Pediatric Clinics of North America
Volume 48 • Number 2 • April 2001
Copyright © 2001 W. B. Saunders Company
PART 2: THE MANAGEMENT OF
BREASTFEEDING
DO BREASTFED INFANTS NEED SUPPLEMENTAL VITAMINS?
Frank R. Greer MD
Departments of Pediatrics and Nutritional Sciences, University of Wisconsin, Madison, Wisconsin
Address reprint requests to
Frank R. Greer, MD
Center for Perinatal Care
Meriter Hospital
202 South Park Street
Madison, WI 53715
e-mail: frgreer@facstaff.wisc.edu
Over the years, there has been considerable disagreement over the use of
supplemental vitamins in breastfed, term infants in the United States.
Deficiencies of the fat-soluble vitamins D and K have been well described in
breastfed infants, and these are the only two vitamins of which supplementation
for breastfed infants is recognized in the current edition of the American
Academy of Pediatrics Pediatric Nutrition Handbook.[23]
FAT-SOLUBLE VITAMINS
Vitamin D
Vitamin D, synthesized in the skin from cholesterol on exposure to ultraviolet (UV) B
radiation and subsequently hydroxylated in the liver (25-OH vitamin D) and kidney
(1,25-OH2 vitamin D), is classified more correctly as a hormone. The parent
compound is found in the diet but also must undergo hydroxylation to become the
active form of the vitamin, 1,25-OH2 vitamin D. Its primary role is to stimulate
intestinal absorption of calcium and phosphorus from the small intestine. It also
promotes renal reabsorption of calcium and phosphorus, and its action on bone
involves bone resorption and bone formation. The molecular effects of 1,25-OH2
vitamin D, like other steroidal hormones, are mediated by intranuclear vitamin D
receptors that bind with 1,25-OH2 vitamin D and act in the cell nucleus to promote
transcription and translation of specific genes to make specific proteins. It is likely
that membrane-bound receptors for 1,25-OH2 vitamin D also are important and act
through signal transduction to promote 1,25-OH2 vitamin D actions such as intestinal
calcium absorption.[20]
Exclusively breastfed infants have several sources of vitamin D, including
transplacental passage, endogenous synthesis (from sunlight exposure), and
exogenous intake. The major metabolite to cross the placenta is 25-OH vitamin D,
and there is a direct relationship between maternal and cord blood levels. Although
relatively little is known about vitamin D storage by the fetus for use after birth,
vitamin D stores of infants born to mothers with a normal vitamin D status are
depleted by 2 months of age.[15]
The vitamin D content of human milk is approximately 20 IU/L, mostly in the form of
25-OH vitamin D (Table 1) . Thus, breast milk is a negligible source for the
recommended vitamin D intake of 300 to 400 IU per day (Table 2) . Vitamin D in
human milk is well correlated with maternal vitamin D intake.[26] Large maternal
intakes of vitamin D (100,000 IU/d) have been reported to increase intake in breastfed
infants to as much as 4500 IU per day, resulting in infantile hypercalcemia.[8] Breast
milk vitamin D concentration also is increased with maternal sunlight exposure,
because the milk concentration is typically higher in the summer months.
Investigators have shown that 1.5 MED (minimal erythemal dose of total body UVB
light exposure, approximately 90 s of irradiation in the white population) to lactating
mothers results in a 10-fold increase in milk vitamin D concentration.[9] Race and
sunlight also affect increased vitamin D levels because blood levels are higher in
white mothers compared with dark-skinned mothers, in whom UVB light absorption
is decreased by skin pigmentation.[26] Sunlight exposure is a source of vitamin D for
breastfed infants because they also show seasonal variations in serum 25-OH vitamin
D concentrations. Investigators have shown that 0.5 to 2.0 hours of sunlight exposure
per week in fully clothed (except for head and hands), white infants in Cincinnati,
Ohio, (39° N latitude) maintain serum 25-OH vitamin D concentrations of more than
11 ng/mL.[26] [27]
TABLE 1 -- VITAMIN CONTENT OF MATURE HUMAN MILK, COW MILK,
AND US FORMULAS
Mature Human
Milk
Cow Milk
Formula
D, IU
<20
24
400
K, mug
2.1
4.9
55
A, IU
2230
1000
2225
E, IU
3.0
0.9
8-20
C, mg
40
17
54-81
Thiamin, B1 , mug
210
300
406-680
Vitamin per Liter
TABLE 1 -- VITAMIN CONTENT OF MATURE HUMAN MILK, COW MILK,
AND US FORMULAS
Mature Human
Milk
Cow Milk
Formula
350
1750
913-1020
93-205
470
406-507
1.5
0.8
5.1-7.1
Folic acid, mug
24-50
50
51-108
B12 , mug
0.5-1.0
4
1.4-2.0
Vitamin per Liter
Riboflavin, B2 , mug
Pyridoxine, B6 ,
mug
Niacin, mg
Data from Committee on Nutrition, American Academy of Pediatrics. In Kleinman RE
(ed): Pediatric Nutrition Handbook, ed 4. Elk Grove Village, IL, American Academy
of Pediatrics, 1998, pp 631-632, 657-658.
TABLE 2 -- VITAMINS SUPPLIED BY MATURE BREAST MILK FEEDINGS OF
120 mL/kg/d (720 mL) TO A HEALTHY 6-kg INFANT
Vitamin
Intake (units/d)
DRI * (units/d)
14.4 IU
300-400 IU
K mug
1.44 mug
5 mug
A IU
1600 IU
375 IU
E IU
2.1 IU
3 IU
C mg
28.8 mg
30 mg
151.2 mug
300 mug
Riboflavin, B2 mug
252 mug
400 mug
Pyridoxine, B6 mug
67-148 mug
300 mug
1.1 mg
5 mg
17-36 mug
25 mug
0.36-0.72 mug
0.3 mug
D IU
Thiamin, B1 mug
Niacin mg
Folic acid mug
B12 , mug
Data from Committee on Nutrition, American Academy of Pediatrics. In Kleinman RE
(ed): Pediatric Nutrition Handbook, ed 4. Elk Grove Village, IL, American Academy
of Pediatrics, 1998, pp 631-632.
*Intake of most water soluble vitamins represents an average value and does not reflect maternal
dietary supplementation.
The supplementation of vitamin D to breastfeeding infants is controversial. In the
United States, where pregnant and lactating women consume vitamin D fortified milk
products and multivitamins containing vitamin D, this issue may be less problematic
than in northern Europe and developing countries, where oral maternal vitamin D
intakes are relatively low.[21] In a study done in white infants in Madison, Wisconsin,
(43° N latitude), infant vitamin D2 supplements during the first 6 months of life were
not necessary to keep 25-OH vitamin D levels (13-25 ng/mL) in unsupplemented,
exclusively breastfed infants (n = 19) in the adult normal range (15-40 ng/mL),
although breastfed infants receiving 400 IU per day vitamin D2 (n = 19) had
significantly higher 25-OH vitamin D serum concentrations (23-37 ng/mL).[11] There
was seasonal variation of serum 25-OH vitamin D3 in this population, reflecting
higher UVB exposure in the summer compared with winter months. The
unsupplemented, breastfed group did not show any evidence of vitamin D
deficiency.[11] At the present time, most cases of vitamin D deficiency rickets in the
United States are reported in dark-skinned, exclusively breastfed infants without
vitamin D supplementation during the first year of life.[3] It is speculated that this
situation is in part caused by poorer penetration of the dark skin by UVB radiation.[30]
Current recommendations by the American Academy of Pediatrics (AAP) state that
"400 IU is recommended for breastfed infants ... as rickets may occur in deeply
pigmented breastfed infants or those with inadequate exposure to sunshine." [23] On the
other hand, the most recent statement from the AAP Work Group on Breastfeeding
states that "Vitamin D may need to be given before 6 months of age in selected
groups of infants.... Vitamin D for infants whose mothers are vitamin D-deficient or
those infants not exposed to adequate sunlight."[4] Also, the most recent Dietary
Reference Intakes from the Institute of Medicine recommends "assuming infants are
not obtaining any vitamin D from sunlight, an AI (adequate intake) of 200 IU/day is
recommended" for infants through the first 12 months of life. They also acknowledge
that "with habitual small doses of sunlight, breastfed infants do not require
supplemental vitamin D."[6] In any event, despite the various recommendations, there
is no known harm from oral vitamin D intakes of 200 to 400 IU per day in breastfed
infants during the first year of life. Also, it would seem prudent that all dark-skinned
infants who are exclusively breastfed be supplemented with 200 to 400 IU per day of
vitamin D. There are two liquid solutions of pure vitamin D available for pediatric
use, but these are so concentrated (8000 IU/mL) that accidental ingestion of them
could result in vitamin D toxicity.
Vitamin K
Vitamin K (phylloquinone) is necessary for the formation of vitamin K dependent
proteins. These proteins have in common gamma-carboxyglutamic acid (Gla), the
unique amino acid formed by the postribosomal enzymatic action of vitamin Kdependent carboxylase. Vitamin K is a necessary cofactor for the activity of this
carboxylase. The formation of the Gla residues on the vitamin K dependent proteins
creates effective calcium binding sites. After the proteins bind calcium, they become
active. Prothrombin is a vitamin K-dependent protein. The precursor of prothrombin,
des-carboxyprothrombin or abnormal prothrombin, is a relatively small molecule
requiring carboxylase and vitamin K for the formation of prothrombin. The presence
of abnormal prothrombin (under carboxylated) in plasma has been proposed as a
measure of subclinical vitamin K deficiency.[14] Other vitamin K-dependent proteins
include coagulation Factors VII and IX and plasma proteins C, S, and Z. Many tissues
have vitamin K-dependent or Gla-containing proteins. This subject has been reviewed
in more detail elsewhere.[14]
The exclusively breastfed infant has limited sources of vitamin K. Compared with
other fat-soluble vitamins, vitamin K is not transported readily across the placenta
from mother to fetus because serum vitamin K concentrations are all but undetectable
in cord blood. Even large maternal doses of vitamin K have little impact on cord
blood concentrations. Like vitamin D, the breast milk concentration of vitamin K is
low and remains low throughout lactation (see Table 1) . On average, the vitamin K
content of human milk is 0.1 to 0.2 mug/dL, which does not supply the current DRI of
1 mug/kg per day (see Tables 1 and 2) . There are large daily variations because the
vitamin K content of milk is affected by dietary intake. Investigators have shown that
maternal pharmacologic supplements of 5 mg per day of vitamin K increase the breast
milk concentration to 4.5 to 6.0 ng/dL and increase serum concentrations in
exclusively breastfed infants to levels comparable with those found in infants fed
formula fortified with vitamin K.[12]
A potential source of vitamin K for newborn infants is the synthesis of vitamin K by
the bacteria of the large intestine; however, for exclusively breastfed infants with an
intestinal predominance of bifidobacteria that do not synthesize vitamin K, this source
is not likely. Investigators have reported that breastfed infants have a near absence of
vitamin K in the stools during the first week of life compared with formula-fed
infants[10] ; however, even for formula-fed infants, these is no clear evidence that
vitamin K synthesized in the large intestine is biologically available.
Vitamin K deficiency in newborns presenting as neonatal hemorrhage is not a major
concern in the United States and Canada, where nearly all newborn infants receive
prophylactic vitamin K at birth. In the classic form of the disease, hemorrhage occurs
in breastfed newborn infants between days 2 and 10 of life, and intracranial
hemorrhage is uncommon. Bleeding may occur from the umbilical cord stump,
gastrointestinal tract, or circumcision site. It is easily treated with parenteral vitamin
K without major sequelae. A second form of the disease, late hemorrhagic disease, is
not as benign. It occurs almost exclusively in breastfeeding infants who have not
received vitamin K prophylaxis or have gastrointestinal disorders associated with fat
malabsorption (e.g., biliary atresia or alpha1 -antitrypsin deficiency) In one series of
131 cases, there were 18 deaths (14%), and 82 (83%) cases of intracranial
hemorrhage. The mean age at onset was 5.6 plus or minus 3.3 weeks.[18] Of the 113
survivors, 27 (24%) had permanent neurologic sequelae. Fifty-five (42%) also had
significant liver disease or malabsorption at diagnosis. A total of 118 infants (90%)
were breastfed. Eighty-nine infants received no newborn vitamin K prophylaxis, and
35 infants received oral prophylaxis. Only five infants were documented to have
intramuscular prophylaxis, and all of these had significant liver disease.
Other than the intramuscular injection of 1 mg of vitamin K at birth, there are no
further recommendations for vitamin K supplements to breastfed infants with wellnourished mothers.[23] If parents refuse the intramuscular injection, then 2 mg of the
parenteral solution should be given orally. Because this is variably absorbed and there
is no well-absorbed liquid product available in the United States for infants, it seems
best to repeat the oral dose at 7 and 28 days after birth, as is done in northern Europe
when oral vitamin K is used in newborns.[13]
Vitamin A
Vitamin A is a generic term for a group of closely related compounds also known as
retinoids. In addition to its role as a chromophore in the retina, it is crucial for
reproduction, cell metabolism, cell differentiation, hematopoiesis, bone development,
and pattern formation during embryogenesis. The retinoids elicit these effects through
their ability to regulate gene expression at specific target sites in the nucleus of cells.
These aspects of vitamin A have been reviewed elsewhere.[14]
Adequate amounts of vitamin A cross the placenta to the fetus, especially in the last
trimester; however, vitamin A stores in the newborn liver are relatively low compared
with those of older infants and children. Mature human milk contains 1850 to 2650
IU/L of vitamin A, and colostrum contains more.[14] Thus, human milk is an excellent
source of vitamin A (see Tables 1 and 2) . In the United States, there is no need to
supplement breastfeeding infants with vitamin A.
Vitamin E
Similar to vitamin A, vitamin E is a generic term for a group of closely related
compounds, the most important of which is alpha-tocopherol. Its primary role in
humans is its ability to serve as an antioxidant in tissues, functioning in cell
membranes as a free radical scavenger. Its metabolism and methods of action have
been reviewed elsewhere.[14]
Transplacental delivery of vitamin E to the fetus is limited, although total body stores
increase in late gestation, together with the amount of adipose tissue. As with vitamin
A, vitamin E is higher in colostrum than in mature milk, which contains
approximately 3 IU/L (see Table 1) . Thus, mature human milk comes close to
meeting the DRI of 3 IU per day of vitamin E[14] (Table 2) . Because no known
deficiencies of vitamin E have been described in healthy term infants fed human milk,
supplements for mothers and their infants are not indicated.
WATER-SOLUBLE VITAMINS
Vitamin C
Vitamin C, or ascorbic acid, is important as an antioxidant and in the synthesis of
neurotransmitters. Placental transfer of vitamin C readily occurs because the
concentration in cord blood exceeds that of the mother's blood. The concentration of
vitamin C in breast milk is generally approximately 40 mg/L (see Table 1) . In wellnourished US women, supplementation of vitamin C does not significantly affect
breast milk concentration. Thus it is not surprising that the DRI for term, breastfed
infants is based on the vitamin C content of mature breast milk and that no
supplementation to infants of well nourished mothers is recommended.[22]
Vitamin B1
Like vitamin B12, vitamin B1 (thiamine) is important as a coenzyme for metabolic
processes, specifically in carbohydrate metabolism. The fetomaternal gradient across
the placenta favors the fetus because fetal blood concentration is higher than is the
maternal concentration. Breast milk concentration is low in colostrum (approximately
20 mug/L) and increases to 210 mug/L in mature milk[22] (see Table 1) . The
requirement for thiamine is related directly to the carbohydrate intake. As with other
water-soluble vitamins, maternal supplementation generally increases the content in
the milk, and infants of well-nourished mothers do not need supplemental vitamin.
The RDA for full-term infants is 300 mug per day. The intake of breastfed infants is
somewhat less than this amount (Table 2) , but deficiency of thiamine (beriberi) is
rare in the United States. Infantile beriberi may occur in mothers who have deficient
intakes of the vitamin, although nursing mothers may not have obvious signs of the
deficiency.[5]
Riboflavin (Vitamin B2 )
Riboflavin is an important component of the coenzymes flavin mononucleotide and
flavin adenine dinucleotide, which function as electron donors and acceptors in
oxidation-reduction systems. They are involved with many metabolic reactions.
Riboflavin readily crosses the placenta, but flavin adenine dinucleotide and flavin
mononucleotide do not. Cord blood concentrations of riboflavin are fourfold greater
than are maternal blood concentrations.[1] The concentration of riboflavin in human
milk, 350 mug/L, does not vary throughout lactation and usually is affected only by
large maternal supplements (three times the maternal RDA)[19] (see Table 1) .
Riboflavin deficiency is rare in mothers in developed countries, and supplements are
not recommended for breastfed infants.
Vitamin B6
Vitamin B6 refers collectively to three naturally occurring pyridines that are important
coenzymes in interconversions of amino acids, neurotransmitter synthesis, and
carbohydrate metabolism, among other functions. Vitamin B6 is readily transported
across the placenta, and this action increases during the third trimester. The maternal
intake of vitamin B6 during the last trimester of pregnancy determines the nutritional
state of the infant with respect to this vitamin. Vitamin concentrations in cord blood
are greater than in maternal blood.[7] Vitamin B6 concentration in human milk
increases with maternal intake or supplementation, but even in mothers whose
average intake is less than the RDA, the milk concentration is approximately 140
mug/L.[16] Thus, if the vitamin B6 intake of the mother is adequate, the healthy
breastfed infant should have sufficient stores of the vitamin to meet all needs, and
additional infant supplements are not necessary.
Niacin
Niacin is a component of the coenzymes nicotinamide adenine dinucleotide and
nicotinamide adenine dinucleotide phosphate, both important in electron transfer and
many metabolic processes. Little is known about placental transfer, but maternal
status is dependent on intakes of niacin and tryptophan, the latter of which is readily
converted to niacin. The concentration of niacin in human milk is 1.5 to 2.0 mg/L and
does not vary with duration of lactation[22] (see Table 1) . As excess dietary tryptophan
is converted to niacin, much of the niacin in human milk is derived from tryptophan.
The RDA for full-term infants is based on the niacin content of human milk. Although
a deficiency state results in the clinical syndrome pellagra, deficiency in breastfed
infants in developed countries is extremely rare, and no supplementation is
recommended.[22]
Folate
Folate, or folic acid, is a coenzyme that participates in the biosynthesis of purines and
pyrimidines, in the metabolism of some amino acids, and in the catabolism of
histidine. Cord blood folate levels are higher than are maternal blood levels, with or
without maternal folate supplements, suggesting a gradient that favors the fetus[17] ;
however, infant folate blood levels decrease quickly during the first 6 weeks of life.
Because the biliary folate content is large, enterohepatic recirculation results in a long
half-life of the vitamin. The folate content of human milk increases from 5 to 10
mug/L to 50 to 100 mug/L at age 3 months.[25] Deficiency states of folate have not
been reported in breastfed, full-term infants, and supplements are not recommended.[24]
Vitamin B12
Vitamin B12 (cobalamin) is important in several metabolic processes. The placenta
concentrates the vitamin, and newborn infants have two- to threefold higher serum
levels than their mothers.[2] Its concentration in human milk decreases from 1.2 mug/L
at age 1 week to 0.5 mug/L at age 6 months (see Table 1) . Maternal supplementation
with vitamin B12 generally increases the content in the milk. Infants of well-nourished
mothers with adequate vitamin B12 intake do not need supplemental vitamin. On the
other hand, it has been reported that infants of strict vegans[28] or mothers with
maternal gastric bypass surgery[29] are at increased risk for vitamin B12 deficiency, and
small supplements of this vitamin may be needed in these clinical situations.
SUMMARY
Table 2 shows that human milk will not meet the DRI for all vitamins in breastfeeding
infants. The most glaring discrepancy between intake and the RDA is for vitamin D,
although, as discussed, infants may synthesize this from sunlight exposure. Vitamin K
must be given in the newborn period. Deficiencies of other vitamins are rare,
especially if mothers are nourished adequately. If breastfeeding infants are to be
supplemented with vitamin D or any other vitamins, the standard liquid preparations
available all contain large amounts of the water-soluble and fat-soluble vitamins
(except for vitamin K), which more than meets the RDA. The milk content of thiamin,
pyridoxine, and niacin is correlated highly with maternal intake, and these vitamins
are all present in relatively large amounts in standard multivitamin tablets given to
lactating mothers. In conclusion, in healthy, breastfed infants of well-nourished
mothers, there is little risk for vitamin deficiencies and the need for vitamin
supplementation is rare. The exceptions to this are a need for vitamin K in the
immediate newborn period and vitamin D in breastfed infants with dark skin or
inadequate sunlight exposure.
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