Micronutrient deficiencies (‘hidden hunger’) are highly prevalent and affect far beyond the known effects like anemia, goiter, asymptomatic to devastating, often hard to recognize, mimic many diseases, have fewer signs but gamut of symptoms, and can involve multiple system. Only few have practicable laboratory diagnosis. Hence they need high index of suspicion and a detailed dietary history for diagnosis. It has potential to affect economic and overall development, as affected populations are unable to achieve full mental and physical potentials, have low work capacity, and are prone to infections [1].

Objectives: Increasing awareness and information mandates need of consensus statement on micronutrient supplementation in making informed decisions on the appropriate nutrition actions; to achieve the Sustainable Development Goals (SDGs) and the global targets set in the Comprehensive Implementation Plan on Maternal, Infant and Young Child Nutrition and the Global Strategy for Women’s, Children’s, and Adolescents’ Health.

A National Consultative Meeting was convened by Infant and Young Child Feeding Chapter (IYCF) of Indian Academy of Pediatrics (IAP) on 17 December, 2016 at Mumbai. IYCF chapter, IAP, United Nations Children Fund, National Institute of Nutrition and Government of India were the participating agencies; and participants representing different parts of India were included.

Methods of search: Cochrane database, e-Library of Evidence for Nutrition Actions (eLENA), MEDLINE through Pubmed, and Google Scholar were searched with preference to recent systematic reviews, using combination of key words "iron (and other micronutrients) status, India, complementary feeding, children, deficiency and supplementation" and further expanded through "related articles" and reference lists of the articles.

Clinical presentations: Apart from anemia, iron deficient young children are vulnerable to socio-emotional behavior issues; irreversible effects on psychomotor skills and cognition and later attention deficits. Presentation with pagophagia, dysphagia, decreased effort tolerance, pica, cold intolerance, altered immunity or cerebral vein thrombosis is known.

Deficiency status and Risk factors: Irrespective of age, geography and socioeconomic status, iron deficiency is still high, underestimated, under-treated and the commonest cause of disability in children [2].

Dietary factors which may result in decreased iron absorption and ultimately iron-deficiency include high phytates (cereals-legumes, roots-tubers, maize, beans, whole wheat flour and sorghum), low ascorbic acid (fruits-vegetables); high animal milk intake; regular tea-coffee with major meals; low consumption of iron supplementation; and low consumption of animal origin foods (meat, fish and poultry) [6]. Cow’s whole milk is a risk factor due to low iron content, poor bioavailability due to high casein and calcium; and increased loss of blood in intestines [7]. However, authors do not suggest exclusion of these from the diet for improving iron status. Parental dietary history per se does not qualify as first stage screening tool for iron deficiency state [8].

Additional risk factors are poor maternal stores; prematurity or low birth weight; exclusive breastfeeding beyond 6 month without iron rich/fortified foods or supplements; worm infestations (hookworm, ascaris and schistosomiasis); low socioeconomic status; migrant worker parents; bottle feeding; and a mother who is currently pregnant [9,10]. Greater than 95th percentile weight and height, and obesity are emerging risk factors for iron-deficiency [11].

Iron-deficiency and iron deficiency anemia (IDA) are incorrectly used synonyms. In healthy appearing infants, anemia is neither a sensitive nor a specific screen for iron-deficiency [12], except for severe cases. In view of high prevalence of iron deficiency, we should have a high index of suspicion even in presence of normal hemoglobin level. Hemoglobin levels as surrogate marker of IDA underestimates iron-deficiency in up to 12-27% [13]. Red cell distribution width should be seen as it is the earliest marker of iron deficiency. It is recommended to treat children with subclinical iron deficiency even in absence of anemia. Serum ferritin <12 ng/mL is sensitive, with high false negative rates being common as it is a acute phase reactant. Transferrin receptor1 and Total iron binding capacity (TIBC) are good to establish iron-deficiency, especially in cases without anemia [14]. Usually a combi-nation of tests is used to diagnose iron deficiency for certain. A cost-effective strategy is a therapeutic trial [15].

For asymptomatic and not at risk children aged 6 to 24 months undergoing primary preventive actions, the current evidence is insufficient to recommend routine screening for IDA [16]. Hemoglobin is the only practical screening test in field settings. All 6 to 36 month children without primary preventive actions should be screened at 9 to 12 months, 6 months later and at 2 year age [17]. At prevalence of anemia <5%, screening is not fruitful as majority of cases are unrelated to iron-deficiency. Screening for programatic purposes should be considered where anemia prevalence is between 5-20% and whole of India comes under this category [18].

Diet: Beyond the age of 6 months, more than 90% of the iron requirements of a breast-fed infant must be met by complementary food rich in bio-available iron [6]. Dietary diversification must be encouraged. Vxegans should be monitored closely and treated early. It is advisable to avoid consumption of beverages like tea and coffee with food as tannin contained in these may interfere with iron absorption. Foods containing ascorbic acid may enhance iron absorption.

Infants with IDA should be screened for cow’s milk protein allergy. Data from Western countries suggest that early introduction of cow’s milk is associated with increased gastrointestinal blood loss [7]. In the absence of Indian data, we do not recommend avoiding whole cow’s milk after 6 months age.

Cooking in cast iron vessels: Cooking of soups containing vegetables of low pH by simmering (heating for a long below boiling point) in cast iron vessels helps in increasing iron intake. This practice should be encouraged. Frying in iron vessels does not usually have similar effect [19].

Food fortification: It is difficult to meet full iron requirements in young children through diet without fortifying complementary feeds or iron supplements. As a public health measure, food fortification can play a major role in decreasing the prevalence of iron deficiency. Except for wheat flour or rice in some state government distribution systems, iron fortified foods are uncommon in India. Multiple Micronutrient Powder (MMNP) fortification should be considered in high-risk settings where above interventions are difficult to implement [20]. Fortification and supplementation together might breach the tolerable upper limit (TUL) for iron intake [21]; though, the clinical significance of this is not clear.

a) In infants >6 month age (Public health measure guidelines): Iron supplementation should be given to children aged 6-60 months in the dose of 10-30 mg /day, three months a year wherever prevalence of anemia is >20% [Strong recommendation, moderate quality evidence]. This comes to about 1-2 mg/kg/day [22] as most of India has >40% prevalence of anemia.

National Health Mission (NHM) guidelines [23] recommend bi-weekly 100 doses/year of 20 mg Fe + 100 mcg FA supplementation in 6-60 months age as syrup. Iron should be withheld in acute illness (fever, acute diarrhea, pneumonia, etc.), severe acute malnutrition (SAM) and hemoglobinopathy or history of repeated blood transfusion. In malaria endemic areas, public health measures to manage malaria must be in place [Strong recommendation]. Folic acid should not be used in malaria endemic areas where antifolate malaria medications are used [24].

b) In infants <6 month age (Individual case based supplementation): Low birth weight [LBW] babies should be supplemented with iron 2-3 mg/kg/day, beginning from 2 weeks for babies with birthweight <1500 g, and 6-8 weeks for babies with birthweight >1500 g [25], till toddlerhood when diet meets the iron requirements. Babies who received multiple transfusions during neonatal care should be clinically and biochemically assessed for need of supplementation at 6-8 weeks [14].

Since large number of term babies (21.4% at 4 months and 36.4% at 5 months) [26] suffer from iron deficiency, it is recommended that iron supplementation be started at 4 months in exclusively breastfed babies, especially where there is high risk of low iron transfer from mothers suffering from malnutrition, anemia, hypertension (with growth retardation) and diabetes.

Ancillary measures

Clinical presentations: There are no pathognomonic features for zinc deficiency except in acrodermatitis enteropathica. Zinc deficiency presents as growth failure, hypogonadism, skin lesions, impaired olfactory and gustatory sense, and impaired resistance to infection. It is pronounced in protein-energy malnutrition, Crohn’s disease, sickle cell anemia and nephrotic syndrome [29].

Deficiency status and risk factors: About 43.8% under-five children in five Indian states have significant zinc deficiency [30]. Zinc is not well conserved in body as there is no conventional tissue reserve. Its status depends on regular dietary zinc intake. Low intake of zinc rich foods (animal or sea products); high intake of inhibitors (phytates) and losses in diarrhea contribute to widespread zinc deficiency.

Laboratory markers are inadequate for practical use due to cost and methodological obstacles even in developed countries, so indirect method of estimating zinc status of diets in various geographic areas are used [31]. Prevalence >20% is indication for public health intervention. Low height for age >20% is a surrogate indicator [32].

Diet: In view of high prevalence of zinc deficiency in population, we recommend food rich in zinc (additional milk, eggs, grains, legumes, nuts and seeds).

Food fortification: Fortification with zinc only has shown to improve serum zinc status [33]. We recommend it to control/eliminate zinc deficiency despite lack of unequivocal evidence on benefits. It is recommended that zinc fortified foods be available.

Adjunct in therapy: Zinc should be prescribed as adjunct therapy for diarrhea as India has high prevalence of zinc deficiency and also malnourished children [34]. The dose recommendation is 10 mg/day for babies below six months and 20 mg/day for babies above six months, using any water soluble zinc salt [35]. In view of vomiting seen with zinc administration we recommend that it can be administered in two divided doses. Zinc should be prescribed as adjunct therapy for conditions like sickle cell disease, preterm babies, protein energy malnutrition, chronic diarrhea, Wilson disease, Thalassemia major.

Supplementation: Zinc supplementation does not have significant impact on all-cause mortality but prevents pneumonia and diarrhea significantly [36-38]. Zinc supplementation in deficient pre-pubertal children shows a significant increment in height and weight, but not weight-for-height, when there was low weight for age and height-for-age [39]. Preterm babies are recommended 2 mg/kg/day supplemental zinc till 3 months corrected age [40]. We recommend co-administration of zinc and iron as it is equally effective [39], contrary to popular belief, for ease of administration.

Clinical presentations: Iodine deficiency disorders (IDD) presents as goiter, cretinism, hypothyroidism, brain damage, abortion, still birth, mental retardation, psychomotor defects, hearing-speech impairment or neuropsychological deficits as subclinical manifestation. It constitutes the largest cause of preventable brain damage worldwide. Children from iodine-deficient areas have lower intelligence quotient by average 10-15 points. Majority of consequences of IDD are invisible and irreversible, but preventable.

Deficiency status and risk factors: WHO estimates a worldwide 37% prevalence of iodine deficiency in school-aged children. The IDD control goal was prevalence <10% in India by 2012 but 325 districts surveyed revealed 263 as endemic [41]. Smoking reduces iodine in breastmilk and needs consideration for supplementation [29].

Median urinary iodine >100 µg/L indicates sufficiency. Ultrasound measurements of thyroid volume are better than clinical assessment. Filter paper TSH test is recommended for neonatal screening. However, its role and cost effectiveness in screening for community iodine deficiency is not established. Filter paper Thyroglobulin (Tg) test is a promising method [42].

Universal Salt Iodization: USI is the most cost effective and sustainable method of iodine supplementation for controlling IDD; we support a ban on availability of non-iodized salt. Iodine is a volatile compound hence the iodized salt should be stored in air-tight containers. Since method of cooking and duration of cooking affect iodine salt content of cooked food, it is advisable to sprinkle salt after cooking or towards end of cooking, wherever possible [43].

In areas of moderate and severe iodine deficiency (median urinary iodine <50 µg/L or total goiter rate >20%) approaches for iodine supplements are described in Table I [44].

A high iodine intake with urinary levels >300 µg/L is to be discouraged, especially in previously deficient populations as it can have an adverse effect of iodine induced hyperthyroidism [42].

Vitamin A deficiency (VAD) is most important preventable cause of blindness in low- and middle-income countries.

Deficiency status and risk factors: Zinc, Iron and protein-calorie deficiencies; recurrent clinical and subclinical infections; and parasitic infestations, adversely affect vitamin A absorption, transport and utilization. Habitual low dietary intake of vitamin A rich animal food or beta carotene-rich vegetables-fruits is the major factor for the poor vitamin A status among the South East Asia Region (SEAR) population. >0.5% Bitot’s spots, >1% night blindness and >0.01% keratomalacia prevalence among under-five children indicates a public health issue.

The NNMB 2006 data from rural India shows 62% prevalence of VAD Disorders (Serum retinol <20 µg/L) in preschoolers [45]. Despite non-significant improvement in dietary intake and vitamin A program coverage, there is decline in clinical VAD in under-5 children in most/countries of SEAR. Keratomalacia is no longer a major public health problem with improved health care, nutrition and measles vaccination, although cases are reported from remote areas [46]. Reappraisal of the prevalence of VAD is warranted at present [47].

Serum retinol, dark adaptometry and Rose-Bengal eye test are useful in detecting VAD. Serum retinol measurements alone, if not adjusted by C-reactive protein (CRP) levels for subclinical infections, can overestimate VAD burden. It may not be an operationally feasible indicator for community use [47].

Diet: Pediatricians should provide guidance to promote vitamin A rich foods routinely (milk products like butter, ghee, yogurt, curd, cheese, eggs, liver and yellow/orange colored vegetables and fruits); more so during diarrhea, measles and respiratory infections [48].

Supplementation: Vitamin A prophylaxis program was started with a view to control blindness due to keratomalacia. Later in 2006, age group was extended to 5 years from initial 3 years. Every six months a mega dose of 2 lakh units (1 lakh for < 8 kg or < 1 year age) of oil based vitamin A is given [48]. Mega dose vitamin A supplementation is not recommended in infants below 6 months age.

Recent data suggests a sharp reduction in the incidence of overt vitamin A deficiency across the country [47], and therefore there is a need for a relook at this program. On basis of possible adverse effects, overdosing, increase in acute respiratory infections, vitamin D and zinc antagonism, and reducing prevalence of deficiency, there is an opinion to adopt a targeted rather than universal mega dose vitamin A supplementation in preschool children [47]. Indian Academy of Pediatrics recommends supplementation till 3 years of age to all, and to older children only in severe malnutrition and measles [49].

Mega dose vitamin A supplementation is recommended in children with severe acute malnutrition (SAM), measles and cholestasis; in addition to those with signs of deficiency like xerotic conjunctiva, Bitot’s spots and keratomalacia. When water soluble injectable preparation is given, oral fat soluble preparation is recommended to replenish stores.

Vitamin A supplementation coverage rate has increased from 16% (NFHS-3, 2005) to 27%-90% in different states (NFHS-4, 2015-16) with a national average of 60.2%. The large dose is well absorbed and stored in the liver, and mobilized over 4-6 months depending on dietary content and utilization rate [50].

Transient side-effects usually disappearing within 24 hours, like headache, nausea, vomiting and diarrhea are reported in 3%-7%, with no long term consequences [50]. There are no known deaths. As overdosing can lead to hypervitaminosis A, special training of field staff is recommended. The supply is irregular and oral syrup is available only to the Government sector, hence many children do not get regular supplementation.

Effects of supplementation: A cochrane review in 2017 found that VA supplementation at 0-6 month does not significantly reduce overall, diarrheal or pneumonia related mortality and morbidity, but increases benign raised fontanel cases [51,52]. VA supplementation in 6-59 month children in low-and middle-income countries with a high prevalence of VAD has shown [50]:

Vitamin D Defeciency

Clinical presentations: Role of vitamin D in bone mineralization and calcium-phosphorus homeostasis is well established with deficiency manifesting as infantile hypocalcemia, rickets, delayed growth and dentition. Lower levels of vitamin D and its binding proteins were seen in children with severe sepsis.

Deficiency status and risk factors: Based on serum levels, vitamin D deficiency is prevalent, largely subclinical, across the country from 70-100% at various times in life cycle, irrespective of gender, region or dietary habits [53]. In infants aged three months and their mothers, prevalence of vitamin D insufficiency was found in 92.6% and two third infants were exclusively breastfed [54]. Prevalence of VDD (serum 25-hydroxyvitamin D <25-30 nmol/L) >20% in whole population or in at-risk population subgroups constitutes a public health issue warranting intervention.

Infants depend upon the vitamin D transferred from mother prenatally. In every deficient mother, evaluate child for calcium and vitamin D and also vice versa. Most infants are born with low vitamin D stores and are dependent on breast milk (containing <25 IU/L), sunlight or supplements as vitamin D sources in initial months of life. Sun exposure may be restricted due to many reasons. Vitamin D deficiency is also prevalent among infants in countries with food fortification and year-round sun exposure.

Laboratories use different methods for assessment. Wide variation in reports on same sample are noted [55]. Based on the observations of relation with calcium absorption and parathormone levels with vitamin D levels most authorities consider >30 ng/ml as sufficient, 20-30 ng/ml as relative insufficiency and <20 ng/ml as deficiency.

Supplementation: Vitamin D supplementation is recommended for children at risk of vitamin D deficiency, especially where sun exposure is not available or is avoided for some reasons.

Recent Cochrane reviews [56] and WHO [57] do not recommend routine supplementation of vitamin D to term infants for preventing rickets or respiratory and diarrheal infections. Cochrane has some evidences for vitamin D supplementation for asthma prevention [58].

There is no national program for prevention of VDD in India. FSSAI has issued recommendation [5] for fortification of vegetable oil with 25 IU/g vitamin A and 4.5 IU/g vitamin D, which cannot meet daily requirements. European Food Safety Authority has set the upper limit of safety at 1000 IU/day for infants and 2000 IU/day for children ages 1 to 10 years [59]. Considering variable concentrations of available preparations, it is imperative to monitor the supplementation to avoid hypervitaminosis D.

Sun exposure: Encourage the socially accepted practice of oil massage under sunlight and promote outdoor activities under sun for older children and adolescents. Skin is a more efficient source for providing vitamin D than ingested form despite slow initial rise in plasma levels [60]. There are no defined recommendations on sunlight exposure. Generally, face, arms, hand and legs should be exposed twice or thrice a week, for the duration causing minimal sunburn [61].

Diet: Encourage children to consume more vitamin D rich or fortified foods. Dietary sources are scarce like fatty fish (wild salmon, mackerel, eel, anchovy, sardines, swordfish, tuna), and lesser extent in egg yolk and fortified foods, milk and dairy products, margarine, etc. [59].

Clinical presentations: Deficiency of B-vitamins can lead to glossitis, angular stomatitis, dermatitis, anemia, hyper-pigmentation or brain dysfunction. Cobalamin stores are so large that clinical deficiency is uncommon without predisposing factors like malabsorptive states; it takes years of inadequate intake or absorption before clinical symptoms. Niacin deficiency is encountered only as epidemic during emergencies in population with maize as staple food and high incidence of infectious diseases and malnutrition; and children may not present with skin changes although diarrhea can occur [62].

Diet: Family education on balanced diet i.e. inclusion of food from vegetable and animal source should be provided. Promote consumption of foods rich in B-vitamins. A useful source is National Institute of Nutrition, Hyderabad manual, which lists the dietary sources and RDA of dietary components [68].

There is very little data on other micronutrients from India. It is felt that the research activity in this area be encouraged to collect evidence for recommendation.

Intramuscular vitamin K administration at birth is recommended.

Routine use of vitamin E for preterm babies is not recommended.

Contributors: All authors approved the final version of manuscript, and are accountable for all aspects related to the study.

Funding: The cost of travel of the members for the consultative meeting for their recommendations was borne by Sun Pharmaceuticals.

Competing interests: None stated.

Acknowledgments: We thankfully acknowledge the help, co-operation, assistance and guidance from Dr. Ajay Khera Deputy Commissioner (Child Health and Immunization) MOHFW, Dr. Sila Deb (Deputy Commissioner - Child Health, MOHFW), Dr. Nimisha Goel (MoHFW Govt of India), Ms. Raji Nair (UNICEF), Dr Pramod Jog (President IAP), WHO, UNICEF, Sun Pharmaceuticals and Smt. Santra Devi Health and Educational Trust for designing and technical assistance.

Disclaimer: These consensus statements are prepared for assisting pediatricians in accordance with current scientific evidence and guidelines for prevention of micronutrient deficiencies in young children; however, many areas are still not clearly defined. These statements cannot establish a standard of care, and decisions about treatment should be based on the judgment of the Pediatricians on merits of individual cases dealt by them.

Revision and Updating: These guidelines were drafted in 2017 and updated in May- June 2018 through email suggestions by the EB members of Central IAP and the writing committee. The recommendations shall be revised after three years i.e. in 2020- 21.

1. Plessow R, Arora NK, Brunner B, Tzogiou C, Eichler K, Brügger U, et al. Social costs of iron deficiency anemia in 6–59-month-old children in India. PLoS One 10:e0136581. Available from: https://doi.org/10.1371/journal.pone. 0136581. Accessed February 10, 2018.

2. World Health Organization. Chilhood and maternal undernutrition. In: Global Health Risks: Mortality and burden of disease attributable to selected major risks. Geneva: WHO Library Cataloguing-in-Publication Data; 2009. P.9.

3. National Nutrition Monitoring Beureau Technical report no. 22. Executive Summary. In: Prevalence of micronutrient deficiencies. Hyderabad: National Institute of Nutrition; 2003. pg. i.

4. Guidelines - Governnment of India. NHM Components: Child Health Guidelines. 2013. Available from: http://nhm.gov.in/nrhm-components/rmnch-a/child-health-immunization/child-health/guidelines.html. Accessed February 10, 2018.

5. Food and Safety Standards Authority of India; 2017. Available from: https://www.fssai.gov.in/dam/jcr.../Direction_Food_Fortification_19_05_2017.pdf%. Accessed February 10, 2018.

6. Iron. In: Human Vitamin and Mineral Requirements: Report of a joint FAO/WHO expert consultation. Bangkok: Food and Nutrition Division FAO Rome; 2001. P. 195–223. Available from: http://www.fao.org/3/a-y2809e.pdf. Accessed July 16, 2018.

7. American Academy of Pediatrics Committee on Nutrition. The use of whole cow’s milk in infancy. Pediatrics. 1992;89;1105.

8. Bogen DL, Duggan AK, Dover GJ, Wilson MH. Screening for iron deficiency anemia by dietary history in a high-risk population. Pediatrics. 2000;105:1254-9.

9. World Health Organization. Vulnerable groups. In: Nutritional Anemias: Tools for effective prevention and control. Geneva: World Health Organization; 2017. P. 4. Available from: http://apps.who.int/iris/bitstream/10665/259425/1/ 9789241513067-eng.pdf?ua=1. Accessed July 16, 2018.

10. Sant-Rayn Pasricha, Black J, Muthayya S, Shet A, Bhat V, Nagaraj S, et al. Determinants of anemia among young children in rural India. Pediatrics. 2010;126:126.

11. Abd-El Wahed MA, Mohamed MH, Ibrahim SS, El-Naggar WA. Iron profile and dietary pattern of primary school obese Egyptian children. J Egypt Public Health Assoc. 2014;89:53-9.

12. White KC. Anemia is a poor predictor of iron deficiency among toddlers in the United States: for heme the bell tolls. Pediatrics. 2005;115:315-20.

13. Ekwochi U, Odetunde O, Maduka I, Azubuike J, Obi I. Iron deficiency among non-anemic under-five children in enugu, South-East, Nigeria. Ann Med Health Sci Res. 2013;3:402-6.

14. Baker RD, Greer FR. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children [0-3 Years of Age]. Pediatrics. 2010;126:1040-50.

15. Lanzkowsky P. Problems in diagnosis of iron deficiency anemia. Pediatr Ann. 1985;14:618,622-3.

16. Albert Sui. Screening for Iron Deficiency Anemia in Young Children: USPSTF Recommendation Statement. Pediatrics. 2015;136:746-52.

17. Kazal LA. Prevention of iron deficiency in infants and toddlers. Am Fam Physician 2002;661217-25.

18. Assessment, surveillance and indicators. In: Iron Deficiency Anemia Assessment, Prevention and Control: A guide for program managers. World Health Organization; 2001. p. 29. Available from: http://www.who.int/nutrition/ publications/en/ida_assessment_prevention_control.pdf Accessed July 16, 2018.

19. Geerligs PDP, Brabin BJ, Omari AAA. Food prepared in iron cooking pots as an intervention for reducing iron deficiency anaemia in developing countries: A systematic review. J Hum Nutr Diet. 2003;16:275-81.

20. WHO. Guideline: Use of multiple micronutrient powders for home fortification of foods consumed by infants and children 6–23 months of age. Geneva: World Health Organization; 2011. Available from: http://www.who.int/about/ licensing/copyright_form/en/index.html. Accessed July 16, 2018.

21. Ghosh S, Sinha S, Thomas T, Sachdev HS, Kurpad AV. Revisiting dietary iron requirement and deficiency in Indian women: Implications for food iron fortification and supplementation. J Nutr. 2019;149:366-71.

22. Guideline: Daily iron supplementation in infants and children. Geneva: World Health Organization; 2016. Available from: http://apps.who.int/iris/bitstream/10665/204712/1/9789241549523_eng.pdf. Accessed July 16, 2018.

23. Supplementation through the Life Cycle. In: Guidelines for Control of Iron Deficiency Anemia. National Health Mission, Ministry of Health and Family Welfare, Government of India; 2013. P. 17–9. Available from: http://nhm.gov.in/nrhm-components/rmnch-a/child-health-immunization/child-health/guidelines.html. Accessed July 16, 2018.

24. Secretariat WHO. Conclusions and recommendations of the WHO Consultation on prevention and control of iron deficiency in infants and young children in malaria- endemic areas. Food Nutr Bull. 2007;28:S621–7. Available from: http://www.who.int/nutrition/publications/micronutrients/FNBvol28N4supdec07.pdf. Accessed February 10, 2018.

25. Shenoi A, Nair SI, Prasad V. Management of Feeding in Low Birth Weight Infants Summary. In: Praveen Kumar, ON Bhakoo, Naveen Jain, Rhishikesh Thakre, Srinivas Murki SV, editor. Evidence Based Clinical Practice Guidelines. Delhi: National Neonatalogy Forum India; 2010. p. 31.

26. Krishnaswamy S, Bhattarai D, Bharti B, Bhatia P, Das R, Bansal D. Iron deficiency and iron deficiency anemia in 35 months-old, breastfed healthy infants. Indian J Pediatr. 2017;84:505-8.

27. McDonald　　SJ, Middleton　　P, Dowswell　　T, Morris　　PS. Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes. Cochrane Database Syst Rev. 2013; CD0040740.

28. Guideline: preventive chemotherapy to control soil-transmitted helminth infections in at-risk population groups. Geneva: World Health Organization. Licence: CC BY-NC-SA 3.0 IGO.; 2017. 3 p. Available from: http://apps.who.int/iris/bitstream/10665/258983/1/97892415 50116-eng.pdf. Accessed July 16, 2018.

29. LD Suskind. Nutritional Deficiencies During Normal Growth. In: Praveen S. Goday, editor. Pediatric Clinics of North America. New Delhi: Reed Elsevier India Pvt. Ltd.; 2009. p. 1035-53.

30. Kapil U, Jain K. Magnitude of zinc deficiency amongst under five children in India. Indian J Pediatr. 2011;78: 1069-72.

31. Caulfield LE, Black RE. zinc deficiency. In: Majid Ezzati, Alan D. Lopez AR, Murray and CJL, editors. Comparative qualifications of health risks: Global and regional burden of disease attributable to selected major risk factors. Geneva: World Health Organization; 2004. p. 257-79. Available from: http://apps.who.int/iris/bitstream/10665/42792/1/9241580348_eng_Volume1.pdf. Accessed February 10, 2018.

32. De Benoist B, Darnton-Hill I, Davidsson L, Fontaine O, Hotz C. Conclusions of the Joint WHO/UNICEF/IAEA/IZiNCG Interagency Meeting on Zinc Status Indicators. Food Nutr Bull. 2007 Sep;28[3_suppl3]:S480–4. Available from:http://journals.sagepub.com/doi/10.1177/1564826 5070283S306. Accessed February 10, 2018.

33. Shah D, Sachdev HS, Gera T, De-Regil LM, Peña-Rosas JP. Fortification of staple foods with zinc for improving zinc status and other health outcomes in the general population. Cochrane Database Syst Rev.2014;CD010697.

34. Lazzerini M, Wanzira H. Oral zinc for treating diarrhoea in children. Cochrane Database Syst Rev. 2016;12: CD005436.

35. Christa L. Fischer Walker and Robert E. Zinc supple-mentation for diarrhoea treatment. e-Library of Evidence for Nutrition Actions [eLENA]. World Health Organization; Mar 2014. Available from: http://www.who. int/elena/titles/commentary/zinc_diarrhoea/en/. Accessed February 10, 2018.

36. Dhingra U, Hiremath G, Menon VP, Dhingra P, Sarkar A, Sazawal S. Zinc deficiency: Descriptive epidemiology and morbidity among preschool children in peri-urban population in Delhi, India. J Health Popul Nutr. 2009;27:632-9.

37. Lassi ZS, Moin A, Bhutta ZA. Zinc supplementation for the prevention of pneumonia in children aged 2 months to 59 months. Cochrane Database Syst Rev. 2016; CD005978.

38. Sazawal S, Black RE, Ramsan M, Chwaya HM, Dutta A, Dhingra U, et al. Effect of zinc supplementation on mortality in children aged 1-48 months: a community-based randomised placebo-controlled trial. Lancet. 2007;369: 927-34.

39. Szymlek-Gay EA, Domellöf M, Hernell O, Hurrell RF, Lind T, Lönnerdal B, et al. Mode of oral iron administration and the amount of iron habitually consumed do not affect iron absorption, systemic iron utilisation or zinc absorption in iron-sufficient infants: a randomized trial. Br J Nutr . 2016;116:1046-60.

40. Mathur NB, Agarwal DK. Zinc Supplementation in Preterm Neonates and Neurological Development: A Randomized Controlled Trial. Indian Pediatr. 2015;52: 951-5.

41. Pandav CS, Yadav K, Srivastava R, Pandav R, Karmarkar MG. Iodine deficiency disorders (IDD) control in India. Indian J Med Res. 2013;138:418-33.

42. WHO Library Cataloguing-in-Publication Data. Indicators of Impact. In: Assessment of iodine deficiency disorders and monitoring their elimination: a guide for program managers. 3rd ed. Geneva: World Health Organization; 2007.p.32-33. Available from:http://apps.who.int/iris/bitstream/10665/43781/1/9789241595827_eng.pdf. Accessed July 16, 2018.

43. Runa R, Raghuvanshi RS. Effect of different cooking methods on iodine loss. J Food Science Technol. 2013;50:1212-6.

44. Reaching Optimal Iodine Nutrition in Pregnant and Lactating Women and Young Children. Geneva: Joint Statement by WHO and UNICEF; 2007. Available from: http://www.who.int/nutrition/publications/micronutrients/ WHOStatement__IDD_pregnancy.pdf. Accessed July 16, 2018.

45. NNMB Technical Report No. 23. Prevalence of vitamin A deficiency among rural preschool children. Hyderabad: National Institute of Nutrition; 2006. p.ii. Available from: http://nnmbindia.org/vad-report-final-21feb07.pdf. Accessed February 10, 2018.

46. Vitamin A deficiency. In: Regional Nutrition Strategy: Addressing malnutrition and micronutrient deficiencies [2011-2015]. New Delhi: World Health Organization; 2012. p. 32–5. Available from: https://apps.who.int/iris/handle/ 10665/205804. Accessed July 16, 2018.

47. Kapil U, Sachdev HPS. Massive dose vitamin A program in India–need for a targeted approach. Indian J Med Res. 2013;138:411-7.

48. Policy on Micronutrient - Vitamin-A. New Delhi: Child Health Division, Dept of Family Welfare, MoH and FW; document No. Z.28020/30/2003-CH. Available from:http://nhm.gov.in/images/pdf/programmes/child-health/guidelines/goi_vit_a.pdf. Accessed Febuary 10, 2018.

49. Recommendations: Eligibility of Children for Vitamin A Supplementation Program. Indian Pediatr. 2005;42:1011-2.

50. WHO Library Cataloguing-in-Publication Data. Guideline: Vitamin A supplementation in infants and children 6–59 months of age. Geneva: World Health Organization; 2011. p.3. Available from: https://apps.who.int/iris/bitstream/handle/10665/44664/9789241501767_eng.pdf? sequence =1. Accessed July 16, 2018.

51. Haider BA, Sharma R, Bhutta ZA. Neonatal vitamin A supplementation for the prevention of mortality and morbidity in term neonates in low and middle income countries. Cochrane Database Syst Rev.2017:CD006980.

52. Imdad A, Ahmed Z, Bhutta ZA. Vitamin A supple-mentation for the prevention of morbidity and mortality in infants one to six months of age. Cochrane Database Syst Rev. 2016:CD007480.

53. Gupta R, Gupta A. Vitamin D deficiency in India: prevalence, causalities and interventions. Nutrients. 2014;6:729-75.

54. Jain V, Gupta N, Kalaivani M, Jain A, Sinha A, Agarwal R. Vitamin D deficiency in healthy breastfed term infants at 3 months and their mothers in India: seasonal variation and determinants. Indian J Med Res. 2011;133:267-73.

55. Lucas R, Neale R. What is the optimal level of vitamin D/ ? Aust Fam Physician. 2014;43:119-22.

56. Wagner CL, Greer FR. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics. 2008;122;1142-52.

57. Braegger C, Campoy C, Colomb V, Decsi T, Domellof M, Fewtrell M, et al. Vitamin D in the Healthy European Pediatric Population: Consensus Statement. J Pediatr Gastroenterol Nutr. 2013;56:692-701.

58. Munns C, Zacharin MR, Rodda CP, Batch JA, Morley R, Cranswick NE, et al. Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: A consensus statement. Med J Aust. 2006; 185:25-729.

59. Khadilkar V. Prevention and Treatment of Vitamin D and Calcium Deficiency in Children and Adolescents: Indian Academy of Pediatrics Guidelines. Indian Pediatr. 2017;54:567-73.

60. Yakoob MY, Salam RA, Khan FR, Bhutta ZA. Vitamin D supplementation for preventing infections in children under five years of age. Cochrane Database Syst Rev. 2017:CD008824.

61. WHO | Vitamin D supplementation in infants. WHO. 2017; Available from: https://www.who.int/elena/titles/vitamind_ infants/en/. Accessed July 16, 2018.

62. Martineau AR, Cates CJ, Urashima M, Jensen M, Griffiths AP, Nurmatov U, et al. Vitamin D for the management of asthma. Cochrane Database Syst Rev.; 2016;9:CD011511.

63. Haddad JG, Matsuoka LY, Hollis BW, Hu YZ, Wortsman J. Human plasma transport of vitamin D after its endogenous synthesis. J Clin Invest. 1993;91:2552-5.

64. Holick MF. Sunlight and vitamin D: both good for cardiovascular health. J Gen Intern Med. 2002;17:733-5.

65. Pellagra and its prevention and control in major emergencies. Geneva: World Health Organization; 2000. 1-6 p. Available from: http://www.who.int/nutrition/publications/en/pell agra_prevention_control.pdf. Accessed July 16, 2018.

66. Mittal M, Bansal V, Jain R, Dabla PK. Perturbing status of Vitamin B12 in indian infants and their mothers. Food Nutr Bull. 2017;38:209-15.

67. Kapil U, Toteja GS, Bhadoria A. Cobalamin and folate deficiencies among children in the age group of 12-59 months in India. Biomed J. 2015;38:162-6.

68. National Institute of Nutrition, Hyderabad. Dietary Guidelines for Indians – A Manual. II edition, 2011.

69. Pasricha SR, Shet AS, Black JF, Sudarshan H, Prashanth NS, Biggs BA. Vitamin B-12, folate, iron, and vitamin A concentrations in rural Indian children are associated with continued breastfeeding, complementary diet, and maternal nutrition. Am J Clin Nutr. 2011;94:1358-70.