Zinc deficiency

Zinc deficiency is defined either as insufficient zinc to meet the needs of the body, or as a serum zinc level below the normal range. However, since a decrease in the serum concentration is only detectable after long-term or severe depletion, serum zinc is not a reliable biomarker for zinc status.[1] Common symptoms include increased rates of diarrhea. Zinc deficiency affects the skin and gastrointestinal tract; brain and central nervous system, immune, skeletal, and reproductive systems.

Zinc deficiency
Causesa diet high in phytate-containing whole grains

Zinc deficiency in humans is caused by reduced dietary intake, inadequate absorption, increased loss, or increased body system use. The most common cause is reduced dietary intake. In the U.S., the Recommended Dietary Allowance (RDA) is 8 mg/day for women and 11 mg/day for men.[2]

The highest concentration of dietary zinc is found in oysters, meat, beans, and nuts. Increasing the amount of zinc in the soil and thus in crops and animals is an effective preventive measure. Zinc deficiency may affect up to 2 billion people worldwide.[3]

Signs and symptoms

Skin, nails and hair

Zinc deficiency may manifest as acne,[4] eczema, xerosis (dry, scaling skin), seborrheic dermatitis,[5] or alopecia (thin and sparse hair).[5][6] It may also impair or possibly prevent wound healing.[6]


Zinc deficiency can manifest as non-specific oral ulceration, stomatitis, or white tongue coating.[5] Rarely it can cause angular cheilitis (sores at the corners of the mouth).[7]

Vision, smell and taste

Severe zinc deficiency may disturb the sense of smell[6] and taste.[8][9][10][11][12][13] Night blindness may be a feature of severe zinc deficiency,[6] although 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).[14]

Immune system

Impaired immune function in people with zinc deficiency can lead to the development of respiratory, gastrointestinal, or other infections, e.g., pneumonia.[6][15][16] The levels of inflammatory cytokines (e.g., IL-1β, IL-2, IL-6, and TNF-α) in blood plasma are affected by zinc deficiency and zinc supplementation produces a dose-dependent response in the level of these cytokines.[17] During inflammation, there is an increased cellular demand for zinc and impaired zinc homeostasis from zinc deficiency is associated with chronic inflammation.[17]


Zinc deficiency contributes to an increased incidence and severity of diarrhea.[15][16]


Zinc deficiency may lead to loss of appetite.[18]

Cognitive function and hedonic tone

Cognitive functions, such as learning and hedonic tone, are impaired with zinc deficiency.[3][19] Moderate and more severe zinc deficiencies are associated with behavioral abnormalities, such as irritability, lethargy, and depression (e.g., involving anhedonia).[20] Zinc supplementation produces a rapid and dramatic improvement in hedonic tone (i.e., general level of happiness or pleasure) under these circumstances.[20] Zinc supplementation has been reported to improve symptoms of ADHD and depression.[3][21][22]

Psychological disorders

Low plasma zinc levels have been alleged to be associated with many psychological disorders. Schizophrenia has been linked to decreased brain zinc levels.[23] Evidence suggests that zinc deficiency could play a role in depression.[23][24][25] Zinc supplementation may be an effective treatment in major depression.[26][27]


Zinc deficiency in children can cause delayed growth[5] and has been claimed to be the cause of stunted growth in one third of the world's population.[28]

During pregnancy

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.[29] These effects may be mediated by the defective functioning of estrogen via the estrogen receptor, which contains a zinc finger protein.[29] 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.[29]

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.[30] Low maternal zinc status has been associated with less attention during the neonatal period and worse motor functioning.[31] 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.[31]

Testosterone production

Zinc is required to produce testosterone. Thus, zinc deficiency can lead to reduced circulating testosterone, which could lead to sexual immaturity (Ananda Parsad, et al.) hypogonadism, and delayed puberty.[5]


Dietary deficiency

Zinc deficiency can be caused by a diet high in phytate-containing whole grains, foods grown in zinc deficient soil, or processed foods containing little or no zinc.[32][33] Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency.[34]

In the U.S., the Recommended Dietary Allowance (RDA) is 8 mg/day for women and 11 mg/day for men. RDA for pregnancy is 11 mg/day. RDA for lactation is 12 mg/day. For infants up to 12 months the RDA is 3 mg/day. For children ages 1–13 years the RDA increases with age from 3 to 8 mg/day.[2] The following table summarizes most of the foods with significant quantities of zinc, listed in order of quantity per serving, unfortified.[35] Note that all of the top 10 entries are meat, beans, or nuts.

Food mg in one serving Percentage of 11 mg recommended daily intake
Oysters, cooked, breaded and fried, 3 ounces (85g) (about 5 average sized oysters) 74.0 673%
Beef chuck roast, braised, 3 ounces (85g) 7.0 64%
Crab, Alaska king, cooked, 3 ounces (85g) 6.5 59%
Beef patty, broiled, 3 ounces (85g) 5.3 48%
Cashews, dry roasted, 3 ounces (85g) 4.8 44%
Lobster, cooked, 3 ounces (85g) 3.4 31%
Pork chop, loin, cooked, 3 ounces (85g) 2.9 26%
Baked beans, canned, plain or vegetarian, 12 cup 2.9 26%
Almonds, dry roasted, 3 ounces (85g) 2.7 25%
Chicken, dark meat, cooked, 3 ounces (85g) 2.4 22%
Yogurt, fruit, low fat, 8 ounces (230g) 1.7 15%
Shredded wheat, unfortified, 1 cup[36] 1.5 14%
Chickpeas, cooked, 12 cup 1.3 12%
Cheese, Swiss, 1 ounce (28g) 1.2 11%
Oatmeal, instant, plain, prepared with water, 1 packet 1.1 10%
Milk, low-fat or non-fat, 1 cup 1.0 9%
Kidney beans, cooked, 12 cup 0.9 8%
Chicken breast, roasted, skin removed, 12 breast 0.9 8%
Cheese, cheddar or mozzarella, 1 ounce (28g) 0.9 8%
Peas, green, frozen, cooked, 12 cup 0.5 5%
Flounder or sole, cooked, 3 ounces (85g) 0.3 3%

Recent research findings suggest that increasing atmospheric carbon dioxide concentrations will exacerbate zinc deficiency problems in populations that consume grains and legumes as staple foods. A meta-analysis of data from 143 studies comparing the nutrient content of grasses and legumes grown in ambient and elevated CO2 environments found that the edible portions of wheat, rice, peas and soybeans grown in elevated CO2 contained less zinc and iron.[37] Global atmospheric CO2 concentration is expected to reach 550 p.p.m. in the late 21st century. At this CO2 level the zinc content of these crops was 3.3 to 9.3% lower than that of crops grown in the present atmosphere. A model of the nutritional impact of these lower zinc quantities on the populations of 151 countries predicts that an additional 175 million people could face dietary zinc deficiency as the result of increasing atmospheric CO2.[38]

Inadequate absorption

Acrodermatitis enteropathica is an inherited deficiency of the zinc carrier protein ZIP4 resulting in inadequate zinc absorption.[6] It presents as growth retardation, severe diarrhea, hair loss, skin rash (most often around the genitalia and mouth) and opportunistic candidiasis and bacterial infections.[6]

Numerous small bowel diseases which cause destruction or malfunction of the gut mucosa enterocytes and generalized malabsorption are associated with zinc deficiency.

Increased loss

Exercising, high alcohol intake, and diarrhea all increase loss of zinc from the body.[5][39] Changes in intestinal tract absorbability and permeability due, in part, to viral, protozoal, or bacteria pathogens may also encourage fecal losses of zinc.[40]

Chronic disease

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.[41][42] It can also occur after bariatric surgery, mercury exposure[43][44] and tartrazine.

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. [24]


As biosystems are unable to store zinc, regular intake is necessary. Excessively low zinc intake can lead to zinc deficiency, which can negatively impact an individual's health.[45] The mechanisms for the clinical manifestations of zinc deficiency are best appreciated by recognizing that zinc functions in the body in three areas: catalytic, structural, and regulatory.[2][46] Zinc (Zn) is only common in its +2 oxidative state, where it typically coordinates with tetrahedral geometry. It is important in maintaining basic cellular functions such as DNA replication, RNA transcription, cell division and cell activations. However, having too much or too little zinc can cause these functions to be compromised.

Zinc is a critical component of the catalytic site of hundreds of kinds of different metalloenzymes in each human being. In its structural role, zinc coordinates with certain protein domains, facilitating protein folding and producing structures such as 'zinc fingers'. In its regulatory role, zinc is involved in the regulation of nucleoproteins and the activity of various inflammatory cells. For example, zinc regulates the expression of metallothionein, which has multiple functions, such as intracellular zinc compartmentalization[47] and antioxidant function.[48][49] Thus 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.[5][50][51]

Pra1 (pH regulated antigen 1) is a candida albicans protein that scavenges host zinc.[52]


Diagnosis is typically made based on clinical suspicion and a low level of zinc in the blood. Any level below 70 mcg/dl (normal 70-120 mcg/dl)is considered as zinc deficiency. Zinc deficiency could be also associated with low alkaline phosphatase since it acts a cofactor for this enzyme.

There is a paucity of adequate zinc biomarkers, and the most widely used indicator, plasma zinc, has poor sensitivity and specificity.[53]


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.[28]


Zinc gluconate tablets
Zinc rich foods. Oysters, beef, peanuts, dark chicken meat

Five interventional strategies can be used:

  • Adding zinc to soil, called agronomic biofortification, which both increases crop yields and provides more dietary zinc.
  • Adding zinc to food, called food fortification. The Republic of China, India, Mexico and about 20 other countries, mostly on the east coast of sub-Saharan Africa, fortify wheat flour and/or maize flour with zinc.[54]
  • Adding zinc rich foods to diet. The foods with the highest concentration of zinc are proteins, especially animal meats, the highest being oysters.[5] Per ounce, beef, pork, and lamb contain more zinc than fish. The dark meat of a chicken has more zinc than the light meat. Other good sources of zinc are nuts, whole grains, legumes, and yeast.[55] Although whole grains and cereals are high in zinc, they also contain chelating phytates which bind zinc and reduce its bioavailability.[5]
  • Oral repletion via tablets (e.g. zinc gluconate) or liquid (e.g. zinc acetate). 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 11 hours.[56]
  • Oral repletion via multivitamin/mineral supplements containing zinc gluconate, sulfate, or acetate. It is not clear whether one form is better than another.[55]


Zinc deficiency affects about 2.2 billion people around the world.[3] Severe zinc deficiency is rare, and is mainly seen in persons with acrodermatitis enteropathica, a severe defect in zinc absorption due to a congenital deficiency in the zinc carrier protein ZIP4 in the enterocyte.[5] Mild zinc deficiency due to reduced dietary intake is common.[5] Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency.[34] Zinc deficiency is thought to be a leading cause of infant mortality.

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.[57]


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.[58] 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.[59] 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.[60] 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.[61] In 2002 the zinc transporter protein ZIP4 was first identified as the mechanism for absorption of zinc in the gut across the basolateral membrane of the enterocyte. By 2014 over 300 zinc containing enzymes have been identified, as well as over 1000 zinc containing transcription factors.

Phytate was recognized as removing zinc from nutrients given to chicken and swine in 1960. That it can cause human zinc deficiency however was not recognized until Reinhold's work in Iran in the 1970s. This phenomenon is central to the high risk of zinc deficiency worldwide.[62]

Soils and crops

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.[63] Many agricultural countries around the world are affected by zinc deficiency.[64] 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 zinc 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.[65]


Soil and foliar application of zinc fertilizer can effectively increase grain zinc and reduce the phytate:zinc ratio in grain.[66][67] People who eat bread prepared from zinc enriched wheat have a significant increase in serum zinc.

Zinc fertilization not only increases zinc content in zinc deficient crops, it also increases crop yields.[65] 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 can improve zinc uptake capacity of plants under soil conditions with low chemical availability of zinc. Breeding can also improve zinc translocation which elevates zinc content in edible crop parts as opposed to the rest of the plant.

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.[68] 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 percent 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.


  1. Hess SY, Peerson JM, King JC, Brown KH (September 2007). "Use of serum zinc concentration as an indicator of population zinc status". Food and Nutrition Bulletin. 28 (3 Suppl): S403-29. doi:10.1177/15648265070283S303. PMID 17988005. S2CID 13748442.
  2. "Zinc" Archived 19 September 2017 at the Wayback Machine, pp. 442–501 in 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.
  3. Prasad AS (June 2012). "Discovery of human zinc deficiency: 50 years later". Journal of Trace Elements in Medicine and Biology. 26 (2–3): 66–9. doi:10.1016/j.jtemb.2012.04.004. PMID 22664333.
  4. Michaëlsson G (February 1981). "Diet and acne". Nutrition Reviews. 39 (2): 104–6. doi:10.1111/j.1753-4887.1981.tb06740.x. PMID 6451820.
  5. 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.
  6. Kumar P, Clark ML (2012). Kumar & Clark's clinical medicine (8th ed.). Edinburgh: Elsevier/Saunders. ISBN 9780702053047.
  7. Scully C (2013). Oral and maxillofacial medicine: the basis of diagnosis and treatment (3rd ed.). Edinburgh: Churchill Livingstone. p. 223. ISBN 9780702049484.
  8. Scully C (2010). Medical problems in dentistry (6th ed.). Edinburgh: Churchill Livingstone. pp. 326. ISBN 9780702030574.
  9. Ikeda M, Ikui A, Komiyama A, Kobayashi D, Tanaka M (February 2008). "Causative factors of taste disorders in the elderly, and therapeutic effects of zinc". The Journal of Laryngology and Otology. 122 (2): 155–60. doi:10.1017/S0022215107008833. PMID 17592661. S2CID 35435439.
  10. Stewart-Knox BJ, Simpson EE, Parr H, Rae G, Polito A, Intorre F, et al. (January 2008). "Taste acuity in response to zinc supplementation in older Europeans". The British Journal of Nutrition. 99 (1): 129–36. doi:10.1017/S0007114507781485. PMID 17651517.
  11. Stewart-Knox BJ, Simpson EE, Parr H, Rae G, Polito A, Intorre F, et al. (November 2005). "Zinc status and taste acuity in older Europeans: the ZENITH study". European Journal of Clinical Nutrition. 59 Suppl 2: S31-6. doi:10.1038/sj.ejcn.1602295. PMID 16254578.
  12. McDaid O, Stewart-Knox B, Parr H, Simpson E (April 2007). "Dietary zinc intake and sex differences in taste acuity in healthy young adults". Journal of Human Nutrition and Dietetics. 20 (2): 103–10. doi:10.1111/j.1365-277X.2007.00756.x. PMID 17374022.
  13. Nin T, Umemoto M, Miuchi S, Negoro A, Sakagami M (May 2006). "[Treatment outcome in patients with taste disturbance]". Nihon Jibiinkoka Gakkai Kaiho (in Japanese). 109 (5): 440–6. doi:10.3950/jibiinkoka.109.440. PMID 16768159.
  14. Preedy VR (2014). Handbook of nutrition, diet and the eye. Burlington: Elsevier Science. p. 372. ISBN 9780124046061.
  15. Penny M. Zinc Protects: The Role of Zinc in Child Health. 2004. Archived 13 May 2008 at the Wayback Machine
  16. Lassi ZS, Moin A, Bhutta ZA (December 2016). "Zinc supplementation for the prevention of pneumonia in children aged 2 months to 59 months". The Cochrane Database of Systematic Reviews. 12 (12): CD005978. doi:10.1002/14651858.CD005978.pub3. PMC 6463931. PMID 27915460.
  17. Foster M, Samman S (July 2012). "Zinc and regulation of inflammatory cytokines: implications for cardiometabolic disease". Nutrients. 4 (7): 676–94. doi:10.3390/nu4070676. PMC 3407988. PMID 22852057.
  18. Suzuki H, Asakawa A, Li JB, Tsai M, Amitani H, Ohinata K, et al. (September 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. doi:10.2174/2212798411103030226. PMID 21846317.
  19. Takeda A (December 2000). "Movement of zinc and its functional significance in the brain". Brain Research. Brain Research Reviews. 34 (3): 137–48. doi:10.1016/s0165-0173(00)00044-8. PMID 11113504. S2CID 13332474.
  20. Mertz W (2012). Trace Elements in Human and Animal Nutrition. Vol. 2 (5th ed.). Elsevier. p. 74. ISBN 9780080924694. Retrieved 18 August 2015.
  21. Chasapis CT, Loutsidou AC, Spiliopoulou CA, Stefanidou ME (April 2012). "Zinc and human health: an update". Archives of Toxicology. 86 (4): 521–34. doi:10.1007/s00204-011-0775-1. PMID 22071549. S2CID 18669835.
  22. Millichap JG, Yee MM (February 2012). "The diet factor in attention-deficit/hyperactivity disorder". Pediatrics. 129 (2): 330–7. doi:10.1542/peds.2011-2199. PMID 22232312. S2CID 14925322.
  23. Petrilli MA, Kranz TM, Kleinhaus K, Joe P, Getz M, Johnson P, et al. (2017). "The Emerging Role for Zinc in Depression and Psychosis". Frontiers in Pharmacology. 8: 414. doi:10.3389/fphar.2017.00414. PMC 5492454. PMID 28713269.
  24. Swardfager W, Herrmann N, Mazereeuw G, Goldberger K, Harimoto T, Lanctôt KL (December 2013). "Zinc in depression: a meta-analysis". Biological Psychiatry. 74 (12): 872–8. doi:10.1016/j.biopsych.2013.05.008. PMID 23806573. S2CID 381132.
  25. Nuttall JR, Oteiza PI (January 2012). "Zinc and the ERK kinases in the developing brain". Neurotoxicity Research. 21 (1): 128–41. doi:10.1007/s12640-011-9291-6. PMC 4316815. PMID 22095091.
  26. Lai J, Moxey A, Nowak G, Vashum K, Bailey K, McEvoy M (January 2012). "The efficacy of zinc supplementation in depression: systematic review of randomised controlled trials". Journal of Affective Disorders. 136 (1–2): e31–e39. doi:10.1016/j.jad.2011.06.022. PMID 21798601.
  27. Swardfager W, Herrmann N, McIntyre RS, Mazereeuw G, Goldberger K, Cha DS, et al. (June 2013). "Potential roles of zinc in the pathophysiology and treatment of major depressive disorder". Neuroscience and Biobehavioral Reviews. 37 (5): 911–29. doi:10.1016/j.neubiorev.2013.03.018. PMID 23567517. S2CID 1725139.
  28. Walker BR, Colledge NR, Ralston SH, Penman I (2013). Davidson's Principles and Practice of Medicine (22nd ed.). Elsevier Health Sciences. ISBN 9780702051036.
  29. Shah D, Sachdev HP (January 2006). "Zinc deficiency in pregnancy and fetal outcome". Nutrition Reviews. 64 (1): 15–30. doi:10.1111/j.1753-4887.2006.tb00169.x. PMID 16491666. Archived from the original on 15 December 2019. Retrieved 3 August 2008.
  30. Sanstead HH, et al. (2000). "Zinc nutriture as related to brain". J. Nutr. 130: 140S–146S.
  31. Black MM (August 1998). "Zinc deficiency and child development". The American Journal of Clinical Nutrition. 68 (2 Suppl): 464S–469S. doi:10.1093/ajcn/68.2.464S. PMC 3137936. PMID 9701161.
  32. Solomons NW (2001). "Dietary Sources of zinc and factors affecting its bioavailability". Food Nutr. Bull. 22 (2): 138–154. doi:10.1177/156482650102200204. S2CID 74543530.
  33. Sandstead HH (August 1991). "Zinc deficiency. A public health problem?". American Journal of Diseases of Children. 145 (8): 853–9. doi:10.1001/archpedi.1991.02160080029016. PMID 1858720.
  34. Maret W, Sandstead HH (2006). "Zinc requirements and the risks and benefits of zinc supplementation". Journal of Trace Elements in Medicine and Biology. 20 (1): 3–18. doi:10.1016/j.jtemb.2006.01.006. PMID 16632171.
  35. Adapted from http://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/#h3.
  36. "Shredded wheat". eatthismuch.com. Retrieved 20 February 2019.
  37. Myers SS, Zanobetti A, Kloog I, Huybers P, Leakey AD, Bloom AJ, et al. (June 2014). "Increasing CO2 threatens human nutrition". Nature. 510 (7503): 139–42. Bibcode:2014Natur.510..139M. doi:10.1038/nature13179. PMC 4810679. PMID 24805231.
  38. Smith MR, Myers SS (2018). "Impact of anthropogenic CO2 emissions on global human nutrition". Nature Climate Change. 8 (9): 834–839. Bibcode:2018NatCC...8..834S. doi:10.1038/s41558-018-0253-3. ISSN 1758-678X. S2CID 91727337.
  39. Castillo-Duran C, Vial P, Uauy R (September 1988). "Trace mineral balance during acute diarrhea in infants". The Journal of Pediatrics. 113 (3): 452–7. doi:10.1016/S0022-3476(88)80627-9. PMID 3411389.
  40. Manary MJ, Hotz C, Krebs NF, Gibson RS, Westcott JE, Arnold T, et al. (December 2000). "Dietary phytate reduction improves zinc absorption in Malawian children recovering from tuberculosis but not in well children". The Journal of Nutrition. 130 (12): 2959–64. doi:10.1093/jn/130.12.2959. PMID 11110854.
  41. "zinc deficiency". GPnotebook.
  42. Prasad AS (February 2003). "Zinc deficiency". BMJ. 326 (7386): 409–10. doi:10.1136/bmj.326.7386.409. PMC 1125304. PMID 12595353.
  43. El-Safty IA, Gadallah M, Shafik A, Shouman AE (September 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". Toxicology and Industrial Health. 18 (8): 377–88. doi:10.1191/0748233702th160oa. PMID 15119526. S2CID 32876828.
  44. Funk AE, Day FA, Brady FO (1987). "Displacement of zinc and copper from copper-induced metallothionein by cadmium and by mercury: in vivo and ex vivo studies". Comparative Biochemistry and Physiology. C, Comparative Pharmacology and Toxicology. 86 (1): 1–6. doi:10.1016/0742-8413(87)90133-2. PMID 2881702.
  45. Prasad AS (March 2013). "Discovery of human zinc deficiency: its impact on human health and disease". Advances in Nutrition. 4 (2): 176–90. doi:10.3945/an.112.003210. PMC 3649098. PMID 23493534.
  46. Cousins RJ (1994). "Metal elements and gene expression". Annual Review of Nutrition. 14: 449–69. doi:10.1146/annurev.nu.14.070194.002313. PMID 7946529.
  47. Maret W (May 2003). "Cellular zinc and redox states converge in the metallothionein/thionein pair". The Journal of Nutrition. 133 (5 Suppl 1): 1460S–2S. doi:10.1093/jn/133.5.1460S. PMID 12730443.
  48. Theocharis SE, Margeli AP, Koutselinis A (2003). "Metallothionein: a multifunctional protein from toxicity to cancer". Int J Biol Markers. 18 (3): 162–169. doi:10.1177/172460080301800302. PMID 14535585.
  49. Theocharis SE, Margeli AP, Klijanienko JT, Kouraklis GP (August 2004). "Metallothionein expression in human neoplasia". Histopathology. 45 (2): 103–18. doi:10.1111/j.1365-2559.2004.01922.x. PMID 15279628. S2CID 41978978.
  50. Kupka R, Fawzi W (March 2002). "Zinc nutrition and HIV infection". Nutrition Reviews. 60 (3): 69–79. doi:10.1301/00296640260042739. PMID 11908743.
  51. Rink L, Gabriel P (November 2000). "Zinc and the immune system". The Proceedings of the Nutrition Society. 59 (4): 541–52. doi:10.1017/S0029665100000781. PMID 11115789.
  52. Citiulo F, Jacobsen ID, Miramón P, Schild L, Brunke S, Zipfel P, et al. (2012). "Candida albicans scavenges host zinc via Pra1 during endothelial invasion". PLOS Pathogens. 8 (6): e1002777. doi:10.1371/journal.ppat.1002777. PMC 3386192. PMID 22761575.
  53. 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.
  54. "Map: Count of Nutrients in Fortification Standards". Food Fortification Initiative. 2018. Retrieved 24 January 2019.
  55. "Zinc in diet: MedlinePlus Medical Encyclopedia". medlineplus.gov. 2 February 2015. Retrieved 21 February 2017.
  56. Lazzerini M, Wanzira H (December 2016). "Oral zinc for treating diarrhoea in children". The Cochrane Database of Systematic Reviews. 12 (4): CD005436. doi:10.1002/14651858.CD005436.pub5. PMC 5450879. PMID 27996088.
  57. "Copenhagen Consensus Center". Retrieved 30 August 2014.
  58. Raulin J (1869). "Chemical studies on vegetation". Annales des Sciences Naturelles. 11: 293–299.
  59. Todd WR, Elvejheim CA, Hart EB (1934). "Zinc in the nutrition of the rat". Am J Physiol. 107: 146–156. doi:10.1152/ajplegacy.1933.107.1.146.
  60. Prasad AS, Miale A, Farid Z, Sandstead HH, Schulert AR (April 1963). "Zinc metabolism in patients with the syndrome of iron deficiency anemia, hepatosplenomegaly, dwarfism, and hypognadism". The Journal of Laboratory and Clinical Medicine. 61: 537–49. PMID 13985937.
  61. Duggan C, Watkins JB, Walker WA (2008). Nutrition in pediatrics : basic science, clinical application (4th ed.). Hamilton: BC Decker. pp. 69–71. ISBN 9781550093612.
  62. Sandstead HH (January 2013). "Human zinc deficiency: discovery to initial translation". Advances in Nutrition. 4 (1): 76–81. doi:10.3945/an.112.003186. PMC 3648742. PMID 23319126.
  63. Korayem, A.M. (1993). "Effect of zinc fertilization on rice plants and on the population of the rice-root nematode Hirschmanniella oryzae". Anz. Schadlingskde., Pflanzenschutz, Umweltschutz. 66: 18–21. doi:10.1007/BF01903608. S2CID 33142627.
  64. "IFA : International Fertilizer Industry Association - Zinc in Soils and Crop Nutrition / Publications / LIBRARY / Home Page / IFA". Archived from the original on 19 December 2008. Retrieved 23 April 2009.
  65. Alloway BJ (2008). "Zinc in Soils and Crop Nutrition, International Fertilizer Industry Association, and International Zinc Association". Archived from the original on 19 February 2013. Retrieved 15 December 2012.
  66. Hussain S, Maqsood MA, Rengel Z, Aziz T (March 2012). "Biofortification and estimated human bioavailability of zinc in wheat grains as influenced by methods of zinc application". Plant and Soil. 361 (1–2): 279–290. doi:10.1007/s11104-012-1217-4. S2CID 16068957.
  67. Fang Y, Wang L, Xin Z, Zhao L, An X, Hu Q (March 2008). "Effect of foliar application of zinc, selenium, and iron fertilizers on nutrients concentration and yield of rice grain in China". Journal of Agricultural and Food Chemistry. 56 (6): 2079–84. doi:10.1021/jf800150z. PMID 18311920.
  68. Cakmak, I. (2008). "Enrichment of cereal grains with zinc: Agronomic or genetic biofortification?". Plant Soil. 302 (1–2): 1–17. doi:10.1007/s11104-007-9466-3. S2CID 34821888.

Further reading

This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.