| content | ||||||||||||||||||||||||||||
| Zinc deficiency Classification and external resources |
|
 |
|
|---|---|
| Zinc | |
| ICD-10 | E60. |
| ICD-9 | 269.3 |
| DiseasesDB | 14272 |
Zinc deficiency is a condition where insufficient zinc is available for metabolic needs.
It is usually nutritional, but can also be associated with malabsorption, acrodermatitis enteropathica, chronic liver disease, chronic renal disease, sickle cell disease, diabetes, malignancy, and other chronic illnesses.[1][2] It can also occur after bariatric surgery.
Zinc deficiency is typically the result of inadequate dietary intake of zinc, disease states that promote zinc losses, or physiological states that require increased zinc. Populations that consume primarily plant based diets that are low in bioavailable zinc often have zinc deficiencies.[3][4] Diseases or conditions that involve intestinal malabsorption promote zinc losses. Fecal losses of zinc caused by diarrhea are one contributing factor.[5], often common in developing countries. Changes in intestinal tract absorbability and permeability due, in part, to viral, protozoal, and bacteria pathogens may also encourage fecal losses of zinc.[6] Physiological states that require increased zinc include periods of growth in infants and children as well as in mothers during pregnancy.[7]
Signs of zinc deficiency include hair loss, skin lesions, diarrhea, and wasting of body tissues. Eyesight, taste,[8][9][10][11][12] smell and memory are also connected with zinc. A deficiency in zinc can cause malfunctions of these organs and functions. Congenital abnormalities causing zinc deficiency may lead to a disease called Acrodermatitis enteropathica. Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency.[13]
Zinc supplementation has been shown to reduce diarrhea prevalence and mortality in children younger than 5 years of age.[14]
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.[15] These effects may be mediated by the defective functioning of estrogen via the estrogen receptor, which contains a zinc finger protein.[15] 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.[15]
Cognitive and motor function may also be impaired in zinc deficient children. Zinc deficiency can interfere with many organ systems especially when it occurs during a time of rapid growth and development when nutritional needs are high, such as during infancy.[16] In animal studies, rats who were deprived of zinc during early fetal development exhibited increased emotionality, poor memory, and abnormal response to stress which interfered with performance in learning situations.[17] Zinc deprivation in monkeys showed that zinc deficient animals were emotionally less mature, and also had cognitive deficits indicated by their difficulty in retaining previously learned problems and in learning new problems.[17] Human observational studies show weaker results. Low maternal zinc status has been associated with less attention during the neonatal period and worse motor functioning.[18] 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.[18]
It is rarely recognised that lack of zinc can contribute to acne. Leukonychia, white spots on the fingernails, are often seen as an indication of zinc deficiency.
High dose of zinc, 30 mg 1-3 times a day, prevents dysmenorrhea.[19]
Plasma zinc levels have been found to be dependent upon vitamins A and D. This suggests that a Vitamin A or D deficiency could cause a secondary zinc deficiency. And that for treatment of zinc deficiency one should ensure adequate vitamin A and D intake.[20]
Zinc deficiency contributes to an increased incidence and severity of diarrhea and pneumonia.[21] Studies have shown that zinc treatment results in a 25 percent reduction in duration of acute diarrhea and a 40 percent reduction in treatment failure or death in persistent diarrhea.[22] The studies determined that a ten-day therapy of zinc treatment can considerably reduce the duration and severity of diarrheal episodes, decrease stool output, and lessen the need for hospitalization. Zinc may also prevent future diarrhea episodes for up to three months. The current World Health Organization recommendation for diarrhea control includes the use of 20 mg per day of zinc supplementation for 10 to 14 days (10 mg per day for infants under the age of six months).[23]
Anorexia nervosa
Zinc deficiency causes a decrease in appetite -- which could degenerate in anorexia nervosa (AN). Appetite disorders, in turn, cause malnutrition and, notably, inadequate zinc intake. Anorexia itself is a cause of zinc deficiency, thus leading to a vicious cycle: the worsening of anorexia worsens the zinc deficiency. The use of zinc in the treatment of anorexia nervosa has been advocated since 1979 by Bakan. At least 15 trials showed that zinc improved weight gain in anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase in the treatment of anorexia nervosa (AN). Deficiency of other nutrients such as tyrosine and tryptophan (precursors of the monoamine neurotransmitters norepinephrine and serotonin, respectively), as well as vitamin B1 (thiamine) could contribute to this phenomenon of malnutrition-induced malnutrition.[24]
References
- ^
- ^ Prasad AS (2003). "Zinc deficiency". BMJ 326 (7386): 409–10. doi:. PMID 12595353. PMC:1125304.
- ^ Solomons, N.W. (2001) Dietary Sources of zinc and factors affecting its bioavailability. Food Nutr. Bull. 22: 138-154
- ^ Sandstead HH (1991). "Zinc deficiency. A public health problem?". Am. J. Dis. Child. 145 (8): 853–9. PMID 1858720.
- ^ Castillo-Duran C, Vial P, Uauy R (1988). "Trace mineral balance during acute diarrhea in infants". J. Pediatr. 113 (3): 452–7. PMID 3411389.
- ^ 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.
- ^ Gibson RS (2006). "Zinc: the missing link in combating micronutrient malnutrition in developing countries". Proc Nutr Soc 65 (1): 51–60. PMID 16441944.
- ^ 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:. PMID 17592661.
- ^ 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:. PMID 17651517.
- ^ 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:. PMID 16254578.
- ^ 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:. PMID 17374022.
- ^ Nin T, Umemoto M, Miuchi S, Negoro A, Sakagami M (2006). "[Treatment outcome in patients with taste disturbance]" (in Japanese). Nippon Jibiinkoka Gakkai Kaiho 109 (5): 440–6. PMID 16768159.
- ^ 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:. PMID 16632171.
- ^ Fischer Walker CL, Black RE (2007). "Micronutrients and diarrheal disease". Clin. Infect. Dis. 45 Suppl 1: S73–7. doi:. PMID 17582575.
- ^ a b c Shah D, Sachdev HP (2006). "Zinc deficiency in pregnancy and fetal outcome". Nutr. Rev. 64 (1): 15–30. PMID 16491666.
- ^ Sanstead, H. H. et al, (2000) Zinc nutriture as related to brain. J. Nutr. 130: 140S-146S
- ^ a b Black MM (2003). "The evidence linking zinc deficiency with children's cognitive and motor functioning". J. Nutr. 133 (5 Suppl 1): 1473S–6S. PMID 12730446.
- ^ a b Black MM (1998). "Zinc deficiency and child development". Am. J. Clin. Nutr. 68 (2 Suppl): 464S–9S. PMID 9701161.
- ^ Eby GA (2007). "Zinc treatment prevents dysmenorrhea". Med. Hypotheses 69 (2): 297–301. doi:. PMID 17289285.
- ^ Potocnik FC, van Rensburg SJ, Hon D, Emsley RA, Moodie IM, Erasmus RT (2006). "Oral zinc augmentation with vitamins A and D increases plasma zinc concentration: implications for burden of disease.". Metab Brain Dis. pages=139-147 21: 134. doi:. PMID 17171460.
- ^ Penny M. Zinc Protects: The Role of Zinc in Child Health. 2004.
- ^ Bhutta ZA, Bird SM, Black RE, et al (2000). "Therapeutic effects of oral zinc in acute and persistent diarrhea in children in developing countries: pooled analysis of randomized controlled trials". Am. J. Clin. Nutr. 72 (6): 1516–22. PMID 11101480.
- ^ World Health Organization. Implementing the New Recommendations on the Clinical Management of Diarrhoea: Guidelines for Policy Makers and Programme Managers. 2006.
- ^ "Neurobiology of Zinc-Influenced Eating Behavior". Retrieved on 2007-07-19.
External links
|
||||||||||||||
