Introduction

Micronutrients play indispensable roles in human health. These nutrients are categorized into two primary groups: vitamins and essential trace elements. Vitamins are further divided into fat-soluble types, including A, D, E, and K, and water-soluble types, comprising the B-complex vitamins and vitamin C. Essential trace elements, vital to numerous bodily functions, consist of a variety of minerals such as calcium, phosphorus, magnesium, sodium, potassium, iron, zinc, fluoride, copper, chromium, manganese, molybdenum, selenium, and iodine [1].

Micronutrients play diverse and vital roles in biochemical processes. Trace elements serve as crucial cofactors in metabolic functions, influence enzyme activity, and constitute essential components of prosthetic enzyme groups. Vitamins and their derivatives function as coenzymes in various metabolic pathways. Many micronutrients possess antioxidant properties that play a significant role in reducing the cell damage caused by free radicals. These micronutrients are essential for various biological functions in the body, including energy production, organ function, RNA and DNA synthesis, promotion of physical growth, sexual maturation, neuromotor development, and immune responses [2].

The objective of this review was to examine the essential roles of selected micronutrients (iron, zinc, vitamin A, vitamin D, iodine, and folate) in the health of children and adolescents, with particular emphasis on growth and development. These micronutrients were chosen based on their high prevalence of deficiency worldwide and their fundamental importance in pediatric development. Through a comprehensive analysis of the current literature, we aimed to synthesize evidence regarding their roles, assessment methods, deficiency patterns, and intervention strategies, while providing evidence-based insights for clinical practice.

Methods

This narrative review comprehensively summarizes recent research trends and guidelines regarding essential micronutrients (iron, zinc, vitamin A, vitamin D, iodine, and folate) crucial for the growth and development of children and adolescents. A literature search was conducted through December 2023 using the PubMed, Embase, and Web of Science databases. The general search strategy employed terms such as [“micronutrients” OR “vitamins” OR “trace elements”] AND [“children” OR “adolescents”] AND [“growth” OR “development”]. When necessary, the search was expanded by combining specific nutrient terms [“iron” OR “zinc” OR “vitamin A” OR “vitamin D” OR “iodine” OR “folate”], along with supplementary keywords related to deficiency, assessment, and supplementation strategies.

As this was a narrative review rather than a systematic review or meta-analysis, we did not employ strict methodological procedures, such as PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) flow diagrams. Instead, we prioritized recent clinical studies, guidelines, high-level evidence (meta-analyses, large cohort studies, and randomized controlled trials [RCTs]), and studies featuring Korean population data to provide clinically relevant information.

Overview: role of micronutrients

Understanding recommended micronutrient intake levels is helpful for evaluating nutritional adequacy and planning appropriate interventions. Table 1 presents the Korean Dietary Reference Intakes of the micronutrients discussed in this review [3]. These reference values provide important benchmarks for assessing nutritional requirements across different age groups and serve as a reference for the following review of each micronutrient. The Dietary Reference Intakes (DRIs) used in Table 1 include several reference values, the definitions of which are as follows. The Estimated Average Requirement (EAR) represents the median daily nutrient intake level that meets the requirements of 50% of healthy individuals and is usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them, although it can also be used to assess individual nutrient intakes. The Recommended Nutrient Intake (RNI) is set at two standard deviations above the EAR, meets the requirements of 97% to 98% of healthy individuals, and is often used to plan nutritionally adequate diets. RNI is the term used in Korean DRIs and is equivalent to the Recommended Dietary Allowance in the United States DRI system. The Adequate Intake (AI) is established when evidence is insufficient to determine EAR based on the median intake levels of healthy individuals from experimental or observational studies, although the extent to which this meets the requirements of the target population is uncertain [3].

To aid clinical practice, Table 2 summarizes the primary physiological roles, key deficiency symptoms, high-risk groups, and prevalence data of these six micronutrients.

Iron

Iron exists primarily in two forms: heme iron from animal sources with higher bioavailability (15%–35%) and nonheme iron from plant sources with lower bioavailability (2%–20%). The absorption of nonheme iron is significantly affected by dietary components, with factors such as phytic acid, polyphenols, calcium, and proteins found in milk, eggs, and soybeans inhibiting absorption. Conversely, enhancers such as ascorbic acid can facilitate the conversion of ferric iron to ferrous iron, thereby promoting iron absorption [4].

The fundamental roles of iron include hemoglobin formation, oxygen transport, myoglobin function, and neural development [5]. Iron deficiency (ID) can manifest with or without anemia. While functional alterations may be present even without anemia, the most severe impairments typically occur with iron deficiency anemia (IDA) [6]. Common causes of ID include an insufficient intake of bioavailable iron, increased demand during rapid growth or menstruation, gastrointestinal blood loss, and impaired absorption [7].

Assessment of iron relies on serum ferritin levels (reflecting storage), transferrin saturation, and hemoglobin levels. Ferritin levels of <12–15 ng/mL typically indicate depleted iron stores, although ferritin levels can be elevated during inflammation. In children and adolescents, IDA is often suspected if the hemoglobin level is <11 g/dL up to 11 years of age and <12 g/dL thereafter [8].

IDA is the most common type of anemia in children and adolescents and one of the most widespread nutritional deficiencies globally [9]. ID can negatively affect motor, cognitive, socioemotional, and neurophysiological development in infants, children, and adolescents in both the short and long term [10]. The impact of iron on fetuses is also significant; ID can lead to changes in hippocampal energy metabolism, striatal dopamine metabolism, and a decrease in myelination, adversely affecting the developing brain behavioral system in fetuses and newborns. Maternal ID is the most common cause of fetal ID [11].

Prevalence data from the Korea National Health and Nutrition Examination Survey (KNHANES) showed higher rates in females, particularly adolescents; boys aged 10 to 14 years had an ID prevalence of 6.8% versus 18.6% in girls, with an IDA prevalence of 1.0% and 2.6%, respectively. Among adolescents aged 15 to 17 years, 3.2% of males had ID, whereas 34.7% and 9.0% of females had ID and IDA, respectively [12]. In the United States, National Health and Nutrition Examination Survey (NHANES) data showed ID, anemia, and IDA prevalence rates of 7.1%, 3.2%, and 1.1%, respectively, in children aged 1 to 5 years, with higher rates in ages of 1 to 2 years. Among females aged 12 to 21 years, the prevalence of ID was 38.6%, and that of IDA was 6.3%, similar to Korean patterns [13].

For these at-risk groups, it is essential to monitor ID and ensure appropriate surveillance. For infants, it is important to introduce complementary foods at the appropriate time and pay careful attention to their diets to ensure adequate iron intake. Nutritional ID occurs when a diet fails to provide sufficient iron to meet the physiological needs of the body. Populations that primarily consume repetitive plant-based diets with minimal meat intake tend to experience reduced bioavailability of dietary iron. This is especially prevalent in diets low in meat, since meat is known to have higher heme iron content, and thus better bioavailability [14]. Incorporating animal-based foods rich in heme iron and coupling them with fresh vegetables and fruits loaded with ascorbic acid can enhance the overall intake and absorption of iron.

A Cochrane Review of 26 studies involving 2,726 preterm and low-birthweight infants found that enteral iron supplementation (≥1 mg/kg/day) reduced the risk of ID [15]. The American Academy of Pediatrics (AAP) recommends iron supplementation of 2 mg/kg/day for preterm infants aged 1 to 12 months who are fed breast milk. For exclusively or primarily breastfed full-term infants, the AAP advises 1 mg/kg of daily iron supplementation from the age of 4 months until they begin consuming iron-containing complementary foods [16]. The European Society for Paediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) recommends that breastfed preterm infants up to 6 months of age receive 2 to 3 mg/kg/day of iron supplements [17].

Meta-analyses and systematic reviews have shown that iron supplementation does not significantly affect the growth of children and adolescents. Some studies have shown that while iron treatment significantly improves hemoglobin levels, it does not significantly affect other anthropometric measures, such as weight, height, mid-upper arm circumference, skinfold thickness, and head circumference [18-20]. In terms of development, iron supplementation has shown positive results in reducing cognitive and motor developmental deficits and improving memory and learning in iron-deficient or anemic children and adolescents [18]. A systematic review indicated that while iron interventions are effective in improving iron status and anemia, there is no evidence that iron status and anemia affect or are associated with the attention, intelligence, or memory of adolescents, nor does iron supplementation improve memory recall or intelligence [21]. Iron plays a crucial role in the growth and development of children and adolescents; however, the effects of iron supplementation can vary based on individual conditions, age, health status, and other variables. Therefore, the approach to iron supplementation should be considered carefully, assessing each child’s iron and nutritional status and providing appropriate iron supplementation when needed.

Zinc

Zinc is abundantly found in meat, fish, and seafood, with oysters notably high in content; meat, particularly beef, accounts for 20% of intake owing to its higher consumption rate. Eggs and dairy also contain zinc. Plant-based sources such as beans, nuts, and whole grains also contain zinc, but their bioavailability is low because of the presence of phytates, which form insoluble complexes that inhibit zinc absorption [22]. Zinc plays a vital role in enzyme catalysis, enhancing immune functions, protein and DNA synthesis, cell signaling, division, growth, tissue repair, and wound healing. It is also involved in lipid and glucose metabolism and in responses to immunity and infection [23]. Zinc supports growth by promoting growth hormone (GH) receptor binding and regulating the expression of GH receptors and insulin-like growth factor 1 (IGF-1) genes in the liver [24].

Symptoms of zinc deficiency vary with age. Diarrhea is a common issue in infants and young children. As children grow older, they may experience growth delays, alopecia, and frequent infections. Additionally, zinc deficiency can affect taste and smell [25]. Acrodermatitis enteropathica is an inherited form of zinc deficiency resulting from impaired absorption and occurs due to an autosomal recessive mutation in the SLC39A4 gene. This condition often becomes symptomatic in infancy after breastfeeding ceases, with clinical symptoms including alopecia, diarrhea, growth impairment, and characteristic skin lesions that predominantly appear as burn-like psoriasiform lesions around the mouth, anus, gluteal region, perineum, and extremities [26].

Typically, serum zinc levels <70 μg/dL for women and <74 μg/dL for men are considered indicative of insufficient zinc status [23]. The International Zinc Nutrition Consultative Group suggests cutoff values for zinc deficiency of <65 µg/dL (9.9 µmol/L) in the morning and <57 µg/dL (8.7 µmol/L) in the afternoon for children under 10 years old [27]. However, these serum values have limitations, as zinc concentrations can vary based on sex, age, and time of day (morning vs. evening); therefore, interpretation requires caution [28].

In the United States, <1% of children aged 2 to 8 years have a zinc intake below the EAR; however, among adolescents aged 14 to 18 years, only 1% of boys fall short compared to 20.9% of girls. The NHANES (2011–2014) further indicates that 3.8% of children <10 years old, 8.6% of males ≥10 years old, and 8.2% of females have serum zinc levels below the sufficiency cutoff, suggesting that adolescents are at potential risk of zinc deficiency [29]. In contrast, Korean data (KNHANES 2016–2019) show that children aged ≥1 year have a zinc intake of 147.4% of the EAR, with those <5 years old consuming more than twice the EAR, suggesting that zinc deficiency is rarely observed in Korea [30].

Several groups should be mindful of zinc inadequacy. Approximately 15% to 40% of individuals with inflammatory bowel disease (IBD) experience zinc deficiency due to inflammation, poor intake, and malabsorption [31]. Children and adolescents receiving parenteral nutrition for long-term intestinal failure are at risk of zinc deficiency if their nutrition lacks adequate zinc [32]. In cystic fibrosis, dermatitis caused by zinc deficiency can be the initial presenting symptom [33]. Vegetarians may encounter zinc inadequacy because the bioavailability of zinc in their diets is low [34]. Additionally, older infants who are exclusively breastfed are at risk of zinc deficiency. The zinc content in breast milk is the highest in the first month after birth and declines by approximately 75% by the ninth month. Therefore, infants older than 6 months who are exclusively breastfed without adequate complementary foods may not receive sufficient zinc [35].

For individuals at risk of zinc deficiency or showing signs or symptoms of zinc deficiency, an assessment of zinc status is necessary. Preventatively, consuming zinc-rich foods such as meat, fish, and seafood are advised. Zinc supplementation is not routinely required for healthy children and adolescents in low-risk environments. Zinc is available in supplements containing only zinc, in combination with other ingredients, and in many multivitamin/mineral products. These supplements contain various forms of zinc, with the amount of elemental zinc indicated on the product label [36]. Regarding gut health, zinc deficiency can alter the composition of the gut microbiome, favoring pathogenic over beneficial bacteria. Adequate zinc levels support intestinal barrier integrity, immune functionality, and overall microbiome health [37]. Studies suggest that zinc, alone or in combination with other treatments, can effectively reduce the duration of diarrhea in children, particularly in low- and middle-income countries [38,39]. The World Health Organization (WHO) recommends a short course (10–14 days) of zinc supplementation to treat diarrhea in children [40]. A recent meta-analysis of the effects of zinc supplementation on growth patterns in healthy children revealed that zinc supplementation significantly enhanced height, weight, and height-for-age in individuals [41]. The positive effects of zinc on weight and height may be related to its effects on GH metabolism. Zinc supplementation increases the levels of IGF-1 and IGF-binding protein-3 in healthy children [42].

Vitamin A

Vitamin A refers to a group of fat-soluble retinoids, most notably retinol and retinyl esters. It is involved in immune responses, growth and development, and reproductive health and aids in the cellular growth and differentiation necessary for the healthy formation and maintenance of vital organs, such as the heart and lungs. Additionally, vitamin A is important for vision, acting as a crucial element of rhodopsin, a light-sensitive protein in the retina, and contributing to the normal differentiation and function of the conjunctival membranes and cornea [43,44].

Humans must obtain vitamin A from their diet either as preformed vitamin A or provitamin A carotenoids. Animal sources such as dairy, eggs, fish, and organ meat provide preformed vitamin A. Provitamin A carotenoids, which are abundant in green leafy vegetables, sweet potatoes, and carrots, are converted into vitamin A in the intestine. In wealthier nations, the majority of vitamin A intake comes from preformed vitamin A, whereas in low-income countries, people primarily consume provitamin A [43].

The first symptom of vitamin A deficiency is night blindness, caused by low retinal rhodopsin levels. The most common clinical manifestation is xerophthalmia, which occurs due to low plasma retinol levels and depletion of vitamin A reserves in the eyes. In extreme cases, long-term vitamin A deficiency can lead to hyperkeratosis of the ocular epithelial tissue and eventually permanent blindness, which is the most common cause of blindness in developing countries [45]. Chronic vitamin A deficiency is also associated with abnormal lung development, pneumonia, increased risk of anemia, and increased mortality [46].

For assessment of vitamin A status, plasma retinol measurement is the standard diagnostic tool, with concentrations of ≤0.70 µmol/L and ≤0.35 µmol/L indicating moderate-severe deficiency, respectively [43]. Although vitamin A deficiency is uncommon in developed countries, it remains a significant public health concern in developing nations, where economic constraints and dietary customs often limit access to both animal-derived foods with preformed vitamin A and plant-based foods rich in provitamin A carotenoids [43]. According to a 2009 WHO report, vitamin A deficiency affected more than 190 million preschool-aged children worldwide, particularly in developing countries [47]. By 2013, the prevalence among children aged 6 to 59 months in low- and middle-income countries was estimated at 29% [48]. In contrast, a 2007 regional study in Korea found that only 2.4% of children aged 2 to 6 years were vitamin A deficient, based on plasma retinol concentrations <0.70 µmol/L [49]. The authors attributed this low prevalence to dietary patterns that rely heavily on plant-based provitamin A carotenoids and the generally good health and balanced nutrition of Korean children [49].

While vitamin A deficiency primarily affects infants and children in low- and middle-income countries, certain individuals, such as preterm infants and those with malabsorptive conditions, including IBD, are also at risk. Premature infants can be vulnerable due to inadequate hepatic vitamin A reserves at birth, with their plasma retinol levels frequently remaining below optimal levels throughout the first year of life. This deficiency is particularly concerning in preterm infants because it increases the risk of developing ocular complications and chronic pulmonary disease [50].

Vitamin D

Vitamin D is synthesized primarily (80%–90%) in the skin upon ultraviolet-B (290–320 nm) exposure, influenced by factors such as skin type, latitude, season, age, and obesity [51]. Only a small portion of vitamin D is provided by the diet, mainly fatty fish (e.g., salmon and mackerel), cod liver oil, and egg yolks, whereas mushrooms contain ergocalciferol [52]. Once produced or ingested, vitamin D binds to vitamin D-binding protein, is hydroxylated in the liver to form 25-hydroxy vitamin D (25(OH)D), and is converted in the kidneys to its active form, 1,25-dihydroxy vitamin D (1,25(OH)D) [53]. Vitamin D aids in calcium absorption in the intestine, maintains adequate calcium and phosphate levels for bone formation, and prevents hypocalcemia. It is also critical for bone remodeling, immune function, and glucose metabolism [54].

In Korea, while the Ministry of Health and Welfare and osteoporosis guidelines consider ≥20 ng/mL as appropriate for skeletal health, clinical practice commonly adopts the criteria of <10 ng/mL for deficiency and <30 ng/mL for insufficiency. The criteria for vitamin D status varies internationally [55]. The U.S. National Institutes of Health considers serum 25(OH)D concentrations <12 ng/mL as deficient, 12 to 20 ng/mL as potentially inadequate, and ≥20 ng/mL as sufficient for most people, with levels >50 ng/mL potentially associated with adverse effects [56].

Vitamin D deficiency is a significant public health concern across various countries and age groups. Data from the KNHANES (2008–2011) demonstrated that among adolescents aged 10 years to 18 years, the prevalence of vitamin D deficiency (<20 ng/mL) and insufficiency (20–29.9 ng/mL) was 73.3% and 24.4%, respectively [57]. Similar patterns were observed in other Asian countries. Studies from Japan have indicated that among 2-year-old children, 24.7% were classified as vitamin D deficient and 51.3% showed insufficient levels [58]. A Chinese study revealed that approximately 66% of children and adolescents aged 6 to 17 years had a suboptimal vitamin D status, using 20 ng/mL as the cutoff value [59]. In the United States, 70% of children and adolescents had suboptimal vitamin D levels (9% deficient and 61% insufficient) [60].

These deficiencies can result from low dietary intake, inadequate sun exposure, impaired renal conversion, or malabsorption. Severe deficiency may cause rickets in children and osteomalacia in adolescents [61]. The risk of vitamin D deficiency is influenced by multiple factors, such as dark skin pigmentation, geographical location (northern latitudes) during winter, consistent use of high sun protection factor sunscreen, cultural practices involving extensive body coverage with clothing, air pollution exposure, and a predominantly indoor lifestyle [62]. These risk factors are likely to be relevant to Korean adolescents.

Children and adolescents who are obese are known to be at risk for vitamin D deficiency or insufficiency [63]. Recent meta-analyses have also confirmed the association between obesity and vitamin D deficiency in adolescents [64]. However, these findings do not conclusively determine whether obesity causes vitamin D deficiency or vice versa. Possible mechanisms include subcutaneous fat-sequestering of vitamin D (limiting its bioavailability), obesity-related leptin pathways inhibiting renal activation, decreased sun exposure, and inadequate dietary intake [65,66]. Some studies have suggested that vitamin D deficiency contributes to obesity through its potential effects on insulin sensitivity and lipid metabolism [67,68]. Obese populations may require higher doses of oral vitamin D supplements [65]; however, the effects of these supplements on metabolic and cardiovascular outcomes remain uncertain. Meta-analyses in adults suggest possible reductions in body mass index and waist circumference with supplementation [69], while pediatric studies (children 6–14 years old) have generally indicated no significant changes in body composition [70,71].

Lactating mothers and their exclusively breastfed infants are considered at high risk for vitamin D deficiency, as human milk typically contains limited amounts of vitamin D (≤25–78 IU/L), with concentrations heavily influenced by maternal vitamin D status [72]. The WHO recommends 200 IU/day of vitamin D for infants [73], and the AAP recommends vitamin D supplementation of 400 IU/day for all infants from birth, including exclusively and partially breastfed infants, continuing until they consume at least 1,000 mL/day of vitamin D-fortified formula or whole milk [72]. The ESPGHAN guidelines recommend oral vitamin D supplementation at 400 IU/day for all infants [74]. The Korean Society of Pediatric Endocrinology suggests a higher supplementation of 400 to 600 IU/day for infants [75]. While sunlight exposure can facilitate vitamin D production in infants, the AAP recommends protecting infants under 6 months of age from direct sunlight through protective clothing and limited sunscreen use when sun exposure cannot be avoided [76].

Iodine

Iodine is a critical component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). Thyroid function is mainly regulated by thyroid-stimulating hormone (TSH), also known as thyrotropin, which is secreted by the pituitary gland. Iodine deficiency can cause a continuous increase in TSH levels, leading to the development of goiter [77]. Earth’s soil contains varying amounts of iodine, which affects the iodine content of crops. Iodine-deficient soils are common in some areas, increasing the risk of iodine deficiency in people consuming local foods. Salt iodization programs have significantly reduced the global prevalence of iodine deficiency globally [35]. Seaweed such as kelp and nori is among the best food sources of iodine. Other seafood and eggs also contain iodine [78].

Iodine status is most effectively evaluated through urinary iodine concentration (UIC), which serves as a sensitive biomarker of current iodine intake because approximately 90% of absorbed iodine is excreted in the urine [79]. While other assessment methods include measuring thyroid size and serum thyroid hormone levels, spot urine measurements are particularly useful as population-level indicators [80]. According to the WHO classification, a median UIC of 100 to 199 μg/L in school-aged children indicates adequate iodine status, while levels <100 μg/L suggest deficiency [81]. Global estimates indicate that 29.8% of school-aged children have insufficient iodine intake [82]. In Korea, an analysis of KNHANES data from 2013 to 2015 showed that only 6.6% of adolescents aged 10 to 18 years had inadequate iodine levels [83].

Iodine deficiency disorders arise when the body cannot produce an adequate level of thyroid hormones owing to insufficient iodine. Their impact can range from mild developmental issues to severe conditions, such as congenital iodine deficiency syndrome, characterized by severe intellectual impairment, hearing loss, muscle spasticity, restricted growth, and delayed sexual development [78]. Prolonged or profound deficiencies can have irreversible effects, particularly during pregnancy or infancy. Consuming <10 to 20 μg of iodine per day may cause hypothyroidism, with goiter often an early sign. In women who are pregnant, deficiency increases the risk of fetal neurodevelopmental deficits, growth retardation, miscarriage, and stillbirth [77].

A meta-analysis showed that lower maternal iodine status in the first trimester was associated with lower verbal intelligence quotient (IQ) in children aged 1.5 to 8 years [84]. Even a mild-to-moderate lack of iodine during pregnancy can compromise fetal development and is linked to a higher incidence of attention deficit hyperactivity disorder in offspring [85]. A meta-analysis found that children (≤5 years old) of iodine-deficient mothers could score 6.910.2 IQ points lower than those of iodine-replete mothers [86]. Research also suggests the partial reversibility of deficits in older children. Two RCTs indicated significant cognitive gains when iodine was provided to school-aged children with mild-to-moderate deficiency (10–12 years in Albania and 10–13 years in New Zealand), indicating that the adverse effects of deficiency may be mitigated, at least until early adolescence [87,88].

Although mild-to-moderate iodine deficiency can adversely affect neurodevelopment, the current evidence remains uncertain as to whether supplementation yields clear benefits in such cases. One RCT found no significant improvements in children’s neurodevelopment by the ages of 5 to 6 years [89], and a systematic review likewise deemed the current data insufficient to establish definitive benefits [90]. Nevertheless, the WHO advises 150 μg/day of iodine for women of childbearing age, rising to 250 μg/day throughout pregnancy and lactation [91]. These guidelines aim to prevent severe deficiencies and mitigate the potential long-term consequences on children’s development, especially in regions without adequate iodized salt programs.

Folate

Folate, an essential water-soluble B vitamin, is found in various foods and is available as a supplement. It plays a crucial role in protein metabolism and DNA and RNA synthesis. Folate participates in two key biochemical processes, converting homocysteine to methionine and methylating deoxyuridylate to form thymidylate, which are critical for DNA synthesis and cell division [92]. Natural food sources of folate include vegetables (particularly spinach, asparagus, and Brussels sprouts), fruits, meat, seafood, dairy products, and liver [92].

Folate status is typically assessed based on serum and red blood cell (RBC) folate levels. Serum folate levels reflect recent dietary or supplemental intake, making them useful for identifying current folate consumption patterns and detecting early signs of folate deficiency. In contrast, RBC folate level reflects long-term status because it remains stable over the 120-day lifespan of erythrocytes and correlates with liver folate stores. This biomarker is commonly used to evaluate chronic folate deficiencies and diagnose conditions associated with folate insufficiency, such as megaloblastic anemia [93]. Folate deficiency is defined as serum levels <6.8 nmol/L, whereas marginal deficiency ranges from 6.8 to 13.4 nmol/L [94]. RBC folate concentrations of <317 nmol/L have been considered indicative of folate deficiency [93].

The prevalence of folate deficiency varies considerably across countries, with reported rates ranging from 1.5% to 40.2% among children and adolescents [95]. In Korea, according to the KNHANES 2013–2015, the prevalence of folate deficiency (<6.8 nmol/L) was 8.6% in males and <2% in females aged ≥10 years [96].

Folate deficiency is relatively rare but is usually seen in conjunction with other nutrient deficiencies, often resulting from poor diet, absorption disorders, or conditions with high cell turnover [92]. Common manifestations of folate deficiency in children include weight loss, headaches, behavioral changes, and stunted growth [97]. Both folate and vitamin B12 are essential for RBC formation and their deficiencies lead to megaloblastic anemia [97]. Insufficient folate intake during pregnancy significantly increases the risk of neural tube defects in infants and is associated with low birth weight, preterm delivery, and fetal growth retardation [92].

To prevent folate deficiency, individuals, especially those in high-risk groups, should consume diets rich in green leafy vegetables and fruits. Daily supplementation with 1 mg of folic acid is typically sufficient for prevention in these populations [98]. Women of childbearing age are strongly recommended to consume folate-rich foods and supplement with at least 0.4 mg of folic acid daily to mitigate the risk of pregnancy complications and fetal anomalies [99].

Conclusion

This comprehensive review demonstrates the fundamental importance of micronutrients in supporting the growth and development of children and adolescents by affecting various physiological processes, including enzymatic activity, immune function, and cellular maintenance. The micronutrients examined (iron, zinc, vitamins A and D, iodine, and folate) exhibit distinct roles and patterns of deficiency. Our review also showed variations in the prevalence of deficiency among nations, with disparities between different age groups. Evidence suggests that while supplementation can be effective, interventions need to be tailored based on individual nutritional status, age-specific requirements, presence of comorbidities, and local dietary patterns. Healthcare providers should remain vigilant in identifying at-risk populations and implementing appropriate interventions, while considering individual and population-specific needs.

Article information

Conflicts of interest

No potential conflict of interest relevant to this article was reported.

Funding

None.

References

• 1. Shenkin A. Micronutrients in health and disease. Postgrad Med J 2006;82:559–67.ArticlePubMedPMCPDF
• 2. Shergill-Bonner R. Micronutrients. Paediatr Child Health 2017;27:357–62.Article
• 3. Ministry of Health and Welfare; The Korean Nutrition Society. Dietary reference intakes for Koreans 2020. Sejong: Ministry of Health and Welfare; 2020.
• 4. Hurrell R, Egli I. Iron bioavailability and dietary reference values. Am J Clin Nutr 2010;91:1461S–1467S.ArticlePubMed
• 5. Aggett PJ. Iron. In: Erdman JW Jr, Macdonald IA, Zeisel SH, editors. Present knowledge in nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012. p. 506–20.
• 6. Wood RJ, Ronnenberg AG. Iron. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern nutrition in health and disease. 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006. p. 248–70.
• 7. Zimmermann MB, Hurrell RF. Nutritional iron deficiency. Lancet 2007;370:511–20.ArticlePubMed
• 8. Lynch S, Pfeiffer CM, Georgieff MK, Brittenham G, Fairweather-Tait S, Hurrell RF, et al. Biomarkers of nutrition for development (BOND)-iron review. J Nutr 2018;148(Suppl 1):1001S–1067S.ArticlePubMedPMC
• 9. Yakoob MY, Lo CW. Nutrition (micronutrients) in child growth and development: a systematic review on current evidence, recommendations and opportunities for further research. J Dev Behav Pediatr 2017;38:665–79.ArticlePubMed
• 10. Iannotti LL, Tielsch JM, Black MM, Black RE. Iron supplementation in early childhood: health benefits and risks. Am J Clin Nutr 2006;84:1261–76.ArticlePubMed
• 11. Lozoff B, Georgieff MK. Iron deficiency and brain development. Semin Pediatr Neurol 2006;13:158–65.ArticlePubMed
• 12. Lee JO, Lee JH, Ahn S, Kim JW, Chang H, Kim YJ, et al. Prevalence and risk factors for iron deficiency anemia in the Korean population: results of the fifth Korea National Health and Nutrition Examination Survey. J Korean Med Sci 2014;29:224–9.ArticlePubMedPMCPDF
• 13. Weyand AC, Chaitoff A, Freed GL, Sholzberg M, Choi SW, McGann PT. Prevalence of iron deficiency and iron-deficiency anemia in US females aged 12-21 years, 2003-2020. JAMA 2023;329:2191–3.ArticlePubMedPMC
• 14. Larocque R, Casapia M, Gotuzzo E, Gyorkos TW. Relationship between intensity of soil-transmitted helminth infections and anemia during pregnancy. Am J Trop Med Hyg 2005;73:783–9.ArticlePubMed
• 15. Mills RJ, Davies MW. Enteral iron supplementation in preterm and low birth weight infants. Cochrane Database Syst Rev 2012;2012:CD005095.ArticlePubMedPMC
• 16. Kleinman RE, Greer FR, editors. Pediatric nutrition. 8th ed. Itasca, IL: American Academy of Pediatrics; 2019.
• 17. Lapillonne A, Bronsky J, Campoy C, Embleton N, Fewtrell M, Fidler Mis N, et al. Feeding the late and moderately preterm infant: a position paper of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition Committee on Nutrition. J Pediatr Gastroenterol Nutr 2019;69:259–70.ArticlePubMed
• 18. Petry N, Olofin I, Boy E, Donahue Angel M, Rohner F. The effect of low dose iron and zinc intake on child micronutrient status and development during the first 1000 days of life: a systematic review and meta-analysis. Nutrients 2016;8:773.ArticlePubMedPMC
• 19. Cantor AG, Bougatsos C, Dana T, Blazina I, McDonagh M. Routine iron supplementation and screening for iron deficiency anemia in pregnancy: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2015;162:566–76.ArticlePubMed
• 20. Baumgartner J, Barth-Jaeggi T. Iron interventions in children from low-income and middle-income populations: benefits and risks. Curr Opin Clin Nutr Metab Care 2015;18:289–94.ArticlePubMed
• 21. Samson KL, Fischer JA, Roche ML. Iron status, anemia, and iron interventions and their associations with cognitive and academic performance in adolescents: a systematic review. Nutrients 2022;14:224.ArticlePubMedPMC
• 22. King JC, Brown KH, Gibson RS, Krebs NF, Lowe NM, Siekmann JH, et al. Biomarkers of nutrition for development (BOND)-zinc review. J Nutr 2015;146:858S–885S.ArticlePubMedPMC
• 23. Ryu MS, Aydemir TB. Zinc. In: Marriott BP, Birt DF, Stallings VA, Yates AA, editors. Present knowledge in nutrition. 11th ed. Cambridge, MA: Wiley-Blackwell; 2020. p. 393–408.
• 24. Sun P, Wang S, Jiang Y, Tao Y, Tian Y, Zhu K, et al. Zip1, Zip2, and Zip8 mRNA expressions were associated with growth hormone level during the growth hormone provocation test in children with short stature. Biol Trace Elem Res 2013;155:11–22.ArticlePubMedPDF
• 25. Roohani N, Hurrell R, Kelishadi R, Schulin R. Zinc and its importance for human health: an integrative review. J Res Med Sci 2013;18:144–57.PubMedPMC
• 26. George AA, Mishra AK, Sahu KK, Sargent J. Acquired acrodermatitis enteropathica. Am J Med 2021;134:e2–3.ArticlePubMed
• 27. International Zinc Nutrition Consultative Group (IZiNCG). Assessing population zinc status with serum zinc concentration. Technical Brief No. 2. Davis, CA: IZiNCG; 2007.
• 28. Hennigar SR, Lieberman HR, Fulgoni VL 3rd, McClung JP. Serum zinc concentrations in the US population are related to sex, age, and time of blood draw but not dietary or supplemental zinc. J Nutr 2018;148:1341–51.ArticlePubMed
• 29. Reider CA, Chung RY, Devarshi PP, Grant RW, Hazels Mitmesser S. Inadequacy of immune health nutrients: intakes in US adults, the 2005-2016 NHANES. Nutrients 2020;12:1735.ArticlePubMedPMC
• 30. Shim JS, Kim KN, Lee JS, Yoon MO, Lee HS. Dietary zinc intake and sources among Koreans: findings from the Korea National Health and Nutrition Examination Survey 2016-2019. Nutr Res Pract 2023;17:257–68.ArticlePubMedPMCPDF
• 31. Ehrlich S, Mark AG, Rinawi F, Shamir R, Assa A. Micronutrient deficiencies in children with inflammatory bowel diseases. Nutr Clin Pract 2020;35:315–22.ArticlePubMedPDF
• 32. Balay KS, Hawthorne KM, Hicks PD, Chen Z, Griffin IJ, Abrams SA. Low zinc status and absorption exist in infants with jejunostomies or ileostomies which persists after intestinal repair. Nutrients 2012;4:1273–81.ArticlePubMedPMC
• 33. Wenk KS, Higgins KB, Greer KE. Cystic fibrosis presenting with dermatitis. Arch Dermatol 2010;146:171–4.ArticlePubMed
• 34. Foster M, Chu A, Petocz P, Samman S. Effect of vegetarian diets on zinc status: a systematic review and meta-analysis of studies in humans. J Sci Food Agric 2013;93:2362–71.ArticlePubMedPDF
• 35. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for vitamin a, vitamin k, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press; 2001.
• 36. Lazzerini M, Ronfani L. Oral zinc for treating diarrhoea in children. Cochrane Database Syst Rev 2013;(1):CD005436.ArticlePubMed
• 37. Kiouri DP, Tsoupra E, Peana M, Perlepes SP, Stefanidou ME, Chasapis CT. Multifunctional role of zinc in human health: an update. EXCLI J 2023;22:809–27.ArticlePubMedPMC
• 38. Lazzerini M, Wanzira H. Oral zinc for treating diarrhoea in children. Cochrane Database Syst Rev 2016;12:CD005436.ArticlePubMed
• 39. Florez ID, Veroniki AA, Al Khalifah R, Yepes-Nuñez JJ, Sierra JM, Vernooij RW, et al. Comparative effectiveness and safety of interventions for acute diarrhea and gastroenteritis in children: a systematic review and network meta-analysis. PLoS One 2018;13:e0207701. ArticlePubMedPMC
• 40. World Health Organization (WHO). Implementing the new recommendations on the clinical management of diarrhoea: guidelines for policy makers and programme managers [Internet]. Geneva: WHO; 2006 [cited 2025 Jan 20]. https://www.who.int/publications/i/item/9241594217.
• 41. Monfared V, Salehian A, Nikniaz Z, Ebrahimpour-Koujan S, Faghfoori Z. The effect of zinc supplementation on anthropometric measurements in healthy children over two years: a systematic review and meta-analysis. BMC Pediatr 2023;23:414.ArticlePubMedPMCPDF
• 42. Cesur Y, Yordaman N, Doğan M. Serum insulin-like growth factor-I and insulin-like growth factor binding protein-3 levels in children with zinc deficiency and the effect of zinc supplementation on these parameters. J Pediatr Endocrinol Metab 2009;22:1137–43.ArticlePubMed
• 43. Blumberg JB, Russell RM. Vitamin A and provitamin A carotenoids. In: Marriott BP, Birt DF, Stallings VA, Yates AA, editors. Present knowledge in nutrition. 11th ed. Cambridge, MA: Wiley-Blackwell; 2020. p. 73–91.
• 44. Carazo A, Macáková K, Matoušová K, Krčmová LK, Protti M, Mladěnka P. Vitamin A update: forms, sources, kinetics, detection, function, deficiency, therapeutic use and toxicity. Nutrients 2021;13:1703.ArticlePubMedPMC
• 45. Perusek L, Maeda T. Vitamin A derivatives as treatment options for retinal degenerative diseases. Nutrients 2013;5:2646–66.ArticlePubMedPMC
• 46. Wiseman EM, Bar-El Dadon S, Reifen R. The vicious cycle of vitamin a deficiency: a review. Crit Rev Food Sci Nutr 2017;57:3703–14.ArticlePubMed
• 47. World Health Organization (WHO). Global prevalence of vitamin A deficiency in populations at risk 1995–2005: WHO global database on vitamin A deficiency [Internet]. Geneva: WHO; 2009 [cited 2025 Jan 20]. https://www.who.int/publications/i/item/9789241598019.
• 48. Stevens GA, Bennett JE, Hennocq Q, Lu Y, De-Regil LM, Rogers L, et al. Trends and mortality effects of vitamin A deficiency in children in 138 low-income and middle-income countries between 1991 and 2013: a pooled analysis of population-based surveys. Lancet Glob Health 2015;3:e528–36.ArticlePubMed
• 49. Kim YN, Giraud DW, Cho YO, Driskell JA. Vitamin A inadequacy observed in a group of 2- to 6-year-old children living in Kwangju, Republic of Korea. Int J Vitam Nutr Res 2007;77:311–9.ArticlePubMed
• 50. Sun H, Cheng R, Wang Z. Early vitamin a supplementation improves the outcome of retinopathy of prematurity in extremely preterm infants. Retina 2020;40:1176–84.ArticlePubMedPMC
• 51. Stechschulte SA, Kirsner RS, Federman DG. Vitamin D: bone and beyond, rationale and recommendations for supplementation. Am J Med 2009;122:793–802.ArticlePubMed
• 52. Park HA, Kim SY. Recent advance on vitamin D. J Korean Med Assoc 2013;56:310–8.Article
• 53. Choi HJ. New insight into the action of vitamin D. Korean J Fam Med 2011;32:89–96.Article
• 54. Jones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, editors. Modern nutrition in health and disease. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2014. p. 278–92.
• 55. Nah EH, Kim S, Cho HI. Vitamin D levels and prevalence of vitamin D deficiency associated with sex, age, region, and season in Koreans. Lab Med Online 2015;5:84–91.Article
• 56. Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, Institute of Medicine; Ross AC, Taylor CL, Yaktine AL, Del Valle HB. Dietary reference intakes for calcium and vitamin D. Washington, DC: National Academies Press; 2011.
• 57. Byun EJ, Heo J, Cho SH, Lee JD, Kim HS. Suboptimal vitamin D status in Korean adolescents: a nationwide study on its prevalence, risk factors including cotinine-verified smoking status and association with atopic dermatitis and asthma. BMJ Open 2017;7:e016409. ArticlePubMedPMC
• 58. Yang L, Sato M, Saito-Abe M, Irahara M, Nishizato M, Sasaki H, et al. 25-Hydroxyvitamin D levels among 2-year-old children: findings from the Japan Environment and Children’s Study (JECS). BMC Pediatr 2021;21:539.ArticlePubMedPMCPDF
• 59. Hu Y, Jiang S, Lu J, Yang Z, Yang X, Yang L. Vitamin D status for Chinese children and adolescents in CNNHS 2016-2017. Nutrients 2022;14:4928.ArticlePubMedPMC
• 60. Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001-2004. Pediatrics 2009;124:e362–70.ArticlePubMedPMCPDF
• 61. Uday S, Högler W. Nutritional rickets and osteomalacia in the twenty-first century: revised concepts, public health, and prevention strategies. Curr Osteoporos Rep 2017;15:293–302.ArticlePubMedPMCPDF
• 62. Tripkovic L, Lambert H, Hart K, Smith CP, Bucca G, Penson S, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr 2012;95:1357–64.ArticlePubMedPMC
• 63. Alemzadeh R, Kichler J, Babar G, Calhoun M. Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season. Metabolism 2008;57:183–91.ArticlePubMed
• 64. Fiamenghi VI, Mello ED. Vitamin D deficiency in children and adolescents with obesity: a meta-analysis. J Pediatr (Rio J) 2021;97:273–9.ArticlePubMedPMC
• 65. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 2000;72:690–3.ArticlePubMed
• 66. Drincic AT, Armas LA, Van Diest EE, Heaney RP. Volumetric dilution, rather than sequestration best explains the low vitamin D status of obesity. Obesity (Silver Spring) 2012;20:1444–8.ArticlePubMedPDF
• 67. Wang L, Wang H, Wen H, Tao H, Zhao X. Relationship between HOMA-IR and serum vitamin D in Chinese children and adolescents. J Pediatr Endocrinol Metab 2016;29:777–81.ArticlePubMed
• 68. Huang K, Jiang YJ, Fu JF, Liang JF, Zhu H, Zhu ZW, et al. The relationship between serum 25-hydroxyvitamin d and glucose homeostasis in obese children and adolescents in Zhejiang, CHINA. Endocr Pract 2015;21:1117–24.ArticlePubMed
• 69. Perna S. Is vitamin D supplementation useful for weight loss programs?: a systematic review and meta-analysis of randomized controlled trials. Medicina (Kaunas) 2019;55:368.ArticlePubMedPMC
• 70. Brzeziński M, Jankowska A, Słomińska-Frączek M, Metelska P, Wiśniewski P, Socha P, et al. Long-term effects of vitamin D supplementation in obese children during integrated weight-loss programme: a double blind randomized placebo-controlled trial. Nutrients 2020;12:1093.ArticlePubMedPMC
• 71. Rajakumar K, Moore CG, Khalid AT, Vallejo AN, Virji MA, Holick MF, et al. Effect of vitamin D3 supplementation on vascular and metabolic health of vitamin D-deficient overweight and obese children: a randomized clinical trial. Am J Clin Nutr 2020;111:757–68.ArticlePubMedPMCPDF
• 72. Wagner CL, Greer FR; American Academy of Pediatrics Section on Breastfeeding; American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008;122:1142–52.ArticlePubMedPDF
• 73. World Health Organization (WHO); Food and Agriculture Organization of the United Nations. Vitamin and mineral requirements in human nutrition [Internet]. 2nd ed. Geneva: WHO; 2004 [cited 2025 Jan 20]. https://www.who.int/publications/i/item/9241546123.
• 74. Płudowski P, Karczmarewicz E, Bayer M, Carter G, Chlebna-Sokół D, Czech-Kowalska J, et al. Practical guidelines for the supplementation of vitamin D and the treatment of deficits in Central Europe - recommended vitamin D intakes in the general population and groups at risk of vitamin D deficiency. Endokrynol Pol 2013;64:319–27.ArticlePubMed
• 75. Lee YA, Kwon A, Kim JH, Nam HK, Yoo JH, Lim JS, et al. Clinical practice guidelines for optimizing bone health in Korean children and adolescents. Ann Pediatr Endocrinol Metab 2022;27:5–14.ArticlePubMedPMCPDF
• 76. Davis CD, Dwyer JT. The “sunshine vitamin”: benefits beyond bone? J Natl Cancer Inst 2007;99:1563–5.ArticlePubMed
• 77. Committee to Assess the Health Implications of Perchlorate Ingestion, National Research Council. Health implications of perchlorate ingestion. Washington, DC: National Academies Press; 2005.
• 78. Zimmermann MB. Iodine deficiency. Endocr Rev 2009;30:376–408.ArticlePubMedPDF
• 79. Wainwright P, Cook P. The assessment of iodine status: populations, individuals and limitations. Ann Clin Biochem 2019;56:7–14.ArticlePubMedPDF
• 80. Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev 2008;13:116–27.PubMed
• 81. World Health Organization (WHO). Iodine deficiency [Internet]. Geneva: WHO; 2023 [cited 2025 Jan 20]. https://www.who.int/data/nutrition/nlis/info/iodine-deficiency.
• 82. Andersson M, Karumbunathan V, Zimmermann MB. Global iodine status in 2011 and trends over the past decade. J Nutr 2012;142:744–50.ArticlePubMed
• 83. Choi YC, Cheong JI, Chueh HW, Yoo JH. Iodine status and characteristics of Korean adolescents and their parents based on urinary iodine concentration: a nationwide cross-sectional study. Ann Pediatr Endocrinol Metab 2019;24:108–115.ArticlePubMedPMCPDF
• 84. Levie D, Korevaar TI, Bath SC, Murcia M, Dineva M, Llop S, et al. Association of maternal iodine status with child IQ: a meta-analysis of individual participant data. J Clin Endocrinol Metab 2019;104:5957–67.ArticlePubMedPMCPDF
• 85. Abel MH, Brandlistuen RE, Caspersen IH, Aase H, Torheim LE, Meltzer HM, et al. Language delay and poorer school performance in children of mothers with inadequate iodine intake in pregnancy: results from follow-up at 8 years in the Norwegian Mother and Child Cohort Study. Eur J Nutr 2019;58:3047–58.ArticlePubMedPMCPDF
• 86. Bougma K, Aboud FE, Harding KB, Marquis GS. Iodine and mental development of children 5 years old and under: a systematic review and meta-analysis. Nutrients 2013;5:1384–416.ArticlePubMedPMC
• 87. Zimmermann MB, Connolly K, Bozo M, Bridson J, Rohner F, Grimci L. Iodine supplementation improves cognition in iodine-deficient schoolchildren in Albania: a randomized, controlled, double-blind study. Am J Clin Nutr 2006;83:108–14.ArticlePubMed
• 88. Gordon RC, Rose MC, Skeaff SA, Gray AR, Morgan KM, Ruffman T. Iodine supplementation improves cognition in mildly iodine-deficient children. Am J Clin Nutr 2009;90:1264–71.ArticlePubMed
• 89. Gowachirapant S, Jaiswal N, Melse-Boonstra A, Galetti V, Stinca S, Mackenzie I, et al. Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. Lancet Diabetes Endocrinol 2017;5:853–63.ArticlePubMed
• 90. Dineva M, Fishpool H, Rayman MP, Mendis J, Bath SC. Systematic review and meta-analysis of the effects of iodine supplementation on thyroid function and child neurodevelopment in mildly-to-moderately iodine-deficient pregnant women. Am J Clin Nutr 2020;112:389–412.ArticlePubMedPDF
• 91. World Health Organization (WHO); United Nations Children's Fund; International Council for the Control of Iodine Deficiency Disorders. Assessment of iodine deficiency disorders and monitoring their elimination: a guide for programme managers [Internet]. 3rd ed. Geneva: WHO; 2007 [cited 2025 Jan 20]. https://www.who.int/publications/i/item/9789241595827.
• 92. Bailey LB, Caudill MA. Folate. In: Erdman JW Jr, Macdonald IA, Zeisel SH, editors. Present knowledge in nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012. p. 321–42.
• 93. Bailey LB, Stover PJ, McNulty H, Fenech MF, Gregory JF 3rd, Mills JL, et al. Biomarkers of nutrition for development: folate review. J Nutr 2015;145:1636S–1680S.ArticlePubMedPMC
• 94. World Health Organization (WHO). Serum and red blood cell folate concentrations for assessing folate status in populations [Internet]. Geneva: WHO; 2014 [cited 2025 Jan 20]. https://www.who.int/publications/i/item/WHO-NMH-NHD-EPG-15.01.
• 95. Khanam A, Gupta S, Singh N, Vohra K, Yadav K. Prevalence of serum cobalamin and serum folate deficiency with associated risk factors among children aged 0 to 19 years in India-a review. Indian J Nutr Diet 2022;59:524–36.ArticlePDF
• 96. Song S, Song BM, Park HY. Folate, vitamin B12, and homocysteine status in the Korean population: data from the 2013-2015 Korea National Health and Nutrition Examination Survey. Epidemiol Health 2024;46:e2024007. ArticlePubMedPDF
• 97. Haslam N, Probert CS. An audit of the investigation and treatment of folic acid deficiency. J R Soc Med 1998;91:72–3.ArticlePubMedPMCPDF
• 98. Centers for Disease Control and Prevention (CDC). CDC Grand Rounds: additional opportunities to prevent neural tube defects with folic acid fortification. MMWR Morb Mortal Wkly Rep 2010;59:980–4.PubMed
• 99. Wilson RD; Genetics Committee; Wilson RD, Audibert F, Brock JA, Carroll J, et al. Pre-conception folic acid and multivitamin supplementation for the primary and secondary prevention of neural tube defects and other folic acid-sensitive congenital anomalies. J Obstet Gynaecol Can 2015;37:534–52.ArticlePubMed

Figure & Data

References

Citations

Citations to this article as recorded by