Contents
The period of childhood between ages 4 and 13 years is characterized by continued physical growth and rapid cognitive, emotional, and social development (1, 2). Many children, especially girls, undergo their pubertal growth spurt between ages 4 and 13. This period of childhood precedes adolescence — the transitional stage of development between childhood and adulthood. Due to increased growth and metabolism, the nutritional requirements of children are higher in proportion to body weight compared with adults (1, 3). Good nutrition throughout childhood is important not only to support normal growth and cognitive development but also to establish healthy eating patterns that are associated with decreased risk of chronic conditions and diseases in adulthood, including obesity, type 2 diabetes, cardiovascular disease, metabolic syndrome, and osteoporosis.
Inadequate intake of nutrients can impair growth and development in children. This article discusses micronutrient (vitamins and nutritionally essential minerals) requirements of children ages 4 to 13 years. The Food and Nutrition Board (FNB) of the Institute of Medicine establishes dietary reference intakes (DRIs) for each micronutrient; these reference values should be used to plan and assess dietary intakes in healthy people (4, 5). The DRIs include the estimated average requirement (EAR), the recommended dietary allowance (RDA), the adequate intake (AI), and the tolerable upper intake level (UL). The RDA, which is the average daily dietary intake level of a nutrient sufficient to meet the requirements of almost all (97.5%) healthy individuals in a specific life stage and gender group, should be used in the planning of diets for individuals (6). An AI recommendation is set when an RDA cannot be determined. In children, these intake recommendations are based on data regarding average micronutrient intakes of children and also on certain criteria for micronutrient adequacy. However, because of limited data, many of the micronutrient intake recommendations for children are extrapolated from recommendations for adults using a formula that accounts for metabolic body weight and growth (3). Metabolic body weight is determined by calculating the 0.75 power of body mass (body mass^0.75) (7). To account for growth, the equation used to derive an RDA or AI involves an age group-specific growth factor (3). The FNB establishes separate dietary intake recommendations for children between the ages of 4 to 8 years and those between the ages of 9 and 13 years (see Ages 4 to 8 Years and Ages 9 to 13 Years).
For each micronutrient, the FNB sets an RDA or AI for children ages 4 to 8 years; these micronutrient intake recommendations do not differ with gender for this age group. Table 1 lists the RDA for each micronutrient. As mentioned above, the RDA should be used in the planning of diets for individuals. A few select micronutrient requirements for children are discussed below.
Micronutrient | Males and Females |
---|---|
Biotin | 12 μg/day (AI) |
Folate | 200 μg/daya |
Niacin | 8 mg/dayb |
Pantothenic Acid | 3 mg/day (AI) |
Riboflavin | 600 μg/day |
Thiamin | 600 μg/day |
Vitamin A | 400 μg/day (1,333 IU/day)c |
Vitamin B6 | 600 μg/day |
Vitamin B12 | 1.2 μg/day |
Vitamin C | 25 mg/day |
Vitamin D | 15 μg/day (600 IU/day) |
Vitamin E | 7 mg/day (10.5 IU/day)d |
Vitamin K | 55 μg/day (AI) |
Calcium | 1,000 mg/day |
Chromium | 15 μg/day (AI) |
Copper | 440 μg/day |
Fluoride | 1 mg/day (AI) |
Iodine | 90 μg/day |
Iron | 10 mg/day |
Magnesium | 130 mg/day |
Manganese | 1.5 mg/day (AI) |
Molybdenum | 22 μg/day |
Phosphorus | 500 mg/day |
Potassium | 2,300 mg/day (AI) |
Selenium | 30 μg/day |
Sodium | 1,000 mg/day (AI) |
Zinc | 5 mg/day |
Cholinee | 250 mg/day (AI) |
α-Linolenic Acide | 900 mg/day (AI) |
Linoleic Acide | 10 g/day (AI) |
AI, adequate intake aDietary Folate Equivalents bNE, niacin equivalent: 1 mg NE = 60 mg tryptophan = 1 mg niacin cRetinol Activity Equivalents dα-Tocopherol eConsidered an essential nutrient, although not strictly a micronutrient |
For each micronutrient, the FNB sets an RDA or AI for children ages 9 to 13 years; these recommendations are gender specific to account for the unique nutritional needs of boys and girls as they undergo puberty. Table 2 lists the RDA for each micronutrient by gender. The RDA should be used in the planning of diets for individuals. A more detailed discussion of the requirements of certain micronutrients for children can be found below.
Micronutrient | Males | Females |
---|---|---|
Biotin | 20 μg/day (AI) | 20 μg/day (AI) |
Folate | 300 μg/daya | 300 μg/daya |
Niacin | 12 mg/dayb | 12 mg/dayb |
Pantothenic Acid | 4 mg/day (AI) | 4 mg/day (AI) |
Riboflavin | 900 μg/day | 900 μg/day |
Thiamin | 900 μg/day | 900 μg/day |
Vitamin A | 600 μg/day (2,000 IU/day)c | 600 μg/day (2,000 IU/day)c |
Vitamin B6 | 1 mg/day | 1 mg/day |
Vitamin B12 | 1.8 μg/day | 1.8 μg/day |
Vitamin C | 45 mg/day | 45 mg/day |
Vitamin D | 15 μg/day (600 IU/day) | 15 μg/day (600 IU/day) |
Vitamin E | 11 mg/day (16.5 IU/day)d | 11 mg/day (16.5 IU/day)d |
Vitamin K | 60 μg/day (AI) | 60 μg/day (AI) |
Calcium | 1,300 mg/day | 1,300 mg/day |
Chromium | 25 μg/day (AI) | 21 μg/day (AI) |
Copper | 700 μg/day | 700 μg/day |
Fluoride | 2 mg/day (AI) | 2 mg/day (AI) |
Iodine | 120 μg/day | 120 μg/day |
Iron | 8 mg/day | 8 mg/day |
Magnesium | 240 mg/day | 240 mg/day |
Manganese | 1.9 mg/day (AI) | 1.6 mg/day (AI) |
Molybdenum | 34 μg/day | 34 μg/day |
Phosphorus | 1,250 mg/day | 1,250 mg/day |
Potassium | 2,500 mg/day (AI) | 2,300 mg/day (AI) |
Selenium | 40 μg/day | 40 μg/day |
Sodium | 1,200 mg/day (AI) | 1,200 mg/day (AI) |
Zinc | 8 mg/day | 8 mg/day |
Cholinee | 375 mg/day (AI) | 375 mg/day (AI) |
α-Linolenic Acide | 1,200 mg/day (AI) | 1,000 mg/day (AI) |
Linoleic Acide | 12 g/day (AI) | 10 g/day (AI) |
AI, adequate intake aDietary Folate Equivalents bNE, niacin equivalent: 1 mg NE = 60 mg tryptophan = 1 mg niacin cRetinol Activity Equivalents dα-Tocopherol eConsidered an essential nutrient, although not strictly a micronutrient |
Vitamin A is a fat-soluble vitamin that is essential for growth and development, normal vision, the expression of selected genes, and immunity (see the article on Vitamin A). Vitamin A deficiency is a major public health problem worldwide. It is the leading preventable cause of blindness among children in developing nations (8). The earliest evidence of vitamin A deficiency is impaired dark adaptation or night blindness. Mild vitamin A deficiency may result in Bitot’s spots, which are changes in the conjunctiva (the mucous membrane that lines the eyelids and the outer surface of the eye). Severe or prolonged vitamin A deficiency causes a condition called xerophthalmia (dry eye), characterized by changes in the cells of the cornea (clear covering of the eye) that ultimately result in corneal ulcers, scarring, and blindness (9, 10).
Vitamin A deficiency also places children at a heightened risk for infectious disease; in fact, vitamin A deficiency can be considered a nutritionally acquired immunodeficiency disorder (11). Even children who are only mildly deficient in vitamin A have a higher incidence of respiratory disease and diarrhea, as well as a higher rate of mortality from infectious disease, compared to children who consume sufficient vitamin A (12). Vitamin A supplementation in children has been found to decrease both the severity and incidence of deaths related to diarrhea and measles in developing countries, where vitamin A deficiency is common (13). The onset of infection reduces blood retinol (preformed vitamin A) levels very rapidly. This phenomenon is generally believed to be related to decreased synthesis of retinol binding protein (RBP) by the liver. In this manner, infection stimulates a vicious cycle, because inadequate vitamin A nutritional status is related to increased severity and likelihood of death from infectious disease (14).
The RDA for vitamin A is based on the amount needed to ensure adequate stores (four months) of vitamin A in the body to support normal reproductive function, immune function, vitamin A-dependent gene expression, and vision (15). Vitamin A intake recommendations for children were derived by extrapolating the recommendation for adults using metabolic body weight, accounting for growth. The RDA for children ages 4 to 8 years is 400 μg/day of Retinol Activity Equivalents (RAE), which is 1,333 international units (IU); the RDA for both boys and girls ages 9 to 13 years is 600 μg/day of RAE, which is equivalent to 2,000 IU. For information on vitamin A content in foods, see the article on Vitamin A.
Vitamin B12 is needed for two sorts of reactions in the human body. One is transmethylation (methyl transfer between two molecules) that leads to the synthesis of the amino acid methionine from homocysteine. Methionine, in turn, is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions, such as the methylation of sites within DNA and RNA (16). The second sort of reaction is isomerization (rearrangement of a molecule). Vitamin B12 acts as a coenzyme for methylmalonyl-CoA mutase to convert methylmalonyl-CoA to succinyl-CoA, an important step for the metabolism of proteins and lipids. Both transmethylation and isomerization reactions are essential for the metabolism of components of the myelin sheath of nerve cells and for the metabolism of neurotransmitters. Accordingly, vitamin B12 deficiency damages the myelin sheath covering cranial, spinal, and peripheral nerves, resulting in neurological damage (17, 18). The myelin sheath is the insulating layer of tissue made up of lipids and proteins that surrounds nerve fibers. This sheath acts as a conduit in an electrical system, allowing rapid and efficient transmission of nerve impulses (19). In some cases, neurologic symptoms caused by vitamin B12 deficiency can be reversed by vitamin treatment (18), but reversibility seems to be dependent upon the duration of the associated neurologic complications (20).
Although myelination primarily occurs during fetal development and early infancy, it continues through childhood, adolescence, and stages of early adulthood (21, 22). Because of the role of vitamin B12 in myelination and other metabolic processes, it is important for children to meet dietary intake recommendations. The RDA of vitamin B12 for children ages 4 to 8 years is 1.2 μg/day, and the RDA for boys and girls ages 9 to 13 years is 1.8 μg/day. This vitamin is naturally present only in animal products, such as meat, poultry, fish (including shellfish), and to a lesser extent in milk, but it is not generally present in plant products or yeast (9). Thus, children who have vegan diets need supplemental vitamin B12 or need adequate intake from fortified foods.
Vitamin C has a number of important roles during growth and development, including being required for the synthesis of collagen, carnitine, and neurotransmitters (23). Vitamin C is also a highly effective antioxidant and is important for immunity (see the article on Immunity). Further, vitamin C strongly enhances the absorption of non heme iron by reducing dietary ferric iron (Fe3+) to ferrous iron (Fe2+) and forming an absorbable, iron-ascorbic acid complex. Specifically, iron absorption is 2- to 3-fold higher with co-ingestion of 25 to 75 mg of vitamin C (24). This has special relevance to child health, considering the fact that iron deficiency is the most common nutrient deficiency in the world (see Iron below). Vitamin C intake recommendations for children are extrapolated from recommendations for adults based on relative body weight. The RDA for children ages 4 to 8 years is 25 mg/day, and the RDA for boys and girls ages 9 to 13 years is 45 mg/day (25). For information on food sources, see the article on Vitamin C.
Vitamin D is a fat-soluble vitamin that is essential for maintaining normal calcium metabolism and is thus necessary for bone health. Severe vitamin D deficiency in infants and children results in the failure of bone to mineralize, leading to a condition known as rickets. Rapidly growing bones are most severely affected by rickets. The growth plates of bones continue to enlarge, but in the absence of adequate mineralization, weight-bearing limbs (arms and legs) become bowed. In severe cases of vitamin D deficiency, low serum calcium levels (hypocalcemia) may induce seizures. Although fortification of foods has led to complacency regarding vitamin D deficiency, nutritional rickets is still being reported in the United States and other nations (26-33).
In the US, fortified foods are a major contributor to dietary vitamin D intake, especially in children, because only a few foods naturally contain vitamin D (see the article on Vitamin D). In the US, milk is voluntarily fortified with 400 IU (10 μg) of vitamin D per quart (946 mL) (34), and other foods may be fortified with varying concentrations of vitamin D. According to a recent report regarding the American food supply, nearly all milk, about 75% of ready-to-eat breakfast cereals, around 50% of milk substitutes, about 25% of yogurts, and 8-14% of juices, cheeses, and spreads are fortified with vitamin D (35). Although not required by the US FDA to be listed on the Nutrition Facts food label, some packaged foods, particularly cereals, include the amount of vitamin D in one serving as the percentage of the Daily Value (DV). The DV is 400 IU, but the RDA for children ages 4 to 8 years and for boys and girls ages 9 to 13 years is 600 IU/day. In Canada, vitamin D fortification of milk and margarine is mandatory, with milk containing 35-45 IU per 100 mL (331-426 IU per quart) and margarine containing 530 IU per 100 grams (34), but vitamin D fortification of foods is less common in European nations (36). In addition to diet, vitamin D can be endogenously synthesized in the skin upon exposure to ultraviolet-B radiation from sunlight; however, sunscreens effectively block synthesis of vitamin D in skin (see the article on Vitamin D).
When setting the RDA for vitamin D, the FNB assumed minimal sun exposure, even though sun exposure could provide most people with their entire vitamin D requirement. For US children to meet the RDA of 600 IU/day (15 μg/day), about 6 cups of milk would need to be consumed each day. Analysis of data from the National Health and Nutrition Examination Survey (NHANES) 2005-2006 found that average total vitamin D intakes (from diet and supplements combined) in US children of ages 4 to 8 were 9.3 μg/day (372 IU/day) for boys and 7.9 μg/day (316 IU/day) for girls (37). Even though the analysis found that 43% of boys and 34% of girls in this age group took supplements containing vitamin D (37), their average total daily intakes were well below the current RDA of 600 IU/day (15 μg/day). Total daily vitamin D intakes were even lower for chilren aged 9 to 13 years (boys, 7.5 μg or 300 IU/day; girls, 7.7 μg or 308 IU/day). Sun exposure can substantially affect body vitamin D levels, and measuring 25-hydroxyvitamin D — the major circulating form of vitamin D — is a useful indicator of vitamin D status. It is assumed that a dietary intake of 600 IU/day results in a serum 25-hydroxyvitamin D level of 50 nmol/L (20 ng/mL), which the FNB considers as the cut-point for vitamin D adequacy (38). However, higher serum 25-hydroxyvitamin D serum levels may benefit health; thus, the Linus Pauling Institute recommends that children ages 4 to 13 years should have a daily intake of 600 to 1,000 IU (15 to 25 μg) of vitamin D, consistent with the recommendations of the Endocrine Society (39). Given the average vitamin D content of the diets of children, supplementation may be necessary to meet these recommendations. The American Academy of Pediatrics currently suggests that all children receive 400 IU of supplemental vitamin D daily (26) — an amount that is typically found in multivitamin supplements.
The tolerable upper intake level (UL) — the highest level of daily intake of a specific nutrient likely to pose no risk of adverse health effects in almost all individuals — for children ages 4 to 8 years is 3,000 IU/day (75 μg/day) of vitamin D; the UL for boys and girls ages 9 to 13 years is 4,000 IU (100 μg/day).
The RDA for vitamin E in children, expressed as an amount of the α-tocopherol form of the vitamin, was based on extrapolations from intake recommendations for adults, accounting for differences in lean body mass and increased needs of growth during childhood. The RDA is 7 mg/day (10.5 IU/day) for children ages 4 to 8 years and 11 mg/day (16.5 IU/day) for boys and girls ages 9 to 13 years (40). A US national survey, NHANES 1999-2000, found that children ages 4 to 8 years had an average intake of 5.2 mg/day of α-tocopherol; this survey found that average α-tocopherol intakes for boys and girls ages 9 to 13 years were 6.0 mg/day and 5.3 mg/day, respectively (41). These intakes are below the current RDA. Surveys in The Republic of Korea and Germany have also reported low intakes of vitamin E in children (42, 43). However, true vitamin E deficiency is rare and has been observed only in cases of severe malnutrition, genetic defects affecting the α-tocopherol protein, and fat malabsorption syndromes; see the article on Vitamin E.
About 99% of calcium in the body is found in bones and teeth (44). Adequate intake of calcium throughout childhood and adolescence is important for proper mineralization of growing bones, attainment of peak bone mass, and reduction of risk for osteoporosis in adulthood (38). Thus, dietary intake recommendations for calcium in children are established based on the calcium intake needed to support bone accretion and overall calcium retention (i.e., the dietary intake needed to achieve positive calcium balance) (38). The RDA is 1,000 mg/day for children ages 4 to 8 years and 1,300 mg/day for boys and girls ages 9 to 13 years. Calcium intake recommendations are higher in children ages 9 to 13 to account for increased needs of the mineral during puberty (38).
Many American children have dietary calcium intakes below current recommendations, with girls having lower intakes than boys. A recent study reported daily calcium intake in children using data from NHANES 2003-2006, a US national survey (37). An estimated 17% of boys and 33% of girls between the ages of 4 and 8 have total calcium intakes (dietary plus supplemental intakes) of 800 mg/day or less. For children in this age group, average intake from supplements in those who took supplemental calcium (29% of boys; 26% of girls) was 99 mg/day and 87 mg/day for boys and girls, respectively. In children 9 to 13 years old, only 23% of boys and 15% of girls met the RDA for calcium, even though 20% of boys and 24% of girls took supplemental calcium (average supplemental calcium intake of 104 mg/day for boys and 80 mg/day for girls) (37). Dairy products, which provide about 72% of the calcium in the American diet (44), represent rich and absorbable sources of calcium. Milk contains 300 mg of calcium per cup; therefore, children ages 4 to 8 and children ages 9 to 13 could meet the RDA for calcium by drinking 3.3 or 4.3 cups of milk daily, respectively. Certain vegetables and grains also provide calcium, but their bioavailability is lower compared with dairy. For more information on dietary sources of calcium and calcium bioavailability, see the article on Calcium. If children do not meet the RDA through diet alone, LPI recommends supplemental calcium. Children’s multivitamin/mineral supplements generally provide no more than 150 mg of calcium.
The Nutrition Facts label of packaged foods lists calcium content in one serving as a percent of the Daily Value (DV), with the DV being 1,000 mg. Since the RDA for children ages 4 to 8 is 1,000 mg/day, the listed amount of calcium on the food label directly provides a percentage of the RDA. However, because the RDA for children ages 9 to 13 years is higher, the percentage of the DV listed would be an overestimation of the percentage of the RDA.
The mineral fluoride is important for the prevention of dental caries (tooth decay). Specific cariogenic (cavity-causing) bacteria found in dental plaque are capable of metabolizing certain carbohydrates (sugars) and converting them to organic acids that can dissolve tooth enamel. If unchecked, the bacteria may penetrate deeper layers of the tooth and progress into the soft pulp tissue at the center. Untreated caries can lead to severe pain, local infection, tooth loss or extraction, nutritional problems, and serious systemic infections in susceptible individuals (45). Increased fluoride exposure, most commonly through water fluoridation, has been found to decrease dental caries (46). Fluoride consumed in water appears to have a systemic effect in children before teeth erupt, as well as a topical (surface) effect in children and adults after teeth have erupted. The FNB set an adequate intake (AI) recommendation based on estimated intakes (0.5 mg/kg of body weight) that have been shown to reduce the occurrence of dental caries most effectively without causing the unwanted side effect of tooth enamel mottling, a white speckling or mottling of the permanent teeth known as dental fluorosis (47). The AI of fluoride for children ages 4 to 8 years is 1 mg/day, and the AI for boys and girls ages 9 to 13 years is 2 mg/day. For information about sources of fluoride, see the article on Fluoride.
Additionally, fluoridated toothpastes are very effective in preventing dental caries but add considerably to fluoride intake of children, especially young children who are more likely to swallow toothpaste. Researchers estimate that children under 6 years of age ingest an average of 0.3 mg of fluoride from toothpaste with each brushing, and swallowing fluoride-containing toothpaste is a major source of excess fluoride intake in this age group. Children who ingest more than two or three times the recommended fluoride intake are at increased risk of dental fluorosis. To prevent dental fluorosis while providing optimum protection from tooth decay, it is recommended that parents supervise children under 6 years of age while brushing with fluoridated toothpaste. In addition to discouraging the swallowing of toothpaste, children should be encouraged to use no more than a pea-size application of toothpaste and to rinse their mouths with water after brushing (47, 48). Fluoride supplements, available only by prescription, are intended for children living in areas with low water fluoride concentrations for the purpose of bringing their intake to approximately 1 mg/day (47). For more information about dental fluorosis, see the article on Fluoride.
Iodine is required for the synthesis of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4). To meet the body's demand for thyroid hormones, the thyroid gland traps iodine from the blood and incorporates it into thyroid hormones that are stored and released into the circulation when needed. In target tissues, such as the liver and the brain, T3, the physiologically active thyroid hormone, can bind to thyroid receptors in the nuclei of cells and regulate gene expression. In target tissues, T4, the most abundant circulating thyroid hormone, can be converted to T3 by selenium-containing enzymes known as deiodinases. In this manner, thyroid hormones regulate a number of physiologic processes, including growth, development, metabolism, and reproductive function (49, 50).
Iodine deficiency is now accepted as the most common cause of preventable brain damage in the world. The spectrum of iodine deficiency disorders (IDD) includes mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities (49, 51). Iodine deficiency is associated with goiter; the incidence of goiter is higher in girls than boys. Children in iodine-deficient areas show poorer school performance, lower IQs, and a higher incidence of learning disabilities than matched groups from iodine-sufficient areas. A meta-analysis of 18 studies concluded that iodine deficiency alone lowered mean IQ scores in children by 13.5 points (52, 53).
Global estimates indicate that 31.5% of children between the ages of 6 and 12 years (266 million total children) has insufficient iodine intake (54). Major international efforts have produced dramatic improvements in the correction of iodine deficiency in the 1990s, mainly through the use of iodized salt in iodine-deficient countries (55). Today, 70% of households in the world use iodized salt (57), but iodine deficiency in children is still a major public health concern worldwide (57-59). For more information on the international effort to eradicate iodine deficiency, visit the websites of the Iodine Global Network or the World Health Organization.
The RDA of iodine for children aged 4 to 8 years is 90 μg/day, and the RDA for boys and girls aged 9 to 13 years is 120 μg/day. The intake recommendation for children in this younger age group was based on results of a balance study in eight-year-old children who did not have goiters (60). Results of a balance study in children ages 9 to 13 years indicated that a minimum of 55 μg/day of iodine is needed (60), but the RDA for this older age group was set by extrapolating from the adult recommendation based on metabolic body weight (55). The amount of iodine in iodized salt and the contribution of iodized salt to total iodine intake vary by nation. In the US, iodized salt contains an average of 45 mg of iodine per kilogram and 20% of the salt consumed by Americans is iodized. Salt used in processed foods and the fast food industry is generally not iodized (61). However, the US is currently considered to be iodine-sufficient (62). Seafood is rich in iodine because marine animals can concentrate the iodine from seawater, and certain types of seaweed (e.g., wakame) are also very rich in iodine (see Table 3 in the article on Iodine). Dairy products are also relatively good sources of iodine. However, iodine content of plant foods depends on the iodine content of the soil (63).
Iron is an essential component of hundreds of proteins and enzymes involved in various aspects of metabolism, including oxygen transport and storage, electron transport and energy metabolism, antioxidant and beneficial pro-oxidant functions, oxygen sensing, and DNA synthesis (9, 64-68); see the article on Iron). Iron is stored in the body as ferritin, and serum level of ferritin is a good clinical indicator of iron status in children (69). Iron deficiency, which is the most common nutritional deficiency in the world, is a major public health problem, especially in developing nations, but it is also prevalent in industrialized nations. Severe iron deficiency leads to iron-deficiency anemia, which affects more than 30% of the global population (2 billion people) (70). Iron-deficiency anemia results when there is inadequate iron to support normal red blood cell formation. The anemia of iron deficiency is characterized as microcytic and hypochromic, meaning red blood cells are measurably smaller than normal and their hemoglobin content is decreased. At this most severe stage of iron deficiency, symptoms may be a result of inadequate oxygen delivery due to anemia and/or sub-optimal function of iron-dependent enzymes. Low red cell count, low hematocrit, and low hemoglobin concentrations are all used in the clinical diagnosis of iron-deficiency anemia (71).
Most observational studies have found relationships between iron-deficiency anemia in children and poor cognitive development, poor school achievement, and behavior problems. However, it is difficult to separate the effects of iron-deficiency anemia from other types of deprivation in such studies, and confounding factors may contribute to the association between iron deficiency and cognitive deficits (72). Yet, several possible mechanisms link iron-deficiency anemia to altered cognition. For example, any cognitive benefit associated with iron supplementation could be possibly due to changes in nerve myelination, which have been observed in iron-deficient animals (73). Iron has an important role in the development of the cells that produce myelin (74); as noted above, the myelin sheath is the insulating layer of tissue comprised of lipids and proteins that surrounds nerve fibers. This sheath acts as a conduit in an electrical system, allowing for rapid and efficient transmission of nerve impulses (19). Iron is also important for enzymes involved in the synthesis of certain neurotransmitters and for DNA synthesis (75).
Children between the ages of 4 and 13 years are at lower risk of iron deficiency compared to younger or older children because infants, toddlers, and adolescents generally have higher growth rates (9). The RDA of iron for children ages 4 to 8 years is 10 mg/day, and the RDA for boys and girls ages 9 to 13 years is 8 mg/day. Girls in this latter age group who start to menstruate need an additional 2.5 mg/day of iron. These intake recommendations were based on a factorial modeling approach that accounts for the amount of iron needed to replace basal losses (losses in urine, feces, and sweat) and the iron requirements associated with growth (increases in hemoglobin, the oxygen-carrying pigment in red blood cells mass; increases in iron content of tissues; and for the younger age group, increases in iron storage). The intake recommendations also account for average bioavailability (the fraction of iron retained and used by the body) of dietary iron in these age groups (76).
The amount of bioavailable iron in food (or supplements) is influenced by the iron nutritional status of the individual and also by the form of iron (heme or nonheme). Individuals who are anemic or iron deficient absorb a larger percentage of the iron they consume (especially nonheme iron) than individuals who are not anemic and have sufficient iron stores (77, 78). In addition, heme iron, found in meat, poultry, and fish, is more readily absorbed and its absorption is less affected by other dietary factors than nonheme iron — the form found in plants, dairy products, fortified foods, and supplements. Although heme iron generally accounts for only 10-15% of the iron found in the diet, it may provide up to one third of total absorbed dietary iron (67, 77). The absorption of nonheme iron is strongly influenced by enhancers and inhibitors present in the same meal (77, 78). For instance, vitamin C strongly enhances the absorption of nonheme iron by reducing dietary ferric iron (Fe3+) to ferrous iron (Fe2+) and forming an absorbable, iron-ascorbic acid complex. Organic acids, such as citric, malic, tartaric, and lactic acids, also enhance nonheme iron absorption. Further, consumption of meat, poultry, and fish enhance nonheme iron absorption, but the mechanism for this increase in absorption is not clear (76, 77). Inhibitors of nonheme iron absorption include phytic acid, which is present in legumes, grains, and rice. In fact, small amounts of phytic acid (5 to 10 mg) can reduce nonheme iron absorption by 50%. The absorption of iron from legumes, such as soybeans, black beans, lentils, mung beans, and split peas, has been shown to be as low as 2% <a href=">(64, 76). Additionally, polyphenols found in some fruit, vegetables, coffee, tea, wines, and spices can markedly inhibit the absorption of nonheme iron, but this effect is reduced by the presence of vitamin C (64, 76). Soy protein, such as that found in tofu, has an inhibitory effect on iron absorption that is independent of its phytic acid content (76).
The mineral magnesium is involved in more than 300 essential metabolic reactions that are generally involved in energy production and the synthesis of nucleic acids (DNA and RNA), proteins, carbohydrates, and lipids (79). Magnesium also plays structural roles in bone, cell membranes, and chromosomes and is also required for various cellular processes, including ion transport across cell membranes, cell signaling, and cell migration (80).
The RDA of magnesium for children ages 4 to 8 years, which is 130 mg/day, was derived by extrapolating data from magnesium balance studies in older children (79). The RDA for boys and girls ages 9 to 13 years is 240 mg/day. This recommendation was based on data from magnesium balance studies in children of this age (81, 82). Good dietary sources of magnesium include nuts and green leafy vegetables because magnesium is part of chlorophyll — the green pigment in plants. Meats and milk have an intermediate magnesium content, with milk providing 24-39 mg per cup (79, 83). Refined foods generally have the lowest magnesium content. Analysis of data from the NHANES study found that US children ages 2 to 12 years who consumed three or more daily servings of whole grains had significantly increased magnesium intakes (84).
The 2010 Dietary Guidelines for Americans recommend that children should limit their sodium intake to 1,500 mg/day to lower blood pressure and thus reduce their risk of cardiovascular and kidney diseases in adulthood (85). In 2004, the FNB set the AI for children by extrapolating from the adult AI using relative energy intakes. The AI for children 4 to 8 years is 1,000 mg/day, which translates to 2.5 grams of salt per day, and the AI for boys and girls 9 to 13 years is 1,200 mg/day, which translates to 3 grams of salt per day (86).
The mineral zinc is essential for growth and development, immune function, neurological function, and reproduction. Zinc plays a number of catalytic, structural, and regulatory roles in cellular metabolism (see the article on Zinc). Zinc deficiency is a major public health concern and has been estimated to affect more than 2 billion people in less developed nations (87). Children are at increased risk for zinc deficiency, which can lead to delayed physical growth, impaired immunity, and possibly to delayed mental development. Mild forms of this mineral deficiency, which are common in both developing and developed nations, appear to have negative effects on growth and development (23, 88). However, the lack of a sensitive indicator of mild zinc deficiency hinders the scientific study of its health implications.
Mild zinc deficiency contributes to impaired physical growth in children (88, 89). Significant delays in linear growth and weight gain, known as growth retardation or failure to thrive, are common features of mild zinc deficiency in children. In the 1970s and 1980s, several randomized, placebo-controlled studies of zinc supplementation in young children with significant growth delays were conducted in Denver, Colorado. Modest zinc supplementation (5.7 mg/day) resulted in increased growth rates compared to placebo (89). More recently, a number of larger studies in developing countries observed similar results with modest zinc supplementation. A meta-analysis of growth data from zinc intervention trials recently confirmed the widespread occurrence of growth-limiting zinc deficiency in young children, especially in developing countries (90). Although the exact mechanism for the growth-limiting effects of zinc deficiency are not known, recent research indicates that zinc availability affects cell-signaling systems that coordinate the response to the growth-regulating hormone, insulin-like growth factor-1 (IGF-1) (91, 92).
Adequate zinc intake in children is essential in maintaining the integrity of the immune system (23, 93), and zinc deficiency is associated with increased susceptibility to a variety of infectious agents (94). The adverse effects of zinc deficiency on immune system function are likely to increase the susceptibility of children to infectious diarrhea, and persistent diarrhea contributes to zinc deficiency and malnutrition. It has been estimated that diarrheal diseases result in the deaths of about 3 million children each year (95). Zinc supplementation in combination with oral rehydration therapy has been shown to significantly reduce the duration and severity of acute and persistent childhood diarrhea and to increase survival in a number of randomized controlled trials (96, 97). Recently, a meta-analysis of randomized controlled trials concluded that zinc supplementation reduces the frequency, severity, and duration of diarrheal episodes in children under five years of age (98). The World Health Organization and the United Nations Children's Fund currently recommend zinc supplementation as part of the treatment for diarrheal diseases in young children (99). Zinc supplementation may also reduce the incidence of lower respiratory infections, such as pneumonia. A pooled analysis of a number of studies in developing countries demonstrated a substantial reduction in the prevalence of pneumonia in children supplemented with zinc (100). A recent meta-analysis found that zinc supplementation reduced the incidence but not duration of pneumonia or respiratory tract illnesses in children under five years of age (98). Due to conflicting reports (101-104), it is not yet clear whether zinc supplementation has utility in treating childhood malaria.
Because a sensitive indicator of zinc nutritional status is not readily available, the RDA for zinc was based on a number of different indicators of zinc nutritional status and represents the daily intake likely to prevent deficiency in nearly all individuals in a specific age and gender group. The RDA for children ages 4 to 8 years is 5 mg/day, and the RDA for boys and girls ages 9 to 13 years is 8 mg/day (105). Shellfish, beef, and other red meats are rich sources of zinc. Nuts and legumes are relatively good plant sources of zinc. Zinc bioavailability (the fraction of zinc retained and used by the body) is relatively high in meat, eggs, and seafood because of the relative absence of compounds that inhibit zinc absorption and the presence of certain amino acids (cysteine and methionine) that enhance zinc absorption. The zinc in whole-grain products and plant proteins is less bioavailable due to their relatively high content of phytic acid, a compound that inhibits zinc absorption (106). The enzymatic action of yeast reduces the level of phytic acid in foods. Therefore, leavened whole-grain breads have more bioavailable zinc than unleavened whole-grain breads (105).
Choline can be synthesized by the body in small amounts, but dietary intake is needed to maintain health (107). Choline and its metabolites have a number of essential biological functions. Choline is used in the synthesis of specific phospholipids (i.e., phosphatidylcholine and sphingomyelin) that are structural components of cell membranes and also precursors for certain cell-signaling molecules. Choline is needed for myelination of nerves and is a precursor for acetylcholine, a neurotransmitter involved in muscle action, memory, and other functions (108-110). For more information about the role of choline in the body, see the article on Choline.
Due to the lack of data in children, intake recommendations for choline in children were extrapolated from adult recommendations using metabolic body weight, accounting for growth. The AI for children aged 4 to 8 years is 250 mg/day, and the AI for boys and girls aged 9 to 13 years is 375 mg/day (108). A number of foods contain choline, but eggs, meats, and milk are the primary sources in the American diet (111).
α-Linolenic acid (ALA), an omega-3 fatty acid, and linoleic acid (LA), an omega-6 fatty acid, are considered essential fatty acids because they cannot be synthesized by humans. The long-chain omega-6 fatty acid, arachidonic acid (AA), can be synthesized from LA, and two long-chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), can be synthesized from ALA (112). These polyunsaturated fatty acids have a number of biological activities that are generally important for the structure and function of cell membranes, vision, eicosanoid synthesis, regulation of gene expression, and nervous system function (see the article on Essential Fatty Acids).
Dietary intake recommendations for ALA and LA in children were based on median intakes of American children, a population where omega-3 and omega-6 fatty acid deficiencies are not observed. The AI of ALA for children ages 4 to 8 years is 0.9 g/day, while the AI of ALA for children ages 9 to 13 years is 1.2 and 1.0 g/day for boys and girls, respectively. The long-chain omega-3 fatty acids, EPA and DHA, can contribute to these intake recommendations. Flaxseeds, walnuts, and their oils are among the richest dietary sources of ALA, but canola oil is also an excellent source of ALA. Oily fish, such as salmon, tuna, trout, and sardines, are the major dietary source of EPA and DHA (113). The AI of LA for children ages 4 to 8 years is 10 g/day, while the AI of LA for boys and girls ages 9 to 13 years is 12 and 10 g/day, respectively. Sources of LA include vegetable oils, such as soybean, safflower, and corn oil, nuts, seeds, and some vegetables (see the article on Essential Fatty Acids).
The FNB sets a tolerable upper intake level (UL) for most micronutrients. The UL is the highest level of daily nutrient intake likely to pose no risk of adverse health effects in almost all individuals of a specified age group. This level applies to total daily intake from food, water, and supplements. Due to the potential for adverse effects, it is recommended that individuals not exceed the UL. Thus, individuals should use the UL as a guide to limit daily micronutrient intake, not as a recommended level of intake (114). Table 3 lists the UL for children ages 4 to 8 years, and Table 4 lists the UL for children ages 9 to 13 years.
Note that many children’s multivitamin/mineral supplements on the market contain more than the RDA for several micronutrients when taken at the suggested dosage by age. Some even contain micronutrients (e.g., vitamin A, folic acid, copper, and zinc) at levels equivalent to the UL; this concern is for children younger than 9 years old. The Food and Nutrition Board of the Institute of Medicine recommends that daily nutrient intake from food and supplements not exceed the UL for each micronutrient. There is no evidence that consumption of micronutrients at or above the UL results in any health benefits in children, and the UL should not be exceeded except under medical supervision. Children often consume vitamin and mineral-fortified foods like cereal, and their total intake of certain micronutrients like vitamin A, folic acid, copper, and zinc from fortified foods, other dietary intake, and from supplements should be determined to ensure that the UL is not exceeded. It is also important to note that the daily values (DVs) listed on supplement labels in the US do not reflect the current intake recommendations (RDA or AI). Another caution is that many children’s supplements look like candy but should never be labeled as such and, because of safety concerns, should be kept out of reach of children.
A healthy diet in children is important to provide nutrients that support optimum physical growth and cognitive development and to also establish healthy eating behaviors that lower risk of chronic diseases in adulthood. Although it is generally advised that micronutrients should be obtained from food, many children do not reach daily intake recommendations for select micronutrients, including vitamins A, C, D, and E, and some minerals, such as calcium and magnesium (37, 115).
Therefore, the Linus Pauling Institute recommends that children ages 4 to 13 years take a daily multivitamin/mineral supplement with 100% of the daily value (DV) for most vitamins and essential minerals, keeping the following suggestions in mind:
Written in August 2011 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in August 2011 by:
Dennis M. Bier, M.D.
Professor of Pediatrics, Baylor College of Medicine
Director, Children’s Nutrition Research Center
Houston, Texas
This article was underwritten, in part, by a grant from Bayer Consumer Care AG, Basel, Switzerland.
DRIs for sodium and potassium updated 4/12/19 Copyright 2011-2024 Linus Pauling Institute
1. Lucas BL, Feucht SA. Nutrition in childhood. In: Mahan LK, Escott-Stump S, eds. Krause's food & nutrition therapy. 12th ed. St. Louis: Saunders Elsevier; 2008:222-45.
2. Wooldridge NH. Child and preadolescent nutrition. In: Brown JE, Issacs JS, Krinke UB, Murtaugh MA, Stang J, Wooldridge NH, eds. Nutrition through the life cycle. Belmont: Wadsworth/Thomson Learning; 2002:283-306.
3. Food and Nutrition Board, Institute of Medicine. Overview and methods. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:44-59. (National Academy Press)
4. Subcommittee on Interpretation and Uses of Dietary Reference Intakes and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes: Applications in Dietary Planning. Washington, D.C.: The National Academies Press; 2003. (The National Academies Press)
5. Subcommittee on Interpretation and Uses of Dietary Reference Intakes. Dietary Reference Intakes: Applications in Dietary Assessment. Washington, D.C.: National Academy Press; 2000. (National Academy Press)
6. Subcommittee on Interpretation and Uses of Dietary Reference Intakes and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Using Dietary Reference Intakes in Planning Diets for Individuals. In: Dietary Reference Intakes: Applications in Dietary Planning. Washington, D.C.: The National Academies Press; 2003:35-54. (The National Academies Press)
7. Kleiber M. Body size and metabolic rate. Physiological reviews 1947;27(4):511-41. (PubMed)
8. Underwood BA, Arthur P. The contribution of vitamin A to public health. FASEB J 1996;10(9):1040-8. (PubMed)
9. Brody T. Nutritional biochemistry. San Diego: Academic Press; 1999.
10. Semba RD. Impact of vitamin A on immunity and infection in developing countries. In: Bendich A, Decklebaum RJ, eds. Preventive nutrition: the comprehensive guide for health professionals. Totowa: Human Press Inc.; 2001:329-46.
11. Semba RD. Vitamin A and human immunodeficiency virus infection. The Proceedings of the Nutrition Society 1997;56(1B):459-69. (PubMed)
12. Field CJ, Johnson IR, Schley PD. Nutrients and their role in host resistance to infection. Journal of leukocyte biology 2002;71(1):16-32. (PubMed)
13. West CE. Vitamin A and measles. Nutrition reviews 2000;58(2 Pt 2):S46-54. (PubMed)
14. Thurnham DI, Northrop-Clewes CA. Optimal nutrition: vitamin A and the carotenoids. The Proceedings of the Nutrition Society 1999;58(2):449-57. (PubMed)
15. Food and Nutrition Board, Institute of Medicine. Vitamin A. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:65-126. (National Academy Press)
16. Shane B. Folic acid. In: Stipanuk M, ed. Biochemical and physiological aspects on human nutrition. Philadelphia: W.B. Saunders Co.; 2000:483-518.
17. Stabler SP. Vitamin B12. In: Bowman BA, Russell RM, eds. Present knowledge in nutrition. 9th ed. Washington, D.C.: ILSI Press; 2006:302-13.
18. Healton EB, Savage DG, Brust JC, Garrett TJ, Lindenbaum J. Neurologic aspects of cobalamin deficiency. Medicine 1991;70(4):229-45. (PubMed)
19. Carter R, Aldridge S, Page M, Parker S. Brain anatomy. In: Frances P, ed. The human brain book. London: Dorling Kindersley; 2009:50-73.
20. Food and Nutrition Board, Institute of Medicine. Vitamin B12. In: Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B6, vitamin B12, pantothenic acid, biotin, and choline. Washington, D.C.: National Academy Press; 1998:306-56. (National Academy Press)
21. Lebel C, Walker L, Leemans A, Phillips L, Beaulieu C. Microstructural maturation of the human brain from childhood to adulthood. NeuroImage 2008;40(3):1044-55. (PubMed)
22. Benes FM. Myelination of cortical-hippocampal relays during late adolescence. Schizophrenia bulletin 1989;15(4):585-93. (PubMed)
23. Maggini S, Wenzlaff S, Hornig D. Essential role of vitamin C and zinc in child immunity and health. The Journal of international medical research 2010;38(2):386-414. (PubMed)
24. Johnston CS. Vitamin C. In: Bowman BA, Russell RM, eds. Present knowledge in nutrition. 9th ed. Washington, D.C.: ILSI Press; 2006:233-41.
25. Food and Nutrition Board, Institute of Medicine. Vitamin C. In: Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, D.C.: National Academy Press; 2000:95-185.
26. Wagner CL, Greer FR. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008;122(5):1142-52. (PubMed)
27. Wharton B, Bishop N. Rickets. Lancet 2003;362(9393):1389-400. (PubMed)
28. Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. The American journal of clinical nutrition 2004;80(6 Suppl):1697S-705S. (PubMed)
29. Mylott BM, Kump T, Bolton ML, Greenbaum LA. Rickets in the Dairy State. Wmj 2004;103(5):84-7. (PubMed)
30. Pettifor JM. Rickets and vitamin D deficiency in children and adolescents. Endocrinology and metabolism clinics of North America 2005;34(3):537-53, vii. (PubMed)
31. Pettifor JM. Nutritional rickets: deficiency of vitamin D, calcium, or both? The American journal of clinical nutrition 2004;80(6 Suppl):1725S-9S. (PubMed)
32. Sills IN, Skuza KA, Horlick MN, Schwartz MS, Rapaport R. Vitamin D deficiency rickets. Reports of its demise are exaggerated. Clinical pediatrics 1994;33(8):491-3. (PubMed)
33. Thacher TD, Fischer PR, Strand MA, Pettifor JM. Nutritional rickets around the world: causes and future directions. Annals of tropical paediatrics 2006;26(1):1-16. (PubMed)
34. Food and Nutrition Board, Institute of Medicine. Overview of vitamin D. In: Dietary reference intakes for calcium and vitamin D. Washington, D.C.: The National Academies Press; 2011:75-124. (The National Academies Press)
35. Yetley EA. Assessing the vitamin D status of the US population. The American journal of clinical nutrition 2008;88(2):558S-64S. (PubMed)
36. Holick MF. Vitamin D deficiency. The New England journal of medicine 2007;357(3):266-81. (PubMed)
37. Bailey RL, Dodd KW, Goldman JA, et al. Estimation of total usual calcium and vitamin D intakes in the United States. The Journal of nutrition 2010;140(4):817-22. (PubMed)
38. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for adequacy: calcium and vitamin D. In: Dietary reference intakes for calcium and vitamin D. Washington, D.C.: The National Academies Press; 2011:345-402. (The National Academies Press)
39. Holick MF, Binkley NC, Bischoff-Ferrari HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. The Journal of clinical endocrinology and metabolism 2011;96(7):1911-1930. (PubMed)
40. Food and Nutrition Board, Institute of Medicine. Vitamin E. In: Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, D.C.: National Academy Press; 2000:186-283. (National Academy Press)
41. Ahuja JK, Goldman JD, Moshfegh AJ. Current status of vitamin E nutriture. Annals of the New York Academy of Sciences 2004;1031:387-90. (PubMed)
42. Giraud DW, Kim YN, Cho YO, Driskell JA. Vitamin E inadequacy observed in a group of 2- to 6-year-old children living in Kwangju, Republic of Korea. International journal for vitamin and nutrition research Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung 2008;78(3):148-55. (PubMed)
43. Stahl A, Vohmann C, Richter A, Heseker H, Mensink GB. Changes in food and nutrient intake of 6- to 17-year-old Germans between the 1980s and 2006. Public health nutrition 2009;12(10):1912-23. (PubMed)
44. Food and Nutrition Board, Institute of Medicine. Overview of calcium. In: Dietary reference intakes for calcium and vitamin D. Washington, D.C.: The National Academies Press; 2011:35-74. (The National Academies Press)
45. Centers for Disease Control. Achievements in public health, 1900-1999: fluoridation of drinking water to prevent dental caries. MMWR 1999;48:933-40.
46. DePaola DP. Nutrition in relation to dental medicine. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern nutrition in health and disease. 9th ed. Baltimore: Lippincott Williams & Wilkins; 1999:1099-124.
47. Food and Nutrition Board, Institute of Medicine. Fluoride. In: Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, D.C.: National Academy Press; 1997:288-313. (National Academy Press)
48. Cerklewski FL. Fluoride bioavailability--nutritional and clinical aspects. Nutr Res 1997;17:907-29.
49. Hetzel BS, Clugston GA. Iodine. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern nutrition in health and disease. 9th ed. Baltimore: Lippincott Williams & Wilkins; 1999:253-64.
50. Dunn JT. What's happening to our iodine? The Journal of clinical endocrinology and metabolism 1998;83(10):3398-400. (PubMed)
51. Assessment of iodine deficiency disorders and monitoring their elimination: a guide for programme managers. World Health Organization, 2007. Accessed 2007. Available at: http://whqlibdoc.who.int/publications/2007/9789241595827_eng.pdf
52. Tiwari BD, Godbole MM, Chattopadhyay N, Mandal A, Mithal A. Learning disabilities and poor motivation to achieve due to prolonged iodine deficiency. The American journal of clinical nutrition 1996;63(5):782-6. (PubMed)
53. Bleichrodt N, Shrestha RM, West CE, Hautvast JG, van de Vijver FJ, Born MP. The benefits of adequate iodine intake. Nutrition reviews 1996;54(4 Pt 2):S72-8. (PubMed)
54. de Benoist B, McLean E, Andersson M, Rogers L. Iodine deficiency in 2007: global progress since 2003. Food and nutrition bulletin 2008;29(3):195-202. (PubMed)
55. Food and Nutrition Board, Institute of Medicine. Iodine. In: Dietary reference intakes for vitamin A, vitamin K, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:258-89. (National Academy Press)
56. United Nations Children's Fund. The state of the world's children 2007. Women and children, the double dividend of gender equality. UNICEF. New York; 2006:109.
57. Andersson M, de Benoist B, Rogers L. Epidemiology of iodine deficiency: Salt iodisation and iodine status. Best practice & research 2010;24(1):1-11. (PubMed)
58. Best C, Neufingerl N, van Geel L, van den Briel T, Osendarp S. The nutritional status of school-aged children: why should we care? Food and nutrition bulletin;31(3):400-17. (PubMed)
59. Zimmermann MB, Andersson M. Prevalence of iodine deficiency in Europe in 2010. Ann Endocrinol (Paris) 2001;72(2):164-166. (PubMed)
60. Malvaux P, Beckers C, De Visscher M. Iodine balance studies in nongoitrous children and in adolescents on low iodine intake. The Journal of clinical endocrinology and metabolism 1969;29(1):79-84. (PubMed)
61. Dasgupta PK, Liu Y, Dyke JV. Iodine nutrition: iodine content of iodized salt in the United States. Environmental science & technology 2008;42(4):1315-23. (PubMed)
62. Caldwell KL, Miller GA, Wang RY, Jain RB, Jones RL. Iodine status of the U.S. population, National Health and Nutrition Examination Survey 2003-2004. Thyroid 2008;18(11):1207-14. (PubMed)
63. Pennington JAT, Schoen SA, Salmon GD, Young B, Johnson RD, Marts RW. Composition of core foods of the U.S. food supply, 1982-1991. III. Copper, manganese, selenium, iodine. J Food Comp Anal 1995;8:171-217.
64. Fairbanks VF. Iron in medicine and nutrition. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern nutrition in health and disease. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 1999:193-221.
65. Jaakkola P, Mole DR, Tian YM, et al. Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Science (New York, NY 2001;292(5516):468-72. (PubMed)
66. Ivan M, Kondo K, Yang H, et al. HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing. Science (New York, NY 2001;292(5516):464-8. (PubMed)
67. Beard JL, Dawson HD. Iron. In: O'Dell BL, Sunde RA, eds. Handbook of nutritionally essential minerals. New York: Marcel Dekker, Inc.; 1997:275-334.
68. Wood RJ, Ronnenberg AG. Iron. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern nutrition in health and disease. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2006:248-70.
69. Owens A, Cloud HH. Special topics in toddler and preschool nutrition: vitamins and minerals in childhood and children with disabilities. In: Edelstein S, Sharlin J, eds. Life cycle nutrition: an evidence-based approach. Boston: Jones and Bartlett Publishers; 2009:183-225.
70. Micronutrient deficiencies: iron deficiency anemia. 2011. http://www.who.int/nutrition/topics/ida/en/. Accessed 5/6/11
71. Disorders of iron metabolism and heme synthesis. In: Lee GR, Foerster J, Lukens J, et al., eds. Wintrobe's Clinical Hematology. 10th ed. Baltimore: Lippincott Williams & Wilkins; 1999:979-1070.
72. Thomas DG, Grant SL, Aubuchon-Endsley NL. The role of iron in neurocognitive development. Developmental neuropsychology 2009;34(2):196-222. (PubMed)
73. Lozoff B. Iron deficiency and child development. Food and nutrition bulletin 2007;28(4 Suppl):S560-71. (PubMed)
74. Todorich B, Pasquini JM, Garcia CI, Paez PM, Connor JR. Oligodendrocytes and myelination: the role of iron. Glia 2009;57(5):467-78. (PubMed)
75. Beard JL. Iron biology in immune function, muscle metabolism and neuronal functioning. The Journal of nutrition 2001;131(2S-2):568S-79S; discussion 80S. (PubMed)
76. Food and Nutrition Board, Institute of Medicine. Iron. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:290-393. (National Academy Press)
77. Lynch SR. Interaction of iron with other nutrients. Nutrition reviews 1997;55(4):102-10. (PubMed)
78. Yip R, Dallman PR. Iron. In: Ziegler EE, Filer LJ, eds. Present knowledge in nutrition. 7th ed. Washington, D.C.: ILSI Press; 1997:277-92.
79. Food and Nutrition Board. Institute of Medicine. Magnesium. In: Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, D.C.: National Academy Press; 1997:190-249. (National Academy Press)
80. Rude RK, Shils ME. Magnesium. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern nutrition in health and disease. 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006:223-47.
81. Andon MB, Ilich JZ, Tzagournis MA, Matkovic V. Magnesium balance in adolescent females consuming a low- or high-calcium diet. The American journal of clinical nutrition 1996;63(6):950-3. (PubMed)
82. Abrams SA, Grusak MA, Stuff J, O'Brien KO. Calcium and magnesium balance in 9-14-y-old children. The American journal of clinical nutrition 1997;66(5):1172-7. (PubMed)
83. US Department of Agriculture National Nutrient Database for Standard Reference, Release 23. 2010. Available at: https://ndb.nal.usda.gov/ndb/ Accessed 4/8/11.
84. O'Neil CE, Nicklas TA, Zanovec M, Cho SS, Kleinman R. Consumption of whole grains is associated with improved diet quality and nutrient intake in children and adolescents: the National Health and Nutrition Examination Survey 1999-2004. Public health nutrition 2011;14(2):347-55. (PubMed)
85. US Department of Agriculture and US Department of Health and Human Services. Dietary Guidelines for Americans, 2010. 7th Edition, Washington, DC: US Government Printing Office, December 2010. Available at: https://health.gov/dietaryguidelines/2010/.
86. Food and Nutrition Board, Institute of Medicine. Sodium and chloride. In: Dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, D.C.: National Academies Press; 2005:269-423. (National Academies Press)
87. Tuerk MJ, Fazel N. Zinc deficiency. Current opinion in gastroenterology 2009;25(2):136-43. (PubMed)
88. Hambidge M. Human zinc deficiency. The Journal of nutrition 2000;130(5S Suppl):1344S-9S. (PubMed)
89. Walravens PA, Hambidge KM, Koepfer DM. Zinc supplementation in infants with a nutritional pattern of failure to thrive: a double-blind, controlled study. Pediatrics 1989;83(4):532-8. (PubMed)
90. Hambidge M, Krebs N. Trace elements in man and animals 10: Proceedings of the tenth international symposium on trace elements in man and animals. In: Roussel AM, ed. New York: Plenum Press; 2000:977-80.
91. Cole CR, Lifshitz F. Zinc nutrition and growth retardation. Pediatr Endocrinol Rev 2008;5(4):889-96. (PubMed)
92. MacDonald RS. The role of zinc in growth and cell proliferation. The Journal of nutrition 2000;130(5S Suppl):1500S-8S. (PubMed)
93. Baum MK, Shor-Posner G, Campa A. Zinc status in human immunodeficiency virus infection. The Journal of nutrition 2000;130(5S Suppl):1421S-3S. (PubMed)
94. Shankar AH, Prasad AS. Zinc and immune function: the biological basis of altered resistance to infection. The American journal of clinical nutrition 1998;68(2 Suppl):447S-63S. (PubMed)
95. Fuchs GJ. Possibilities for zinc in the treatment of acute diarrhea. The American journal of clinical nutrition 1998;68(2 Suppl):480S-3S. (PubMed)
96. Fischer Walker CL, Black RE. Micronutrients and diarrheal disease. Clin Infect Dis 2007;45 Suppl 1:S73-7. (PubMed)
97. Bhutta ZA, Bird SM, Black RE, et al. Therapeutic effects of oral zinc in acute and persistent diarrhea in children in developing countries: pooled analysis of randomized controlled trials. The American journal of clinical nutrition 2000;72(6):1516-22. (PubMed)
98. Aggarwal R, Sentz J, Miller MA. Role of zinc administration in prevention of childhood diarrhea and respiratory illnesses: a meta-analysis. Pediatrics 2007;119(6):1120-30. (PubMed)
99. The United Nations Children's Fund/World Health Organization. WHO/UNICEF Joint Statement: Clinical Management of Acute Diarrhoea. Geneva; New York; 2004:1-8. Available at: http://www.unicef.org/publications/index_21433.html.
100. Bhutta ZA, Black RE, Brown KH, et al. Prevention of diarrhea and pneumonia by zinc supplementation in children in developing countries: pooled analysis of randomized controlled trials. Zinc Investigators' Collaborative Group. The Journal of pediatrics 1999;135(6):689-97. (PubMed)
101. Sazawal S, Black RE, Ramsan M, et al. Effect of zinc supplementation on mortality in children aged 1-48 months: a community-based randomised placebo-controlled trial. Lancet 2007;369(9565):927-34. (PubMed)
102. Shankar AH. Nutritional modulation of malaria morbidity and mortality. The Journal of infectious diseases 2000;182 Suppl 1:S37-53. (PubMed)
103. Zinc Against Plasmodium Study Group. Effect of zinc on the treatment of Plasmodium falciparum malaria in children: a randomized controlled trial. The American journal of clinical nutrition 2002;76(4):805-12. (PubMed)
104. Muller O, Becher H, van Zweeden AB, et al. Effect of zinc supplementation on malaria and other causes of morbidity in west African children: randomised double blind placebo controlled trial. BMJ (Clinical research ed 2001;322(7302):1567. (PubMed)
105. Food and Nutrition Board, Institute of Medicine. Zinc. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:442-501. (National Academy Press)
106. King JC, Cousins RJ. Zinc. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern nutrition in health and disease. 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006:271-85.
107. Blusztajn JK. Choline, a vital amine. Science (New York, NY 1998;281(5378):794-5. (PubMed)
108. Food and Nutrition Board, Institute of Medicine. Choline. In: Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B-6, folate, vitamin B-12, pantothenic acid, biotin, and choline. Washington, D.C.: National Academy Press; 1998:390-422. (National Academy Press)
109. Zeisel SH, Niculescu MD. Choline and phosphatidylcholine. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern nutrition in health and disease. Philadelphia: Lippincott Williams & Wilkins; 2006:525-36.
110. Zeisel SH. Choline: an essential nutrient for humans. Nutrition (Burbank, Los Angeles County, Calif 2000;16(7-8):669-71. (PubMed)
111. Zeisel SH, da Costa KA. Choline: an essential nutrient for public health. Nutrition reviews 2009;67(11):615-23. (PubMed)
112. Nakamura MT, Nara TY. Structure, function, and dietary regulation of delta6, delta5, and delta9 desaturases. Annual review of nutrition 2004;24:345-76. (PubMed)
113. Food and Nutrition Board, Institute of Medicine. Dietary fats: total fat and fatty acids. In: Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Washington, D.C.: The National Academies Press; 2005:422-541. (The National Academies Press)
114. Food and Nutrition Board, Institute of Medicine. Summary. In: Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:1-28. (National Academy Press)
115. Moshfegh A, Goldman J, Cleveland L. 2005. What We Eat in America, NHANES 2001-2002: Usual Nutrient Intakes from Food Compared to Dietary Reference Intakes. US Department of Agriculture, Agricultural Research Service. Available at: http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/0102/usualintaketables2001-02.pdf