics of in soils, understanding of the uptake and transport of zinc in crops and characterizing the response of crops to zinc deficiency are essential steps in achieving sustainable solutions to the problem of zinc deficiency in crops and humans.[39]

Fortification[edit]

Soil and foliar application of zinc fertilizer can effectively increase grain zinc and reduce the phytate:zinc ratio in grain.[40][41] People who eat bread prepared from zinc enriched wheat have a significant increase in serum zinc.{citation needed}

Zinc fertilization not only increases zinc content in zinc deficient crops, it also increases crop yields.[39] Balanced crop nutrition supplying all essential nutrients, including zinc, is a cost effective management strategy. Even with zinc-efficient varieties, zinc fertilizers are needed when the available zinc in the topsoil becomes depleted.

Plant breeding, including modern biotechnology, can improve:

Zinc uptake capacity of plants under soil conditions with low chemical availability of zinc; Zinc translocation, thus elevating zinc content in edible crop parts rather than the rest of the plant; Zinc bioavailability For optimal efficiency, zinc-efficient genotypes should be associated with complementary soil crop management (including fertilization) to ensure adequate zinc uptake by roots and thus enhance zinc nutrition of crops and humans.[42]

Central Anatolia, in Turkey, was a region with zinc-deficient soils and widespread zinc deficiency in humans. In 1993, a research project found that yields could be increased by 6 to 8-fold and child nutrition dramatically increased through zinc fertilization.[43] Zinc was added to fertilizers. While the product was initially made available at the same cost, the results were so convincing that Turkish farmers significantly increased the use of the zinc-fortified fertilizer (1 per cent of zinc) within a few years, despite the repricing of the products to reflect the added value of the content. Nearly ten years after the identification of the zinc deficiency problem, the total amount of zinc-containing compound fertilizers produced and applied in Turkey reached a record level of 300,000 tonnes per annum. It is estimated that the economic benefits associated with the application of zinc fertilizers on zinc deficient soils in Turkey is around US$100 million per year. Zinc deficiency in children has been dramatically reduced.

References[edit]

  1. ^ a b Brian R. Walker, Nicki R Colledge, Stuart H. Ralston, Ian Penman (2013). Davidson's Principles and Practice of Medicine (22nd ed.). Elsevier Health Sciences. ISBN 9780702051036. 
  2. ^ a b c d e f g h i j k l m n o p Yamada T, Alpers DH, et al. (2009). Textbook of gastroenterology (5th ed.). Chichester, West Sussex: Blackwell Pub. pp. 495, 498, 499, 1274, 2526. ISBN 978-1-4051-6911-0. 
  3. ^ Gerd Michaelsson (1981). "Diet and Acne". Nutrition Reviews 39 (2): 104–106. doi:10.1111/j.1753-4887.1981.tb06740.x. PMID 6451820. 
  4. ^ a b c d e f g h Kumar P; Clark ML (2012). Kumar & Clark's clinical medicine (8th ed.). Edinburgh: Elsevier/Saunders. ISBN 9780702053047. 
  5. ^ Scully C (2013). Oral and maxillofacial medicine: the basis of diagnosis and treatment (3rd ed.). Edinburgh: Churchill Livingstone. p. 223. ISBN 9780702049484. 
  6. ^ Gurvits, Grigoriy E. "Burning mouth syndrome". World Journal of Gastroenterology 19 (5): 665. doi:10.3748/wjg.v19.i5.665. PMC 3574592. 
  7. ^ Scully C (2010). Medical problems in dentistry (6th ed.). Edinburgh: Churchill Livingstone. p. 326. ISBN 9780702030574. 
  8. ^ Ikeda M, Ikui A, Komiyama A, Kobayashi D, Tanaka M (2008). "Causative factors of taste disorders in the elderly, and therapeutic effects of zinc". J Laryngol Otol 122 (2): 155–60. doi:10.1017/S0022215107008833. PMID 17592661. 
  9. ^ Stewart-Knox BJ, Simpson EE, Parr H et al. (2008). "Taste acuity in response to zinc supplementation in older Europeans". Br. J. Nutr. 99 (1): 129–36. doi:10.1017/S0007114507781485. PMID 17651517. 
  10. ^ Stewart-Knox BJ, Simpson EE, Parr H et al. (2005). "Zinc status and taste acuity in older Europeans: the ZENITH study". Eur J Clin Nutr. 59 Suppl 2: S31–6. doi:10.1038/sj.ejcn.1602295. PMID 16254578. 
  11. ^ McDaid O, Stewart-Knox B, Parr H, Simpson E (2007). "Dietary zinc intake and sex differences in taste acuity in healthy young adults". J Hum Nutr Diet 20 (2): 103–10. doi:10.1111/j.1365-277X.2007.00756.x. PMID 17374022. 
  12. ^ Nin T, Umemoto M, Miuchi S, Negoro A, Sakagami M (2006). "[Treatment outcome in patients with taste disturbance]". Nippon Jibiinkoka Gakkai Kaiho (in Japanese) 109 (5): 440–6. doi:10.3950/jibiinkoka.109.440. PMID 16768159. 
  13. ^ Preedy VR (2014). Handbook of nutrition, diet and the eye. Burlington: Elsevier Science. p. 372. ISBN 9780124046061. 
  14. ^ a b Penny M. Zinc Protects: The Role of Zinc in Child Health. 2004.
  15. ^ a b [1]
  16. ^ Suzuki, H; Asakawa, A; Li, JB; Tsai, M; Amitani, H; Ohinata, K; Komai, M; Inui, A (Sep 2011). "Zinc as an appetite stimulator - the possible role of zinc in the progression of diseases such as cachexia and sarcopenia.". Recent patents on food, nutrition & agriculture 3 (3): 226–31. PMID 21846317. 
  17. ^ "Neurobiology of Zinc-Influenced Eating Behavior". Retrieved 2007-07-19. 
  18. ^ Shay NF, Mangian HF. (2000). Neurobiology of Zinc-Influenced Eating Behavior.
  19. ^ Sanstead, H. H. et al., (2000) Zinc nutriture as related to brain" J. Nutr 130: 140S-146S
  20. ^ a b Black MM (1998). "Zinc deficiency and child development". Am. J. Clin. Nutr. 68 (2 Suppl): 464S–9S. PMC 3137936. PMID 9701161. 
  21. ^ a b Swardfager W (2013). "Zinc in depression: a meta-analysis". Biol Psychiatry 74 (12): 872–8. doi:10.1016/j.biopsych.2013.05.008. PMID 23806573. 
  22. ^ Nuttall, J; Oteiza (2012). "Zinc and the ERK kinases in the developing brain". Neurotoxicity Research 21: 128–141. doi:10.1007/s12640-011-9291-6. PMID 22095091. 
  23. ^ Swardfager, W; Herrmann, N; McIntyre, R. S.; Mazereeuw, G; Goldberger, K; Cha, D. S.; Schwartz, Y; Lanctôt, K. L. (2013). "Potential roles of zinc in the pathophysiology and treatment of major depressive disorder". Neuroscience & Biobehavioral Reviews 37 (5): 911–29. doi:10.1016/j.neubiorev.2013.03.018. PMID 23567517.  edit
  24. ^ a b c Shah D, Sachdev HP (2006). "Zinc deficiency in pregnancy and fetal outcome". Nutr. Rev. 64 (1): 15–30. doi:10.1111/j.1753-4887.2006.tb00169.x. PMID 16491666. 
  25. ^ Solomons, N.W. (2001) Dietary Sources of zinc and factors affecting its bioavailability. Food Nutr. Bull. 22: 138-154
  26. ^ Sandstead HH (1991). "Zinc deficiency. A public health problem?". Am. J. Dis. Child. 145 (8): 853–9. doi:10.1001/archpedi.1991.02160080029016. PMID 1858720. 
  27. ^ a b Maret W, Sandstead HH (2006). "Zinc requirements and the risks and benefits of zinc supplementation". J Trace Elem Med Biol 20 (1): 3–18. doi:10.1016/j.jtemb.2006.01.006. PMID 16632171. 
  28. ^ Castillo-Duran C, Vial P, Uauy R (1988). "Trace mineral balance during acute diarrhea in infants". J. Pediatr. 113 (3): 452–7. doi:10.1016/S0022-3476(88)80627-9. PMID 3411389. 
  29. ^ Manary MJ, Hotz C, Krebs NF et al. (2000). "Dietary phytate reduction improves zinc absorption in Malawian children recovering from tuberculosis but not in well children". J. Nutr. 130 (12): 2959–64. PMID 11110854. 
  30. ^ Gibson RS (2006). "Zinc: the missing link in combating micronutrient malnutrition in developing countries". Proc Nutr Soc 65 (1): 51–60. doi:10.1079/PNS2005474. PMID 16441944. 
  31. ^ 886046736 at GPnotebook
  32. ^ Prasad AS (2003). "Zinc deficiency : Has been known of for 40 years but ignored by global health organisations". BMJ 326 (7386): 409–10. doi:10.1136/bmj.326.7386.409. PMC 1125304. PMID 12595353. 
  33. ^ El-Safty, Ibrahim A M, Gadallah, Mohsen, Shafik, Ahmed, Shouman, Ahmed E (2002) Effect of mercury vapour exposure on urinary excretion of calcium, zinc and copper: relationship to alterations in functional and structural integrity of the kidney Toxicol Ind Health 18 (8) 377-388 [2]
  34. ^ Funk, Day, Brady (1987) Displacement of zinc and copper from copper-induced metallothionein by cadmium and by mercury: in vivo and ex vivo studies Comp Biochem Physiol C 86 (1) 1-6 [3]
  35. ^ Lazzerini, Marzia; Ronfani, Luca (2005). "Oral zinc for treating diarrhoea in children". Cochrane Database of Systematic Reviews. Retrieved 30 August 2014. 
  36. ^ "Copenhagen Consensus Center". Retrieved 30 August 2014. 
  37. ^ Duggan C; Watkins JB; Walker WA (2008). Nutrition in pediatrics : basic science, clinical application (4th ed.). Hamilton: BC Decker. pp. 69–71. ISBN 9781550093612. 
  38. ^ Effect of zinc fertilization on rice plants and on the population of the rice-root nematodeHirschmanniella oryzae Jzincournal of Pest Science
  39. ^ a b Alloway, Brian J. (2008). "Zinc in Soils and Crop Nutrition , International Fertilizer Industry Association, and International Zinc Association". 
  40. ^ Hussain et al. 2012. Plant and Soil 361:279-290
  41. ^ Effect of Foliar Application of Zinc, Selenium, and Iron Fertilizers on Nutrients Concentration and Yield of Rice Grain in China Journal of Agriculture and Food Chemistry, 2008
  42. ^ Hussain et al. 2012. Euphytica 186:153-163
  43. ^ Enrichment of cereal grains with zinc: Agronomic or genetic biofortification? Cakmak Ismail, in Plant and Soil, 2007

Further reading[edit]

External links[edit]