Micronutrient Needs During Pregnancy and Lactation

Introduction

Nutrient needs during the life stages of pregnancy and lactation are increased relative to women who are not pregnant or lactating. Mathematical models predict that energy requirements increase by an estimated 300 kcal/day during the second and third trimesters of pregnancy and by 500 kcal/day during lactation (1). In practice, most women will require only approximately 200 additional kcal/day due to reduced levels of physical activity during pregnancy and to increased lipolysis of fat stores during breast-feeding [personal communication with Dr. Berthold Koletzko]. Relative to the increased energy requirement, the requirements for many micronutrients (vitamins and nutritionally essential minerals) are even higher during pregnancy and lactation; this article discusses micronutrient needs during these life stages.

Micronutrient Requirements During Pregnancy

Pregnancy is associated with increased nutritional needs due to physiologic changes of the woman and the metabolic demands of the embryo/fetus. Proper maternal nutrition during pregnancy is thus imperative for the health of both the woman and the offspring. Maternal malnutrition during pregnancy has been associated with adverse outcomes, including increased risk of maternal and infant mortality, as well as low-birth-weight newborns (<2,500 grams) — a measure that accounts for preterm birth and intrauterine growth restriction of the fetus (2, 3). Select nutrient deficiencies have also been linked to congenital anomalies and birth defects. In addition, gestational undernutrition has been implicated in increasing the offspring’s susceptibility to chronic disease (i.e., type 2 diabetes, hypertension, coronary heart disease, and stroke) in adulthood, a phenomenon sometimes called Barker’s hypothesis, the thrifty phenotype hypothesis, or the fetal origin of adult disease hypothesis (4, 5). Maternal undernutrition often refers to malnutrition caused by insufficient caloric (energy) intake from macronutrients (carbohydrates, proteins, and lipids) during pregnancy, but micronutrient deficiencies are also a form of undernutrition. Multiple micronutrient deficiencies commonly co-exist in pregnant women (6).

Daily requirements for many micronutrients during pregnancy are higher to meet the physiologic changes and increased nutritional needs of pregnancy. Good nutritional status prior to conception is also important for a healthy pregnancy. For instance, folic acid supplementation during the periconceptional period (about one month before conception until the end of the first trimester) dramatically reduces the incidence of devastating birth defects called neural tube defects (see Folate below). Thus, folic acid supplementation (at least 400 μg/day) is recommended for all women capable of becoming pregnant (7-9). A well-balanced diet throughout pregnancy is necessary to supply the developing embryo/fetus with micronutrients. In addition to folic acid supplementation, iron supplementation is generally needed to meet the increased demands for this mineral during pregnancy (see the section on Iron below).

The Food and Nutrition Board (FNB) of the Institute of Medicine establishes life-stage specific dietary reference intakes (DRIs) for each micronutrient; these reference values should be used to plan and assess dietary intakes in healthy people (10, 11). 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 (12). The FNB establishes an AI when an RDA cannot be determined. The below recommendations are specific to the life stages of pregnancy and lactation. For most micronutrients, the RDA or AI for pregnant women is increased compared to nonpregnant women of the same age (Table 1). The discussion below largely focuses on these recommendations for select micronutrients during pregnancy but also notes major concerns for micronutrient toxicity or teratogenicity. The UL is the highest level of daily intake that is likely to pose no risk of adverse health effects in almost all individuals of a specified life stage. For the UL for each micronutrient during pregnancy, see Table 2.

Table 1. RDA for Micronutrients During Pregnancy
Micronutrient  Age  RDA 
Biotin  14-50 years  30 μg/day (AI
Folate 14-50 years  600 μg/daya 
Niacin  14-50 years  18 mg/dayb 
Pantothenic Acid  14-50 years  6 mg/day (AI) 
Riboflavin  14-50 years  1.4 mg/day 
Thiamin  14-50 years  1.4 mg/day 
Vitamin A  14-18 years  750 μg (2,500 IU)/dayc 
  19-50 years  770 μg (2,567 IU)/dayc 
Vitamin B6  14-50 years  1.9 mg/day 
Vitamin B12  14-50 years  2.6 μg/day 
Vitamin C  14-18 years  80 mg/day 
  19-50 years  85 mg/day 
Vitamin D  14-50 years  15 μg (600 IU)/day 
Vitamin E  14-50 years  15 mg (22.5 IU)/dayd 
Vitamin K  14-18 years  75 μg/day (AI) 
  19-50 years  90 μg/day (AI) 
Calcium  14-18 years  1,300 mg/day 
  19-50 years  1,000 mg/day 
Chromium  14-18 years  29 μg/day (AI) 
  19-50 years  30 μg/day (AI) 
Copper  14-50 years  1 mg/day 
Fluoride  14-50 years  3 mg/day (AI) 
Iodine  14-50 years  220 μg/day 
Iron  14-50 years  27 mg/day 
Magnesium  14-18 years  400 mg/day 
  19-30 years  350 mg/day 
  31-50 years  360 mg/day 
Manganese  14-50 years  2 mg/day (AI) 
Molybdenum  14-50 years  50 μg/day 
Phosphorus  14-18 years  1,250 mg/day 
  19-50 years  700 mg/day 
Potassium  14-50 years  4,700 mg/day (AI) 
Selenium  14-50 years  60 μg/day 
Sodium  14-50 years  1,500 mg/day (AI) 
Zinc  14-18 years  12 mg/day 
  19-50 years  11 mg/day 
Cholinee  14-50 years  450 mg/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

Vitamins

Biotin

Biotin is needed as a cofactor for carboxylase enzymes and for the attachment of biotin to molecules, such as proteins, in a process known as "biotinylation" (13). Rapidly dividing cells of the developing fetus require the vitamin for synthesis of essential carboxylase enzymes and for histone biotinylation. Although maternal biotin deficiency in certain strains of mice causes malformations in the offspring, namely cleft palate and limb shortening (14, 15), a link between biotin deficiency and birth defects in humans has not been observed.

Experimentally induced, marginal biotin deficiency results in the increased urinary excretion of 3-hydroxyisovaleric acid (3-HIA) and decreased urinary excretion of biotin and the biotin catabolites, bisnorbiotin (BNB) and biotin disulfoxide (BSO) (16, 17). Abnormally elevated urinary excretion of 3-HIA and abnormally decreased urinary excretion of biotin are the most extensively validated biomarkers of low biotin status (18).

Two observational studies have reported that there is an increased urinary excretion of 3-HIA during pregnancy, though other indices of biotin status were not consistently altered (19, 20). Similarly, a 2014 feeding study in which all subjects consumed a mixed diet with a known amount of biotin (average daily intake, 57 μg biotin/day), urinary 3-HIA excretion was higher in pregnant compared to nonpregnant women, while urinary biotin and BNB excretion did not differ between the groups (21). Supplementation with biotin (300 μg/day for 14 days) reduced urinary 3-HIA and increased urinary biotin excretion in pregnant women with elevated 3-HIA; however, this intervention did the same for nonpregnant controls considered to have normal biotin status (22).

Elevated urinary excretion of 3-HIA during pregnancy could be due to several possibilities. Some suggest that it reflects marginal biotin deficiency and the need for more biotin during pregnancy (23, 24). Alternatively, increased 3-HIA in isolation could reflect altered leucine metabolism or renal handling of organic acids during pregnancy (18).

At this time, the AI for biotin (30 μg/day) is the same for pregnant and nonpregnant women. Biotin is widespread in food, though its concentration varies substantially (see the article on Biotin). Based on dietary intake data from the National Health and Nutrition Examination Survey (NHANES) II (18, 25) and the above-mentioned feeding study (21), a typical mixed diet provides approximately 40 to 60 μg of biotin/day.

Folate

The terms folate and folic acid are often used interchangeably, but folic acid is the synthetic form of the vitamin that is only found in fortified food and supplements. Folic acid is more bioavailable than folate from food (see the article on Folate); folic acid is converted to biologically active forms of folate in the body. Folate is needed for amino acid and nucleic acid (DNA and RNA) metabolism. Adequate folate status is critical to embryonic and fetal growth — developmental stages characterized by accelerated cell division. In particular, folate is needed for closure of the neural tube early in pregnancy, and periconceptional supplementation with folic acid has been shown to dramatically reduce the incidence of neural tube defects (NTDs) (reviewed in 26 and 27). NTDs are devastating congenital malformations that can occur as either anencephaly or spina bifida. Because these birth defects occur between 21 to 27 days after conception (28), often before many women recognize their pregnancy, it is recommended in the US that all women capable of becoming pregnant take supplemental folic acid (7).

A recent systematic review of five trials, including 7,391 women, found that periconceptional folic acid supplementation, alone or with other micronutrients, was associated with a 69% lower risk of NTDs (risk ratio (RR), 0.31; 95% confidence interval (CI), 0.17 to 0.58) (29). The RDA for pregnant women is 600 μg/day of dietary folate equivalents (DFE), which is equivalent to 300 μg/day of synthetic folic acid on an empty stomach or 353 μg/day of synthetic folic acid with a meal (see the article on Folate). The US Preventive Services Task Force recommends a daily supplement of 400-800 μg of folic acid, in addition to consuming food folate from a varied diet, for all women planning or capable of pregnancy (9). Supplemental folic acid use at the higher end of this suggested range has been recommended by some (27, 30), and 800 μg/day from supplements plus dietary intake is safe for women of childbearing age.

Multivitamin/mineral supplements marketed in the US commonly contain 400 μg of folic acid, and many prenatal supplements marketed in the US contain 800 μg of folic acid. Folic acid may also be present in the food supply: several countries have programs of mandatory folic acid fortification to help reduce the incidence of NTDs; for example, the US FDA implemented legislation in 1998 requiring the fortification of all enriched grain products with folic acid at a level of 140 μg folic acid/100 g of product (31). Mandatory fortification in the US has resulted in a 28 percent reduction (an estimated 1,326 births/year) in the prevalence of NTDs (32).

Doses greater than 1 mg/day of folic acid are used pharmacologically to treat hyperhomocysteinemia and to prevent reoccurrence of NTDs (33). Women who have had a previous NTD-affected pregnancy may be advised to consume up to 5 mg/day (5,000 μg/day) of folic acid if they are planning a pregnancy, but this level of supplementation should be prescribed by their medical provider (see the CDC recommendations and the World Health Organization [WHO] guidelines).

A new form of folate, 5-methyltetrahydrofolate (5-MTHF), has been proposed as an alternative to folic acid. 5-MTHF is less likely to mask a severe vitamin B12 deficiency, exhibits lower interaction potential with antimalarial drugs, and may be preferable for women with an MTHFR polymorphism (26, 34). While the effect of 5-MTHF supplementation on NTDs has not yet been evaluated, it is at least as effective as folic acid at raising red blood cell folate status and reducing homocysteine concentrations in nonpregnant healthy young women (35-38) and lactating women (39).

Inadequate folate status may also be linked to other birth defects, such as cleft lip, cleft palate, and limb malformations, but there are insufficient data to evaluate the effect of folic acid supplementation on these outcomes (26). However, results of some case-control studies (40-44) and controlled trials (45, 46) have suggested that periconceptional supplementation with a multivitamin containing folic acid may protect against congenital cardiovascular malformations, especially conotruncal (outflow tract) and ventricular septal defects. A 2006 systematic review and meta-analysis concluded that such supplementation was associated with a 22% lower risk of cardiovascular defects in case-control studies and a 39% lower risk in cohort studies and randomized controlled trials (47).

Impaired folate status during pregnancy may also be associated with other adverse pregnancy outcomes. Elevated blood homocysteine concentrations, considered an indicator of functional folate deficiency, have been associated with increased risk of preeclampsia, premature delivery, low placental weight, low birth weight, very low birth weight (<1,500 grams), small for gestational age, neural tube defects (NTDs), and stillbirth (48-50). Thus, it is reasonable to maintain folic acid supplementation throughout pregnancy, even after closure of the neural tube, in order to decrease the risk of other potential problems during pregnancy.

Riboflavin

Riboflavin is a component of flavocoenzymes involved in energy metabolism, as well as antioxidant functions. The Food and Nutrition Board of the Institute of Medicine recommends that all pregnant women consume 1.4 mg of riboflavin daily. Riboflavin deficiency has been implicated in preeclampsia — a pregnancy-associated complication characterized by elevated blood pressure, protein in the urine, and edema (significant swelling). Preeclampsia is estimated to affect 2%-8% of all pregnancies (51), and about 5% of women with preeclampsia progress to eclampsia, a significant cause of maternal death (52). Eclampsia is characterized by seizures, in addition to high blood pressure and increased risk of hemorrhage (severe bleeding) (52). Although the specific causes of preeclampsia are not known, decreased intracellular concentrations of flavocoenzymes could cause mitochondrial dysfunction, increase oxidative stress, and interfere with nitric oxide release and thus blood vessel dilation. All of these changes have been associated with preeclampsia, but there have been few studies on the association of riboflavin nutritional status and the condition. A study in 154 pregnant women at high risk for preeclampsia found that those who were riboflavin deficient were 4.7 times more likely to develop preeclampsia than those who had adequate riboflavin nutritional status (53). However, a small randomized, double-blind, placebo-controlled trial in 450 pregnant women at high risk for preeclampsia found that supplementation with 15 mg of riboflavin daily did not prevent the condition (54).

Vitamin A

Adequate maternal status of vitamin A is critical for a healthy pregnancy. Forms of the vitamin, known as retinoids, are involved in the regulation of gene expression, cellular proliferation and differentiation, growth and development, vision, and immunity (see the article on Vitamin A). The retinoids, retinol and retinoic acid, are essential for embryonic and fetal development (55); for example, retinoic acid functions in forming the heart, eyes, ears, and limbs (56). Animal studies demonstrate that severe vitamin A deficiency or excess during critical periods of development results in a spectrum of malformations, especially affecting craniofacial structures, limbs, and visceral organs (57).

Forms of vitamin A are also necessary for maternal health. Vitamin A deficiency during pregnancy has been linked to impaired immunity, increased susceptibility to infection, increased risk of maternal morbidity and mortality (58-61), and night blindness (62). Vitamin A deficiency may exacerbate iron-deficiency anemia (see section on Iron below); co-supplementation with vitamin A and iron seems to ameliorate anemia more effectively than either micronutrient supplement alone (63). Vitamin A deficiency is a major public health problem in developing nations, where availability of foods containing preformed vitamin A (retinol) and provitamin A carotenoids is limited (for information on food sources of vitamin A, see the article on Vitamin A). The RDA during pregnancy is 750 to 770 μg/day (2,500 to 2,567 IU/day) of preformed vitamin A (see Table 1 above).

Although normal embryonic and fetal development require sufficient maternal vitamin A intake, consumption of excess preformed vitamin A during pregnancy causes birth defects. An increased risk of vitamin A-associated birth defects has not been observed at supplemental doses below 3,000 μg (10,000 IU)/day of preformed vitamin (64). However, because a number of foods in the US are fortified with preformed vitamin A, the Linus Pauling Institute recommends that pregnant women avoid multivitamin or prenatal supplements that contain more than 750 μg (2,500 IU) of preformed vitamin A. Vitamin A from β-carotene is not known to increase the risk of birth defects (58), although the safety of high-dose β-carotene supplements in pregnancy has not been well studied. Moreover, pharmacological use of retinoids by pregnant women causes serious birth defects; thus, tretinate, isotretinoin (Accutane), and other retinoids should not be used during pregnancy or if there is a possibility of becoming pregnant (65). Use of tretinoin (Retin-A), a topically applied retinoid, exhibits very low systemic absorption, but is not recommended during pregnancy due to possible risks (66). It is important to note that retinoids tend to be very long acting; birth defects have been reported to occur months after discontinuing retinoid therapy (57). Retinoids are used therapeutically to treat retinitis pigmentosa, acute promyelocytic leukemia, various skin diseases, and other conditions.

Vitamin B6

Vitamin B6 has diverse roles in the body, including nervous system function, red blood cell formation and function, steroid hormone function, nucleic acid synthesis, and niacin formation. Pyridoxal, pyridoxine, and pyridoxamine are three forms of the vitamin. The RDA for vitamin B6 during pregnancy is 1.9 mg/day. Vitamin B6 has been used since the 1940s to treat nausea during pregnancy. The results of two double-blind, placebo-controlled trials that used 25 mg of pyridoxine every eight hours for three days (67) or 10 mg of pyridoxine every eight hours for five days (68) suggest that vitamin B6 may be beneficial in alleviating morning sickness. Each study found a slight but significant reduction in nausea or vomiting in pregnant women. A third randomized trial compared high-dose (10 mg/day) and low-dose (1.28 mg/day) vitamin B6 in 60 pregnant women experiencing nausea and/or vomiting prior to the twelfth week of gestation (69). After two weeks, nausea and vomiting scores decreased to an equal extent in both supplementation groups. A 2014 pooled analysis indicates that supplemental vitamin B6 alone may be effective in alleviating nausea, but not vomiting, during pregnancy (70). Vitamin B6 at the above-mentioned dosages is considered safe during pregnancy, and the vitamin has been used in pregnant women without any evidence of fetal harm (68, 71).

Vitamin B6 was included in the medication Bendectin (a delayed-release formulation of 10 mg doxylamine succinate [an antihistamine] and 10 mg pyridoxine hydrochloride [vitamin B6]), which was prescribed for the treatment of morning sickness and later withdrawn from the market in 1983 due to unproven concerns that it increased the risk of birth defects (72). Since that time, several investigations have shown the combination of doxylamine/pyridoxine to be both effective and safe, and in 2013, the US Food and Drug Administration approved this same formulation for the treatment of nausea and vomiting in pregnancy (reviewed in 73 and 74). The American and Canadian Colleges of Obstetrics and Gynecology and the Association of Professors of Gynecology and Obstetrics recommend the combination of doxylamine/pyridoxine as first-line therapy for nausea and vomiting during pregnancy (reviewed in 75).

The tolerable upper intake level (UL) for vitamin B6 during pregnancy is 80 to 100 mg/day; see Table 2.

Vitamin B12

In humans, vitamin B12 is needed as a cofactor for two enzymes. One converts homocysteine to the amino acid, methionine. Methionine is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions (76). DNA methylation that occurs during embryonic and fetal development modulates gene expression, cell differentiation, and the formation of organs (77). Thus, adequate vitamin B12 status during pregnancy is critical.

Inadequate dietary intake of vitamin B12 causes elevated homocysteine concentrations, which have been associated with adverse pregnancy outcomes, including preeclampsia, premature delivery, low placental weight, low birth weight, very low birth weight (<1,500 grams), small for gestational age, neural tube defects (NTDs), and stillbirth (48-50). Moreover, low serum concentrations of vitamin B12 during pregnancy have been linked to an increased risk for NTDs (78), and there is concern that folic acid supplementation during pregnancy may mask the clinical diagnosis of vitamin B12 deficiency. For these reasons, adequate vitamin B12 intake during pregnancy (RDA=2.6 μg/day) is important.

To ensure a daily intake of 6 to 30 μg of vitamin B12 in a form that is easily absorbed, the Linus Pauling Institute recommends that women who are planning a pregnancy take a daily multivitamin supplement or eat a breakfast cereal fortified with vitamin B12 (for more information, see the article on Vitamin B12).

Vitamin C and Vitamin E

Because oxidative stress has been implicated in the pathogenesis of preeclampsia (79), nutritional status of the two antioxidant vitamins, vitamin C and vitamin E, may be important in preventing the condition. These vitamins have other biological functions; for more information, see the separate articles on Vitamin C and Vitamin E. Several trials have investigated whether supplementation with vitamins C and E improves pregnancy-associated hypertension or preeclampsia, but evidence supporting such an effect is largely lacking. An early placebo-controlled trial found that supplementation with 1,000 mg/day of vitamin C and 400 mg of vitamin E (RRR-α-tocopherol) was associated with a 61% reduction in the incidence of preeclampsia in women at increased risk for the condition (80). However, more recent randomized controlled trials have not found supplementation at these dosages to be effective in preventing preeclampsia in high- or low-risk women (81-84). Nevertheless, adequate intake of antioxidant vitamins is important throughout pregnancy. According to data from the US National Health and Nutrition Examination Survey (NHANES), 42%-46% and 85%-94% of US adults do not meet the estimated average requirement (EAR) for vitamin C and vitamin E, respectively (85). The Linus Pauling Institute’s recommends that adults, including pregnant women, reach daily intakes of at least 400 mg of vitamin C and 15 mg (22.5 IU) of vitamin E.

Vitamin D

In 2010, the FNB of the Institute of Medicine set the RDA for vitamin D at 15 μg (600 IU)/day for all pregnant women (86). The FNB based this recommendation on a limited number of studies using bone health as the only indicator, assuming minimal sun exposure. Vitamin D, however, has a number of other roles in disease prevention and health (see the article on Vitamin D), and several vitamin D researchers believe that vitamin D requirements for adults, including pregnant women, are higher than the current RDA (87-91). Moreover, a number of studies indicate that vitamin D deficiency and insufficiency are quite common among pregnant women (92-101).

Low vitamin D status in pregnancy has been associated with an increased risk of adverse outcomes for both the mother and the infant. For pregnant women, vitamin D deficiency (serum 25-hydroxyvitamin D less than 50 nmol/L [20 ng/mL]) has been associated with an increased risk of preeclampsia and gestational diabetes (102, 103). For infants, low maternal vitamin D status has been associated with an increased risk of preterm birth (birth before 37 weeks of gestation) and low birth weight (a newborn weighing less than 2,500 grams) (104-106). A pooled analysis of 15 randomized controlled trials concluded that vitamin D supplementation raises serum 25-hydroxyvitamin D during pregnancy and may reduce the risk of preeclampsia, low birth weight, and preterm birth; notably, combined supplementation of vitamin D and calcium may increase the risk of preterm birth (107).

Vitamin D is found in very few foods, and prenatal supplements often contain only 10 μg (400 IU) of vitamin D. Sunlight exposure is the main source of the vitamin: vitamin D3 (cholecalciferol) is synthesized in skin cells following exposure to ultraviolet-B radiation. However, the contribution of sun exposure to vitamin D status depends on many factors, including latitude, skin color, amount of skin exposed, duration of exposure, and the use of sunscreens, which effectively block skin production of vitamin D. Thus, vitamin D supplementation throughout pregnancy is likely needed to achieve body concentrations thought to benefit fetal and maternal health. The Linus Pauling Institute recommends that generally healthy adults, including pregnant women, take 2,000 IU (50 μg) of supplemental vitamin D daily. Because sun exposure, diet, skin color, and obesity have variable, substantial impact on body vitamin D concentrations, measuring serum concentrations of 25-hydroxyvitamin D — the clinical indicator of vitamin D status — is important. The Linus Pauling Institute recommends aiming for a serum 25-hydroxyvitamin D level of at least 75 nmol/L (30 ng/mL).

Vitamin K

The adequate intake (AI) for vitamin K (90 μg/day for women aged 19-50 years and 75 μg/day for those aged 14-18 years) is not increased during pregnancy, and a tolerable upper intake level (UL) has not been set for vitamin K. However, if taken during pregnancy, a number of drugs, including warfarin, rifampin, isoniazid, and anticonvulsants, may increase the risk of neonatal vitamin K deficiency and hemorrhagic disease of the newborn (108).

Placental transfer of vitamin K is low, thus all infants are born with low concentrations of vitamin K. A small proportion of newborns (0.25 to 1.1%) does not have enough vitamin K to make their blood clot and may develop vitamin K deficiency bleeding (VKDB) (109). There are three categories of VKDB depending on the age of onset: early (0-24 hours), classic (one to seven days), and late (two to 12 weeks) (110-112). Early VKDB is seen mainly in infants of mothers taking drugs that inhibit vitamin K, as listed above. Classic VKDB is more common and presents as bruising, gastrointestinal blood loss, or bleeding from the umbilicus, skin, or site of circumcision. Late VKDB is particularly concerning as it can lead to life-threatening intracranial bleeding. Randomized controlled trials have demonstrated that prophylactic intramuscular (IM) vitamin K injection of the newborn raises plasma vitamin K concentration, reduces PIVKA II (a marker of vitamin K deficiency), improves prothrombin time, and decreases the risk of classic VKDB compared to placebo (reviewed in 111). Administration of multiple oral doses of vitamin K can reduce PIVKA II concentrations and raise plasma vitamin K concentration but is associated with an increased incidence of late VKDB (109, 111, 113). The American Academy of Pediatrics and several international professional organizations recommend that all babies receive 0.5 to 1.0 mg intramuscular vitamin K1 injection shortly after birth to prevent VKDB (109, 110, 114)

Minerals

Calcium

Although 200 to 250 mg/day of calcium is transferred to the fetus, primarily in the last trimester, dietary intake requirements of calcium are not increased due to maternal physiological adaptations. In particular, the efficiency of intestinal calcium absorption doubles during pregnancy, and the mineral can also be transiently mobilized from maternal stores (i.e., the skeleton) to support fetal needs for calcium. Permanent demineralization of bone during pregnancy has not been observed (86, 115). Moreover, there is no evidence from randomized controlled trials that calcium supplementation during pregnancy confers any benefit to maternal or fetal bone health (116, 117). The RDA is 1,300 mg/day for women aged 14-18 years and 1,000 mg/day for women aged 19-50 years.   

Calcium intake during pregnancy, however, may influence the risk for pregnancy-induced hypertension (PIH). PIH, which occurs in 10% of pregnancies and is a major health risk for pregnant women and the fetus, is a term that includes gestational hypertension, preeclampsia, and eclampsia. Gestational hypertension is defined as an abnormally high blood pressure that usually develops after the 20th week of pregnancy. In addition to gestational hypertension, preeclampsia includes the development of edema (severe swelling) and proteinuria (protein in the urine). Preeclampsia may progress to eclampsia in which life-threatening convulsions and coma may occur (118). Risk factors for PIH include first pregnancies, multiple gestations (e.g., twins or triplets), chronic high blood pressure, diabetes, and some autoimmune diseases. Although the cause of PIH is not entirely understood, calcium metabolism appears to play a role. Low calcium intake during pregnancy may: (1) stimulate parathyroid hormone release, thereby increasing intracellular calcium and vascular smooth muscle contractility; and/or (2) stimulate renin release, leading to vasoconstriction and retention of sodium and fluid (119). Data from observational studies suggest an inverse relationship between dietary calcium intake and the incidence of PIH (120). Additionally, a recent systematic review of randomized, placebo-controlled trials (RCTs) reported that calcium supplementation during pregnancy (≥1,000 mg/day) was associated with a 35% lower risk of high blood pressure and a 55% lower risk of preeclampsia; the risk reduction for preeclampsia was even stronger for women considered to be at high risk for the condition (78% lower risk compared to placebo) and women with low dietary intake of calcium (64% lower risk compared to placebo) (121). This analysis also found that calcium supplementation lowered the risk of preterm birth by 24%, but no significant effect of calcium supplementation was found regarding the risk of stillbirth, admission to neonatal intensive care unit, or neonatal mortality before hospital discharge. Of four RCTs that monitored maternal death or serious morbidity, one RCT (122) reported a 20% reduced risk for the "severe maternal morbidity and mortality index" (a summary indicator defined as the presence of at least one of the following outcomes: maternal admission to intensive care or any special care unit, eclampsia, severe preeclampsia, placental abruption, HELLP syndrome [hemolysis, elevated liver enzymes, and low platelet count], renal failure, or death) with calcium supplementation; no events occurred in the other three RCTs (121).

Chromium

Chromium is known to enhance the action of insulin; therefore, several studies have investigated the utility of chromium supplementation for the control of blood glucose concentrations in type 2 diabetes (see the article on Chromium). However, its use in gestational diabetes — a condition that affects 4.6%-9.2% of all pregnancies in the US (123) — has not been well studied. Gestational diabetes is a glucose intolerance that usually appears in the second or third trimester of pregnancy; blood glucose concentrations must be tightly controlled to prevent adverse effects on the developing fetus and other pregnancy complications. After delivery, glucose tolerance generally reverts to normal, but women are at a heightened risk of developing type 2 diabetes (124). In fact, a recent systematic review and meta-analysis found that the risk of developing type 2 diabetes in women diagnosed with gestational diabetes is more than 7-fold higher than women not diagnosed with gestational diabetes (125). Gestational diabetes is also considered a risk factor for cardiovascular disease (124). Two observational studies found that serum concentrations of chromium in pregnant women were not associated with glucose intolerance or gestational diabetes (126, 127), although serum chromium concentrations may not necessarily reflect tissue chromium concentrations. An eight-week placebo-controlled trial in 24 women with gestational diabetes found that supplementation in the form of chromium picolinate (4 μg/day of chromium per kilogram of body weight) was associated with lower fasting blood glucose and insulin concentrations (128). However, it is important to note that insulin therapy was still required to normalize the severely elevated blood glucose concentrations. Thus, more research, especially from randomized controlled trials, is needed to determine whether chromium supplementation has any utility in the treatment of gestational diabetes. 

Iodine

Iodine requirements are increased by more than 45% during pregnancy: the RDA for pregnant women is 220 μg/day compared to 150 μg/day for women who are not pregnant. Adequate intake of this mineral is needed for maternal thyroid hormone production, and thyroid hormone is needed for myelination of the central nervous system and is thus essential for normal fetal brain development (129). If iodine deficiency leads to inadequate production of thyroid hormone during pregnancy, irreversible brain damage in the fetus may occur (130). Severe maternal iodine deficiency has also been associated with increased incidence of miscarriage, stillbirth, and birth defects (131).

One of the most devastating effects of severe maternal iodine deficiency is congenital hypothyroidism (132). A severe form of congenital hypothyroidism may lead to a condition that is sometimes referred to as cretinism and result in irreversible mental retardation. Cretinism occurs in two forms, neurologic and myxedematous, although there is considerable overlap between them. The neurologic form is characterized by mental and physical retardation and deafness; it results from maternal iodine deficiency that affects the fetus before its own thyroid is functional. The myxedematous or hypothyroid form is characterized by short stature and mental retardation (133). Severe maternal iodine deficiency has also been linked to neurocognitive deficits in the offspring (134). In severely iodine-deficient pregnant women, iodine supplementation effectively reduces rates of cretinism, and improves offspring cognitive function and survival (reviewed in 135). The timing of iodine supplementation appears to be important: supplementation should be initiated prior to conception and early in pregnancy (before the 10th week of gestation) in order to see beneficial effects on offspring neurocognitive outcomes (135).

Even mild forms of maternal iodine deficiency may have adverse effects on cognitive development in the offspring (136), though this outcome is less well studied. Randomized controlled trials conducted in moderately iodine deficient pregnant women demonstrate that iodine supplementation increases thyroid gland volume but has no effect on thyroid hormone concentrations compared to placebo (reviewed in 130 and 135). The extent to which supplementation in moderately iodine deficient pregnant women affects neurocognitive outcomes in their offspring is currently under investigation (137).

Iodine deficiency is now accepted as the most common cause of preventable brain damage in the world (131). Thus, adequate intake of the mineral throughout pregnancy is critical. A daily supplement providing 150 μg of iodine, as recommended by the American Thyroid Association (138), will help to ensure that US pregnant women consume sufficient iodine. However, it is important to note that several prenatal supplements and some multivitamin/mineral supplements on the market in the US do not contain iodine (139), presumably because manufacturers assume that women receive sufficient iodine through iodized salt and other food sources. For more information on iodine and iodine deficiency disorders, see the article on Iodine.

Iron

Iron requirements are significantly increased during pregnancy: the RDA is 27 mg/day for pregnant women of all ages compared to 15 to 18 mg/day for nonpregnant women. Many women have dietary iron intakes below current recommendations. National surveys in the US indicate that the average dietary iron intake is about 12 mg/day in nonpregnant women and 15 mg/day in pregnant women (140). Iron is needed for a number of biological functions (see the article on Iron), but during pregnancy, the mineral is generally needed to support growth and development of the fetus and placenta and to meet the increased demand for red blood cells to transport oxygen. Intestinal absorption of dietary iron increases during the second and third trimesters to accommodate for expansion of red cell mass (140). Maternal blood volume expands by almost 50% during pregnancy, which results in a hemodilution of red blood cells (141).

Despite maternal physiologic changes that enhance iron absorption, many women develop iron-deficiency or iron-deficiency anemia during pregnancy. The World Health Organization estimates that the worldwide prevalence of anemia among pregnant women is 42%; the prevalence of anemia is much higher in less developed nations compared with industrialized nations, with almost 90% of these anemic women living in Africa or Asia (142). In pregnant women in the US, the prevalence of iron deficiency is 18%, and the prevalence of iron-deficiency anemia is 5% (143). Anemias can be caused by deficiencies in other micronutrients, such as folate or vitamin B12, but iron deficiency is the primary cause of anemia during pregnancy (1). Severe iron-deficiency anemia has been associated with an increased risk of maternal death (142) and with an increased risk of low birth weight infants (<2,500 grams), premature delivery, and perinatal mortality (144).

Two 2015 systematic reviews evaluated the effect of routine iron supplementation compared to placebo or no treatment on maternal and birth outcomes (145, 146). Both reviews found that routine supplementation with iron improved maternal iron status and decreased the risk of iron deficiency and iron-deficiency anemia at term. There is some indication that maternal iron supplementation could improve birth outcomes (namely preterm birth and low birth weight) in developing countries, but the evidence was deemed of low quality (146). Women taking higher doses of iron (≥60 mg/day) tended to have abnormally high hemoglobin values at term and were more likely to report side effects (146); side effects of high-dose iron supplements include nausea, constipation, vomiting, and diarrhea.

Iron status of the woman at the time of conception is important for a healthy pregnancy, to avoid postpartum anemia, and to provide the breast-feeding infant with sufficient iron stores until six months of age, when complementary feeding is recommended. Because of the increased demands for the mineral during the second and third trimesters of pregnancy, iron supplementation (30 mg/day) is usually recommended beginning at 12 weeks’ gestation (147). Absorption of nonheme iron, which is the form of iron found in supplements, is affected by a number of enhancers (e.g., vitamin C) as well as inhibitors (e.g., polyphenols found in tea and coffee). In general, iron supplements are better absorbed on an empty stomach. High doses of iron supplements taken together with zinc supplements on an empty stomach can inhibit the absorption of zinc (140, 148); supplemental iron at 38 to 65 mg/day of elemental iron may decrease zinc absorption (149). For more information about dietary and supplemental sources of iron, as well as the side effects and safety of iron, see the article on Iron

Magnesium

The mineral magnesium plays a number of important roles in the structure and the function of the human body (see the article on Magnesium), and adequate intake of the mineral is needed for normal embryonic and fetal development. National dietary surveys indicate that magnesium insufficiency is relatively common in the US, with 56% of American adults not meeting the EAR — the nutrient intake value that is estimated to meet the requirement of half of the healthy individuals in a particular life stage and gender group (150). Good sources of magnesium include green leafy vegetables, whole grains, and nuts (see the article on Magnesium). Several multivitamin/mineral and prenatal supplements do not contain magnesium or contain no more than 100 mg of magnesium.

Preeclampsia-eclampsia is a disease that is unique to pregnancy and may occur anytime after 20 weeks’ gestation. Preeclampsia is defined as the presence of elevated blood pressure and protein in the urine; severe swelling (edema) may also be present. Eclampsia occurs with the addition of seizures to these symptoms. Approximately 5%-8% of women with preeclampsia go on to develop eclampsia in developing countries, which is a significant cause of maternal death (84).

A 2014 pooled analysis of randomized controlled trials concluded that oral magnesium supplementation during pregnancy has no significant effect on perinatal mortality, small-for-gestational age, or the risk of preeclampsia (151). Intravenous administration of high-dose magnesium sulfate has been the treatment of choice for preventing eclamptic seizures that may occur in association with preeclampsia-eclampsia in late pregnancy or during labor (152-154). Magnesium is believed to relieve cerebral blood vessel spasm and promote peripheral vasodilation, thereby increasing blood flow to the brain (155-157).

Zinc

The RDA for zinc is increased during pregnancy (from 8 mg/day-9 mg/day to 11 mg/day-12 mg/day), and pregnant women, especially teenagers, are at increased risk of zinc deficiency. It has been estimated that 82% of pregnant women in the world may have inadequate intake of dietary zinc (158), leading to poor nutritional status of the mineral. Poor nutritional status of zinc during pregnancy has been associated with a number of adverse outcomes, including low birth weight (<2,500 grams), premature delivery, labor and delivery complications, and congenital anomalies (159). However, the results of maternal zinc supplementation trials in the US and developing countries have been mixed (160). A 2014 systematic review of 16 randomized controlled trials found that zinc supplementation during pregnancy was associated with a 14% reduction in premature deliveries; the lower incidence of preterm births was observed mainly in low-income women (161). This analysis, however, did not find zinc supplementation to benefit other indicators of maternal or infant health.

It is important to note that supplemental levels of iron (38 to 65 mg/day of elemental iron), but not dietary levels of iron, may decrease zinc absorption (149). Because iron supplementation is often recommended during pregnancy (see Iron above), pregnant women who take more than 60 mg/day of elemental iron may want to take a prenatal or multivitamin-mineral supplement that also includes zinc (162).

Other Nutrients

Choline

Choline can be synthesized by the body in small amounts, but dietary intake is needed to maintain health (163). Choline is essential for embryonic and fetal brain development, liver function, and placental function (164). The choline metabolite betaine is a source of methyl (CH3) groups required for methylation reactions; DNA methylation that occurs during embryonic and fetal development modulates gene expression, cell differentiation, and the formation of organs (77). A mother delivers large amounts of choline to the fetus across the placenta and to the infant via breast milk, placing an increased demand on maternal stores of choline during pregnancy and lactation (164). The induction of de novo choline synthesis by the high levels of estrogen during pregnancy helps to meet this increased demand (165). Additionally, pregnant women are encouraged to consume choline-rich foods, such as eggs, meat, and seafood (for dietary sources, see the article on Choline). The adequate intake (AI) for pregnant women is 450 mg/day of choline, slightly higher than the 425 mg/day recommended for nonpregnant women (166).

Case-control studies have reported mixed results regarding the relationship between dietary choline intake or blood choline concentration and the risk of neural tube defects (NTDs). One case-control study reported a lower risk of having an NTD-affected pregnancy in those with the highest intake of betaine and choline combined (167), while two other studies found no association between maternal choline intake and NTD risk (168, 169). Similarly, one case-control study found low serum choline concentration was associated with a higher risk of NTDs (170), while another study found no such association (171). Additionally, it is not known if supplementation with choline or betaine, like supplementation with folic acid (see Folate above), will lower the incidence of NTDs. More research is needed to determine whether choline is involved in the etiology of NTDs.

Maternal intake of choline during pregnancy could possibly affect cognitive abilities of the offspring. Choline supplementation in pregnant rats, as well as rat pups during the first month of life, leads to improved performance in spatial memory tests months after choline supplementation has been discontinued (172). A review by McCann et al. discusses the experimental evidence from rodent studies regarding the availability of choline during prenatal development and cognitive function in the offspring (173). It is not clear whether findings in rodent studies are applicable to humans. One randomized controlled trial demonstrated that choline supplementation (750 mg/day of choline in the form of phosphatidylcholine administered from week 18 of gestation through 90 days postpartum) in pregnant women consuming a moderate-choline diet (approximately 360 mg/day) was safe but did not enhance infant cognitive function at 10 or 12 months of age (174).

Finally, choline is important for homocysteine metabolism during pregnancy. Methyl groups derived from choline may be used to convert homocysteine to methionine. Elevated blood homocysteine concentrations have been associated with increased risk of preeclampsia, premature delivery, low placental weight, low birth weight (<2,500 grams), very low birth weight (<1,500 grams), small for gestational age, NTDs, and stillbirth (48-50).

Essential fatty acids

Although not micronutrients, certain fatty acids are required in the maternal diet during pregnancy and lactation; the US Institute of Medicine’s adequate intake (AI) recommendations for omega-3 and omega-6 fatty acids during pregnancy and lactation are listed in the separate article on Essential Fatty Acids. For more information on the importance of omega-3 fatty acids during these life stages, see two sections in the separate article on essential fatty acids: Visual and neurological development and Pregnancy and lactation. Information about environmental contaminants in fish and supplements is included in the sections, Contaminants in fish and Contaminants in supplements

Safety in Pregnancy

Table 2. UL for Micronutrients During Pregnancy
Micronutrient  Age  UL 
Biotin  14-50 years  NDa 
Folate 14-18 years  800 μg/dayb 
  19-50 years  1,000 μg/dayb 
Niacin  14-18 years  30 mg/dayb 
  19-50 years  35 mg/dayb 
Pantothenic Acid  14-50 years  ND 
Riboflavin  14-50 years  ND 
Thiamin  14-50 years  ND 
Vitamin A  14-18 years  2,800 μg (9,333 IU)/dayc 
  19-50 years  3,000 μg (10,000 IU)/dayc 
Vitamin B6  14-18 years  80 mg/day 
Vitamin B6  19-50 years  100 mg/day 
Vitamin B12  14-50 years  ND 
Vitamin C  14-18 years  1,800 mg/day 
  19-50 years  2,000 mg/day 
Vitamin D  14-50 years  100 μg (4,000 IU)/day 
Vitamin E  14-18 years  800 mg (1,200 IU)/dayd 
  19-50 years  1,000 mg (1,500 IU)/dayd 
Vitamin K  14-50 years  ND 
Calcium  14-18 years  3,000 mg/day 
  19-50 years  2,500 mg/day 
Chromium  14-50 years  ND 
Copper  14-18 years  8 mg/day 
  19-50 years  10 mg/day 
Fluoride  14-50 years  10 mg/day 
Iodine  14-18 years  900 μg/day 
  19-50 years  1,100 μg/day 
Iron  14-50 years  45 mg/day 
Magnesium  14-50 years  350 mg/daye 
Manganese  14-18 years  9 mg/day 
  19-50 years  11 mg/day 
Molybdenum  14-18 years  1,700 μg/day 
  19-50 years  2,000 μg/day 
Phosphorus  14-50 years  3,500 mg/day 
Potassium  14-50 years  ND 
Selenium  14-50 years  400 μg/day 
Sodium  14-50 years  2,300 mg/day (AI) 
Zinc  14-18 years  34 mg/day 
  19-50 years  40 mg/day 
Cholinef  14-18 years  3,000 mg/day 
  19-50 years  3,500 mg/day 
aND, not determinable because data are lacking
bApplies to the synthetic form in fortified foods and supplements
cApplies to only preformed vitamin A (retinol)
dApplies to any form of supplemental α-tocopherol
eApplies only to the supplemental form
fConsidered an essential nutrient, although not strictly a micronutrient

Maternal Micronutrient Requirements During Lactation

Breast-feeding confers health benefits to the child, as well as the mother (175). Breast milk is the ideal source of nutrition for the infant and also contains a number of bioactive compounds important in immunity, such as antibodies, cytokines, antimicrobial agents, and oligosaccharides (176). The American Academy of Pediatrics recommends exclusive breast-feeding for the first six months of infancy, followed by continued breast-feeding as complementary foods are introduced, with continuation of breast-feeding until 12 months postpartum or longer as mutually desired by the mother and child (177). The World Health Organization recommends exclusive breast-feeding for the first six months of life and continued breast-feeding, with complementary feeding, up to two years or more postpartum (178). There are, however, a few exceptions when breast-feeding is contraindicated, including those listed on the CDC website.

Lactation is extremely energy expensive (exceeding pre-pregnancy demands by approximately 500 kcal/day), and macronutrient requirements for breast-feeding women are even higher than during pregnancy (175). Likewise, the intake recommendations (RDA or AI) for most micronutrients, which are based on amounts secreted in breast milk, are higher for lactating women compared to pregnant women (see Table 3). One notable exception is the RDA for iron, which is significantly lower during lactation (9 to 10 mg/day) compared to pregnancy (27 mg/day) (140). Breast milk is considered to be low in iron; however, the iron content of breast milk is not influenced by changes in maternal iron status, such as through maternal supplementation (59). The RDA for folate is also lower during lactation compared with pregnancy. Dietary intake recommendations for calcium remain unchanged for lactating women compared to recommendations for nonlactating women, and calcium content in breast milk does not reflect maternal intake of the mineral. Adequate calcium is maintained in breast milk because of maternal physiological changes that involve transient bone resorption; increased maternal intake of calcium through diet and supplementation does not prevent maternal bone demineralization, and studies have shown that maternal bone mineral content is restored upon weaning (179).

In general, the amounts of water-soluble vitamins (B vitamins and vitamin C) in breast milk reflect maternal intake from diet and/or supplements. Thus, meeting daily intake recommendations for these micronutrients is important for the health of the child. Maternal vitamin deficiencies can negatively affect infant growth and development; for instance, vitamin B12 deficiency during infancy can impair brain development and cause neurological problems (180). Vitamin B12 deficiency has been documented in nursing infants of mothers who have untreated pernicious anemia and also in women who are strict vegetarians (vegans) (181). Vitamin B12 is found only in foods of animal origin and fortified foods, and lactating women who follow vegetarian diets should take supplemental vitamin B12. Vitamin B12 deficiency that results from pernicious anemia can easily be corrected with high-dose daily supplementation or with monthly intramuscular injections of the vitamin (see the article on Vitamin B12). However, there has been relatively little research on the effect of oral vitamin B12 supplementation in lactating women, and it has been suggested that supplementation during lactation may be too late to restore adequate milk concentrations and infant status (182). Supplementation during pregnancy may more effectively improve infant vitamin B12 status. For instance, oral daily vitamin B12 supplementation (50 μg/day) administered from <14 weeks gestation through 6 weeks postpartum significantly increased maternal plasma and breast milk concentrations of vitamin B12 and improved infant vitamin B12 status (183). The concentrations of other water-soluble vitamins in breast milk, including thiamin, riboflavin, and vitamin B6, are also strongly dependent on maternal intake of these vitamins (59, 182). Likewise, vitamin C concentration in human milk varies with the vitamin C status of the mother. Vitamin C supplementation can moderately increase concentrations of the vitamin in breast milk, especially in lactating women with poor vitamin C status (184), and maternal intakes of 100 mg/day maximize the amount of vitamin C in breast milk (185).

Compared to water-soluble vitamins, the concentrations of fat-soluble vitamins (vitamins A, D, E, and K) in breast milk are less correlated with maternal dietary intake. The RDA for vitamin A during lactation is 1,200 to 1,300 μg/day (4,000 to 4,333 IU/day). At such levels of maternal intake, breast milk is a good source of vitamin A and provides the infant with a sufficient amount of the vitamin (186). In contrast, breast milk is considered to be low in vitamins D and K. Vitamin D concentrations in human milk are dependent on maternal vitamin D status, which is determined by the woman’s sun exposure and dietary and supplemental intake. Vitamin D concentrations are low in breast milk, presumably because many women have insufficient vitamin D status. Vitamin D supplementation during lactation has been shown to improve vitamin D status in the woman and the infant (187). The RDA for lactating women is 600 IU/day of vitamin D, but intake at this level in the absence of sun exposure likely results in insufficient amounts for the infant. To prevent vitamin D deficiency and rickets in infants, the American Academy of Pediatrics recommends that all breast-fed and partially breast-fed infants be given a vitamin D supplement of 400 IU/day (177). Liquid vitamin D supplements are commercially available for infant supplementation. The Linus Pauling Institute recommends that all adults take 2,000 IU/day of supplemental vitamin D and aim for a serum 25-hydroxyvitamin D level of at least 75 nmol/L (30 ng/mL). Human milk is also relatively low in vitamin K. Thus, exclusively breast-fed newborns are at increased risk for vitamin K deficiency. In general, newborns have low vitamin K status for the following reasons: (1) vitamin K is not easily transported across the placental barrier; (2) the newborn's intestines are not yet colonized with bacteria that synthesize vitamin K; and (3) the vitamin K cycle may not be fully functional in newborns, especially premature infants (188). Vitamin K deficiency in newborns may result in a bleeding disorder called vitamin K deficiency bleeding (VKDB). Because VKDB is life-threatening and easily prevented, the American Academy of Pediatrics and a number of similar international organizations recommend that an injection of phylloquinone (vitamin K1) be administered to all newborns shortly after birth (110, 114, 177). Additionally, the vitamin E content in breast milk varies with maternal diet and vitamin E supplement use (184, 186). The RDA for vitamin E during lactation is 19 mg/day (28.5 IU/day) of α-tocopherol. National surveys indicate that more than 90% of US adults have daily vitamin E intakes below 12 mg (18 IU) (85)

Maternal dietary intake recommendations for the 14 essential minerals during lactation are shown in Table 3. The content of minerals in breast milk does not correlate well with maternal intake or status, except for iodine and selenium (1, 176). Iodine requirements are increased during lactation: breast-feeding women require 290 μg/day of iodine compared to 220 μg/day for pregnant women and 150 μg/day for nonpregnant, nonlactating women (129). Iodine-deficient women who are breast-feeding may not be able to provide sufficient iodine to their infants who are particularly vulnerable to the effects of iodine deficiency (see the article on Iodine). A daily supplement providing 150 μg of iodine, as recommended by the American Thyroid Association (138), will help to ensure that US breast-feeding women consume sufficient iodine during these critical periods. Additionally, the RDA for selenium is slightly higher for lactating women (from 60 to 70 μg/day), and selenium content in breast milk reflects maternal intake (189).

Table 3. RDA for Maternal Micronutrients During Lactation
Micronutrient  Age  RDA 
Biotin  14-50 years  35 μg/day (AI
Folate 14-50 years  500 μg/daya 
Niacin  14-50 years  17 mg/dayb 
Pantothenic Acid  14-50 years  7 mg/day (AI) 
Riboflavin  14-50 years  1.6 mg/day 
Thiamin  14-50 years  1.4 mg/day 
Vitamin A  14-18 years  1,200 μg (4,000 IU)/dayc 
  19-50 years  1,300 μg (4,333 IU)/dayc 
Vitamin B6  14-50 years  2.0 mg/day 
Vitamin B12  14-50 years  2.8 μg/day 
Vitamin C  14-18 years  115 mg/day 
  19-50 years  120 mg/day 
Vitamin D  14-50 years  15 μg (600 IU)/day 
Vitamin E  14-50 years  19 mg (28.5 IU)/dayd 
Vitamin K  14-18 years  75 μg/day (AI) 
  19-50 years  90 μg/day (AI) 
Calcium  14-18 years  1,300 mg/day 
  19-50 years  1,000 mg/day 
Chromium  14-18 years  44 μg/day (AI) 
  19-50 years  45 μg/day (AI) 
Copper  14-50 years  1.3 mg/day 
Fluoride  14-50 years  3 mg/day (AI) 
Iodine  14-50 years  290 μg/day 
Iron  14-18 years  10 mg/day 
  19-50 years  9 mg/day 
Magnesium  14-18 years  360 mg/day 
  19-30 years  310 mg/day 
  31-50 years  320 mg/day 
Manganese  14-50 years  2.6 mg/day (AI) 
Molybdenum  14-50 years  50 μg/day 
Phosphorus  14-18 years  1,250 mg/day 
  19-50 years  700 mg/day 
Potassium  14-50 years  5,100 mg/day (AI) 
Selenium  14-50 years  70 μg/day 
Sodium  14-50 years  1,500 mg/day (AI) 
Zinc  14-18 years  13 mg/day 
  19-50 years  12 mg/day 
Cholinee  14-50 years  550 mg/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

Safety in Lactation

The tolerable upper intake level (UL) for each micronutrient is shown in the Table 4. The UL, established by the Food and Nutrition Board of the Institute of Medicine, is the highest level of daily intake that is likely to pose no risk of adverse health effects in almost all individuals.

Table 4. UL for Maternal Micronutrients During Lactation
Micronutrient  Age  UL 
Biotin  14-50 years  NDa 
Folate 14-18 years  800 μg/dayb 
  19-50 years  1,000 μg/dayb 
Niacin  14-18 years  30 mg/dayb 
  19-50 years  35 mg/dayb 
Pantothenic Acid  14-50 years  ND 
Riboflavin  14-50 years  ND 
Thiamin  14-50 years  ND 
Vitamin A  14-18 years  2,800 μg (9,333 IU)/dayc 
  19-50 years  3,000 μg (10,000 IU)/dayc 
Vitamin B6  14-18 years  80 mg/day 
Vitamin B6  19-50 years  100 mg/day 
Vitamin B12  14-50 years  ND 
Vitamin C  14-18 years  1,800 mg/day 
  19-50 years  2,000 mg/day 
Vitamin D  14-50 years  100 μg (4,000 IU)/day 
Vitamin E  14-18 years  800 mg (1,200 IU)/dayd 
  19-50 years  1,000 mg (1,500 IU)/dayd 
Vitamin K  14-50 years  ND 
Calcium  14-18 years  3,000 mg/day 
  19-50 years  2,500 mg/day 
Chromium  14-50 years  ND 
Copper  14-18 years  8 mg/day 
  19-50 years  10 mg/day 
Fluoride  14-50 years  10 mg/day 
Iodine  14-18 years  900 μg/day 
  19-50 years  1,100 μg/day 
Iron  14-50 years  45 mg/day 
Magnesium  14-50 years  350 mg/daye 
Manganese  14-18 years  9 mg/day 
  19-50 years  11 mg/day 
Molybdenum  14-18 years  1,700 μg/day 
  19-50 years  2,000 μg/day 
Phosphorus  14-50 years  4,000 mg/day 
Potassium  14-50 years  ND 
Selenium  14-50 years  400 μg/day 
Sodium  14-50 years  2,300 mg/day (AI) 
Zinc  14-18 years  34 mg/day 
  19-50 years  40 mg/day 
Cholinef  14-18 years  3,000 mg/day 
  19-50 years  3,500 mg/day 
aND, not determinable because data are lacking
bApplies to the synthetic form in fortified foods and supplements
cApplies to only preformed vitamin A (retinol)
dApplies to any form of supplemental α-tocopherol
eApplies only to the supplemental form
fConsidered an essential nutrient, although not strictly a micronutrient

Authors and Reviewers

Originally written in July 2011 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in March 2016 by:
Giana Angelo, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in August 2016 by:
Berthold V. Koletzko, M.D., Ph.D.
Professor for Paediatrics, Ludwig-Maximilians-University of Munich
Dr. von Hauner Children’s Hospital, Univ. of Munich Medical Center,
Campus Innenstadt
Munich, Germany

The 2016 update of this article was underwritten, in part, by a grant from Bayer Consumer Care AG, Basel, Switzerland.

Copyright 2011-2017  Linus Pauling Institute


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