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EDITORIAL
Year : 2012  |  Volume : 18  |  Issue : 2  |  Page : 55-57

Role of vitamin D in prevention of deafness


Chief, Indian Institute of Ear Diseases, Resident, Department of E.N.T., Subharti Medical College and University, Meerut, Uttar Pradesh, India

Date of Web Publication6-Sep-2012

Correspondence Address:
Mahendra K Taneja
Chief, Indian Institute of Ear Diseases, Resident, Department of E.N.T., Subharti Medical College and University, Meerut, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-7749.100692

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How to cite this article:
Taneja MK, Taneja V. Role of vitamin D in prevention of deafness. Indian J Otol 2012;18:55-7

How to cite this URL:
Taneja MK, Taneja V. Role of vitamin D in prevention of deafness. Indian J Otol [serial online] 2012 [cited 2018 Nov 20];18:55-7. Available from: http://www.indianjotol.org/text.asp?2012/18/2/55/100692

There are numerous causes of deafness or hearing loss, which have been well researched, documented, universally accepted, and very well practiced with the preventable/curable techniques and their results. However, there are some indirect causes, which may have significant role to play in hearing loss. These are either not universally accepted or not so well-documented/researched. Few of these as deficiency of vitamin D, use of tobacco, bottle feeding of infants in lying down position etc. In this article, I would like to dwell on the deficiency of vitamin D, its causes, its consequences, or possible effect on hearing problems.

The most common cause of deafness in Indian children is ear discharge, which in majority is as a result of recurrent otitis media, which is usually almost always a result of common cold or upper respiratory tract infection (URTI). The URTI results in swelling and blockage of Estachian tube opening, leading to acute otitis media. Acute otitis media may lead to: (1) negative pressure, which may cause retraction pocket and cholesteatoma, (2) secretary otitis media, in which there is glue formation, (3) acute suppurative otitis media that may lead to perforation and chronic suppurative otitis media (CSOM). All together or any of these sequlae can lead to permanent hearing loss. Fortunately, all these are curable.

There are about 200 viruses apart from pneumococci, meningocci, and streplococci, which can cause common cold and acute otitis media. These all pathogens are sensitive to anti-mierobials cathelieidin, and defensin released by the body defense mechanism under the influence of vitamin D. [1],[2],[3],[4] The URTI result in acute neutrophilic infiltration in respiratory epithelium and production of mucous. With increased amount of mucous, infant is more prone to infections and decrease in pancreatic secretion, which may result in malabsorption of fat, consequently decreased absorption of vitamin D. [5]

The prophylactic role of vitamin C has been embarked and been used for decade in the prevention of recurrent URTI. The ergocalciferol and cholecalciferol are less commonly used as vitamin supplement and are rarely used as immunomodulator. Though some food also contain these pro vitamin, due to inadequate sunlight exposure or dark skin, active vitamin D (25 hydroxy vitamin D and 25 (OH)D) level varies in the body, which may result in reduced innate immunity. Wintertime vitamin D insufficiency may explain seasonal variation and more frequent URTI. Apart from darker pigmentation, use of sun screens, wearing of clothing, clouds, environmental pollution limits the penetration of ultraviolet light B. Aging is associated with decrease concentration of 7 dehydro cholesterol in skin; a common reason may be attributed for vitamin D insufficiency and old age deafness.

The role of vitamin D supplementation in primary tuberculosis and lower respiratory tract infection is known and is observed in various epidemiological studies. [5],[6],[7],[8] Daily administration of 600-700 IU vitamin D from cod-liver oil and multivitamin supplementation or 60,000 IU weekly of vitamin D and calcium supplementation has been observed to decrease the incidence of RTI. [9],[10]

Vitamin D deficiency is now associated with increased risk of certain cancer, autoimmune and infectious diseases. [11] Vitamin D regulates more than 200 genes including genes for cellular proliferation, differentiation, and apoptosis. [5] Vitamin D regulates gene expression through binding with vitamin D receptor (VDR), which modulate the expression of genes.

Pathogenic antigens interact with toll-like receptors on macrophages to up regulate the expression of gene that codes for the vitamin D receptor and for the 1 a hydroxylase enzyme that converts 25 (OH) D to the biologically active 1,25 dihydroxy vitamin D [12],[13],[14] and it enhances the production of cathelicidin hCAP-18 (LL-37), [3],[15] which enhances microbial killing in phagocytic vacuoles, acts as a chemotractant for neutrophils and monocytes. [16],[17]

The respiratory epithelium can also convert inactive vitamin D to active 1,25 (OH) D3 to increase the expression of vitamin D regulated genes, which provide definite innate immunity at the site. [18] Thus, vitamin D is a key immunomodulator and its deficiency will increase the incidence of URTI leading to otitis media a retraction pocket and cholesteatoma, again deficiency of vitamin D will lead to low bone density and osteoporosis, hence osteoclastic activity of cholesteatoma will be enhanced.

An inverse association between maternal intake of vitamin D during pregnancy and incidence of respiratory infection, low birth weight, premature birth has been reported. [19],[20] Hence, low serum vitamin D levels in the pregnant woman must be considered, which may result in severe congenital hearing loss.

Deficiency of vitamin D has been attributed to cochlear demineralization and cochlear deafness. The deficient vitamin D may exert its effect by disturbed calcium metabolism as calcium ions play an important role in membrane permeability. Ionized calcium is necessary for normal function of the nerve and its deficiency may affect the action potential generation in cochlea. Low level of vitamin D and calcium may lead to demineralization of otic capsule, degenerative changes in the spiral ligament, stria vascularis, and cochlear hair cells. [21] Brooks et al. has reported improvement in the degree of hearing after restoration of serum vitamin D level. [22]

Thus, I conclude that adequate serum level of vitamin D (Serum 25 (OH) D) is essential; its deficiency may lead to recurrent respiratory tract and ear infection, which may end up with significant morbidity in terms of hearing loss, poor language, communication, and mental health. The serum 25 (OH) D levels below 30 ng/ml are considered as deficient and below 10 ng/ml as grossly deficient. The emerging consensus is that vitamin D level below 80 n mol/L should be labeled as insufficient. The provitamin D can be procured from fortified dairy products, cereals, oily fish, and fish liver oil. Vitamin D synthesized or absorbed from the gut is hydroxylated to its active form in the liver, hence may be low where absorption or liver function are affected/inadequate, hence in cases of recurrent otitis media/cholesteatoma, estimation and supplementation of vitamin D is hallmark in their management.

To prevent congenital deafness due to premature birth, birth asphyxia, and low birth weight and infentile pneumonia, adequate supplemental of vitamin D in all pregnant woman should be considered.

 
  References Top

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3.Yim S, Dhawan P, Ragunath C, Christakos S, Diamond G. Induction of cathelicidin in normal and CF bronchial epithelial cells by 1,25- D3. J Cyst Fibros 2007;6:403-10.  Back to cited text no. 3
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4.Wayse W, Yousafzai A, Mogale K, Filteau S. Association of subclinical dihydroxivitamin vitamin D deficiency with severe acute lower respiratory tract infections in Indian children under 5 year. Eur J Clin Nutr 2004;58:563-7.  Back to cited text no. 4
    
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7.Najada AS, Habashneh MS, Khader M. The frequency of nutritional rickets among hospitalized infants and its relation to respiratory diseases. J Trop Pediatr 2004;50:364-8.  Back to cited text no. 7
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8.Walker VP, Modlin RL. The vitamin D connection to pediatric infections and immune function. Pediatr Res 2009;65(5 Pt 2):106R-113R.  Back to cited text no. 8
    
9.Linday LA, Shindledecker RD, Tapia-Mendoza J, Dolitsky JN. Effect of daily cod liver oil and a multivitamin-mineral supplement with selenium on upper respiratory tract pediatric visit by young, inner-city, Latino children: Randomized pediatric sites. Ann Otol Rhinol Laryngol 2004;113:891-901.  Back to cited text no. 9
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10.Rehman PK. Sub-clinical rickets and recurrent infection (research letter). J Trop Pediatr 1994;40:58.  Back to cited text no. 10
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11.Holick MF, Chen TC. Vitamin D deficiency: A worldwide problem with health consequences. Am J Clin Nutr 2008;87:1080S-6S.  Back to cited text no. 11
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12.Ginde AA, Mansbach JM, Camargo CA Jr. Association between Serum 25-Hydroxyvitamin D level and upper respiratory tract infection in the third national health and nutrition examination survey. Arch Intern Med 2009;169:384-90.  Back to cited text no. 12
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13.Reichel H, Koeffler HP, Bishop JE, Norman AW. 25-Hydroxyvitamin D 3 metabolism by lipopolysaccharide-stimulated normal human macrophages. J Clin Endocrinol Metab 1987;64:1-9.  Back to cited text no. 13
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14.Liu PT, Stenger S, Li H, Wenzel L, Tan BH, Krutzik SR, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science 2006;311:1770-3.  Back to cited text no. 14
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15.Webber G, Heilborn JD, Chamorro Jimenez Cl, Hammarsjo A, Torma H, Stahle M. Vitamin D induces the antimicrobial protein hCAP18 in human skin. J Invest Dermatol 2005;124:1080- 2.  Back to cited text no. 15
    
16.Gombart AF, Borregaard N, Koeffler HP. Human cathelicidin antimicrobial peptide (CAMP) is a direct target of the vitamin D receptor and is strong up-regulated in myeloid cells by 1,25-dihydroxyvitamin D 3 . FASEB J 2005;19:1067-77.  Back to cited text no. 16
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17.Liu PT, Stenger S, Tang DH, Modlin RL. Cutting edge: Vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin. J Immunol 2007;179:2060-3.  Back to cited text no. 17
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18.Hansdottir S, Monick MM, Hinde SL, Lovan N, Look DC, Hunninghake GW. Respiratory epithelial cells convert inactive vitamin D to its active form: Potential effects on host defense. J Immunol 2008;181:7090-9.  Back to cited text no. 18
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19.Cammargo CA Jr, Rifas-Shiman SL, Liuonjua AA, Burris HH, Kleinman K, Huh SY, et al. Prospective study of maternal intake of vitamin D during pregnancy and risk of wheezing illeness in children at age 2 years. J Allergy Clin Immunol 2006;117:721-2.  Back to cited text no. 19
    
20.Devereux G, Litonjua AA, Turner SW, Craig LC, McNeill G, Martindale S, et al. Maternal vitamin D intake during pregnancy and early childhood wheezing. Am J Clin Nutr 2007;85:853-9.  Back to cited text no. 20
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21.Weir N. Sensorineural deafness associated with recessive hypophosphataemic rickets. J Laryngol Otol 1977;91:717-22.  Back to cited text no. 21
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22.Brookes EB, Morrison AW. Vitamin D deficiency and deafness. Br Med J (Clin Res Ed) 1981;283:273-4.  Back to cited text no. 22
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