Iron supplementation of breastfed infants nure_438 71..

77

Ekhard E Ziegler, Steven E Nelson, and Janice M Jeter

Reported here are three studies performed with the objective of finding ways to
improve the iron status of breastfed infants and to prevent iron deficiency (ID).
Participating infants were exclusively breastfed until 4 months of age; thereafter,
they could receive complementary foods and, in some studies, supplemental
formula. In the first study, infants were given medicinal iron between the ages of 1
and 5.5 months. During this period, iron status improved and ID was prevented;
however, these benefits did not continue after the intervention ceased. In the second
study, infants received medicinal iron or an equivalent amount of iron from an
iron-fortified cereal between the ages of 4 and 9 months. Again, iron
supplementation largely prevented ID from occurring, while non-anemic ID and ID
anemia occurred in the control group as well as in the intervention groups before the
intervention began. In the third study, infants received dry cereals fortified with
electrolytic iron or with ferrous fumarate between the ages of 4 and 9 months. The
cereals were equally effective in providing relative protection from ID. The results of
these three studies indicate it is possible to protect breastfed infants from ID and IDA.
© 2011 International Life Sciences Institute

INTRODUCTION estimated at 6.9 mg per day between 7 and 12 months of

When high need for a nutrient meets with a diet that is
low in the nutrient in question, there is a risk of defi-
ciency. The breastfed infant exemplifies this constellation
with regard to iron. The need for iron is high due to rapid
growth, and the diet (breast milk and typical complemen-
tary foods) is low in iron. During the first few months of
life, the breastfed infant is protected from iron deficiency
(ID) by the usually generous amount of iron the infant
receives from the mother. This birth iron endowment
(BIE) provides the infant for some time after birth with
the iron needed for growth. This independence from
dietary iron ends when the iron endowment becomes
exhausted, which usually happens around 4–6 months of
age. The infant then needs iron from exogenous sources
to meet its needs for growth and the replacement of inevi-
table losses. Breast milk contains only small amounts of
iron (0.2–0.4 mg/L), which, in spite of being highly bio-
available,1,2 meet only a fraction of the infant’s needs,
age.3 Given these facts, it is not too surprising that ID and
even iron deficiency anemia (IDA) can occur in breastfed
infants. For the present discussion, ID is defined as a state
with exhausted iron stores, indicated by a plasma ferritin
concentration of <10 mg/L. When ID is accompanied by
evidence of limited tissue iron availability, such as
anemia, ID is considered severe.
IRON DEFICIENCY AMONG BREASTFED INFANTS
Iron deficiency in the first six months of life
It is well documented that some breastfed infants develop
ID before 6 months of age, a condition known as early ID.
Makrides et al.4 reported that, in Australia, 15% of
6-month-old breastfed infants had ID and 1% had IDA.
In Sweden, Domellöf et al.5 found the prevalence of IDA
among 5-month-old infants to be about 1% and Lind
et al.6 found IDA in 2% of 6-month-old infants. For

Affiliations: EE Ziegler, SE Nelson, and JM Jeter are with the Fomon Infant Nutrition Unit, Department of Pediatrics, University of Iowa, Iowa
City, Iowa, USA.
Correspondence: EE Ziegler, Fomon Infant Nutrition Unit, Department of Pediatrics, A-136 MTF, Oakdale Research Park, 2501 Crosspark
Road, Coralville, IA 52241-8802, USA. E-mail: ekhard-ziegler@uiowa.edu, Phone: +1-319-335-4570, Fax: +1-319-335-4856.
Key words: breastfeeding, complementary feeding, infants, iron supplementation

doi:10.1111/j.1753-4887.2011.00438.x
Nutrition Reviews® Vol. 69(Suppl. 1):S71–S77 S71
Norway, Hay et al.7 reported the prevalence of “low iron
status” to be 4% at 6 months. For Chile, Lozoff et al.8
reported that 3.6% of predominantly breastfed infants
had IDA at 5–6 months of age, while in Turkey, Arvas
et al.9 found IDA in 9.5% of breastfed infants at 4 months
of age. Denmark seems to be an exception in that no ID
was found at 6 months of age.10 In our own studies of
breastfed infants in the United States, early ID and IDA
have been observed with regularity (see below).11–13 It is
thus evident that not all breastfed infants are protected
from ID by their BIE during the first 6 months of life.
A measure of the size of an infant’s BIE may be
obtained from the concentration of ferritin in cord blood
or blood obtained within 2 months of birth. Based on
ferritin concentrations, which show variation as large as
20-fold,11–17 the size of the BIE is known to vary greatly.
Infants born with a low BIE would be expected to be at
high risk of ID before the age of 6 months. Tamura et al.15
showed that infants born with cord ferritin concentrations
in the lowest quartile (<76 mg/L) were at risk of impaired
mental and psychomotor development at 5 years of age.
Georgieff et al.18 reported that infants born with low iron
stores have poorer iron nutritional status at 9 months
of age than infants born with normal stores. Our own
observations11–13 seem to be the first to show that a low BIE
can lead to ID in the first 6 months of life. Without excep-
tion, infants who developed IDA in the first 6 months of
life were born with a low BIE, whereas those who devel-
oped ID only were not uniformly born with a very low BIE.
Although the cause of variation in BIE is not known, it
must be assumed that low maternal iron status plays a role,
albeit a role of unknown magnitude.
Iron deficiency late in the first year of life
During the second 6 months of life, most infants have
used up the iron provided to them by their mothers. Only
the infants born with the largest BIEs continue to derive
protection against ID.16 After the BIE has been used up,
iron status reflects the balance between iron intake and
iron use for growth. Given the low iron content of breast
milk, it is not too surprising that an association between
the duration of breastfeeding and the occurrence of ID
has been documented in several localities, including
Canada,19 Korea,20 Turkey,9 Mexico,21,22 and the United
States.23 In our own studies of breastfed infants about 6%
of infants developed ID between 6 and 12 months of
age.11,12 In contrast with infants who developed ID before
6 months of age, these infants were not born with par-
ticularly low BIE and ID was mostly mild, i.e., without
anemia. Typical complementary foods are low in iron
content and many infants do not regularly consume
meats or iron-fortified foods that are the most reliable
sources of iron for infants.24
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Iron deficiency during the second year of life
During the second year of life the majority of infants have
been weaned off the breast and those who continue to be
breastfed consume a variety of other foods. Iron needs
continue to be relatively large and are not always met by
the typical toddler diet. That ID is relatively common in
the second year of life is thus not too surprising and is
well documented in the literature7,20,25–30; its prevalence
has also not changed much in recent decades.29 In one of
our own studies11 the prevalence of ID at 15 and 18
months of age was 12%, and in another study12 37% of
toddlers between the ages of 12 and 24 months had ID. In
neither study did we observe any IDA during the second
year of life.
Iron supplementation and growth
In some studies a negative effect of iron supplementation
on the growth of infants has been observed.31,32 The effect
on growth was seen only in iron-replete infants and not
in those with low or depleted iron stores. We similarly
observed small but significant effects on growth.11,12
Although the effects on growth are small, they suggest
that iron supplementation should be undertaken only
with good reason and probably not in infants with replete
iron stores.
IRON SUPPLEMENTATION STUDIES
Given the potential of severe ID to impair the neurocog-
nitive development of infants,33–35 prevention of ID in
breastfed infants is of considerable importance. To be
useful, preventive measures must not only be effective,
they should also be free of adverse effects and should be
simple to administer. Our group has undertaken several
studies that examined different means of iron supple-
mentation of breastfed infants. In each of the studies,
infants were breastfed exclusively until 4 months of age.
After 4 months infants could receive complementary
foods and, with the exception of the DryCereal study
described below, could receive some formula. Breastfeed-
ing continued up to 5.5 months in all infants; in many
infants it continued much longer, even into the second
year of life in some. In each study, infants visited the study
center every 4 weeks and had capillary blood drawn at
predetermined ages. In the first study (EarlyFe), medici-
nal iron was given between the ages of 1 and 5.5 months.
In the second study (FeCereal) medicinal iron drops or a
wet-pack cereal were given between 4 and 9 months of
age. The third study (DryCereal) compared two sources
of iron (electrolytic iron and ferrous fumarate) as fortifi-
cants of dry infant cereals, which were given between the
ages of 4 and 9 months.
Nutrition Reviews® Vol. 69(Suppl. 1):S71–S77
Figure 1 Plasma ferritin concentrations of breastfed infants receiving medicinal iron (Fe) or placebo from 1 to 5.5
months of age. Reproduced with permission from Ziegler et al.11
The EarlyFe study11 was a prospective double-blind
study that was designed to answer the question of
whether iron supplementation from an early age can
augment iron stores, which at that age tend to be large,
and whether such augmentation, if it occurred, was
carried forward beyond the period of actual supplemen-
tation. In other words, could early iron supplementation
also protect against iron deficiency later in the first year of
life? Breastfed infants were enrolled at 1 month of age and
randomly assigned to a daily supplement of 7 mg of iron
in the form of ferrous sulfate, or to a placebo of similar
appearance and taste. The intervention, from 1 to 5.5
months of age, was completed by 31 infants in the iron
group and 32 infants in the placebo group. Infants were
followed up to 18 months.
Figure 1 shows that plasma ferritin levels were sig-
nificantly increased during the supplementation period,
indicative of augmentation of iron stores. However, soon
after the iron supplementation ceased, the difference in
ferritin levels disappeared, indicating that augmentation
of iron stores did not extend much beyond the period of
actual supplementation. Plasma concentration of sTfR
was significantly lower at 5.5 months in the iron group
than in the placebo group, but there was no difference in
hemoglobin concentration at any time. Small differences
in relative distribution width and mean corpuscular
volume were observed during, as well as after, the inter-
vention period. In the placebo group, one infant devel-
oped IDA and one developed ID by 5.5 months of age,
whereas in the Fe group no infant developed ID. After the
intervention, one infant in the Fe group developed IDA at
Nutrition Reviews® Vol. 69(Suppl. 1):S71–S77
9 months. Six subjects (among 52 followed to 18 months)
developed ID at 15 and/or 18 months (prevalence 12%),
but none developed IDA. Although weight gain among
females was significantly slower in the Fe group, overall,
there was no significant effect of iron supplementation on
weight gain or length gain. Of note is that plasma ferritin
concentrations tracked very strongly from 1 month all
the way to 18 months.
The FeCereal study12 was a randomized open-label
study designed to examine, in comparative fashion, two
regimens of providing iron to infants from 4 to 9 months
of age. The primary aim of this study was to examine iron
nutrition during the period when infants begin to exhaust
their BIE and become dependent on exogenous sources of
iron. Around the age of 4 months infants begin to receive
complementary foods, but many of these foods are poor
sources of iron.24 We hypothesized that the regular con-
sumption of iron either in the form of medicinal iron or in
the form of iron-fortified cereal would protect infants
from ID and maintain iron status at a higher level than that
of control infants lacking regular consumption of iron.
Exclusively breastfed infants were randomized at 4
months to either medicinal iron (FeMed) in the amount of
7 mg per day,or to a wet-pack cereal (FeCer) that provided
7 mg of iron each day, or to a control group in which
infants received complementary foods entirely at the
parents’discretion.Medicinal iron and the wet-pack cereal
both provided iron from ferrous sulfate.
Iron status was improved by medicinal iron and wet-
pack cereal to about the same degree. Plasma ferritin con-
centrations in both intervention groups were significantly
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Figure 2 Plasma ferritin concentrations of breastfed infants receiving medicinal iron (FeMed) or iron-fortified cereal
(FeCer) from 4 to 9 months of age. Reproduced with permission from Ziegler et al.12
higher than in the control group (Figure 2). As in the
EarlyFe study, the effect on iron status was limited to the
intervention period, with no effect on iron status soon
after termination of the intervention. One infant devel-
oped IDA at the age of 2 months and was not random-
ized. In the control group, two infants developed IDA (by
5.5 months) and six infants developed ID. The 14.3%
prevalence was significantly (P = 0.016) greater than in
the combined FeMed and FeCer groups, for which it was
2.5%. At 12 months of age, 12 infants (9.6%) had ID.
During the second year of life, 37% of subjects had ID on
one, two, or three occasions, but none had IDA. The
prevalence of ID was significantly (P < 0.001) higher in
the control group than in the combined intervention
groups, suggesting there was still some effect from the
intervention. As noted in the earlier study, plasma ferritin
tracked strongly from 1 month to 24 months. Growth
(weight and length gain) was significantly lower
(P = 0.027 for weight, P = 0.011 for length) in the FeMed
group compared to the control group.
Our third study, the DryCereal study,13 was a ran-
domized double-blind study designed to compare ferrous
fumarate as fortification iron of a dry infant cereal with
electrolytic iron, the widely used source of fortification
iron. Because of its organoleptic properties, electrolytic
iron is widely used to fortify infant cereals, but its bio-
availability is considered to be poor.36,37 Ferrous fumarate,
on the other hand, is more available and is suitable as a
fortificant of cereals in that it does not cause discoloration
or changes of taste.38 We therefore hypothesized that
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cereal fortified with ferrous fumarate would be more effi-
cacious in maintaining iron status and preventing ID
than cereal fortified with electrolytic iron. Exclusively
breastfed infants were enrolled at age 2 months and were
assigned at random to one of the two cereals, which were
fed daily between the ages of 4 and 9 months. The amount
of cereal fed was greater than the amount that free-living
infants typically consume. Three infants developed
IDA by 4 months of age; they were not randomized and
were treated. Three additional infants developed ID at 4
months and these infants were randomized.
As Figure 3 shows, ferritin concentrations were quite
similar during the intervention. The small persistent dif-
ferences in favor of ferrous fumarate were not statistically
significant. During the intervention, none of the study
infants developed IDA, but four infants developed ID
(two each with fumarate and electrolytic iron), including
the two infants who already had ID at the time of ran-
domization. The prevalence of ID during the intervention
(4.2%) was lower than the prevalence observed in the
control group of the FeCereal study (14.3%), suggesting
that iron-fortified dry cereal is effective in providing rela-
tive protection of infants from ID. It was concluded that
electrolytic iron and ferrous fumarate were equally effec-
tive as fortification sources of iron in infant cereals.
Iron deficiency during the first year of life
ID and IDA were observed during the first 6 months of
life in each of our supplementation studies of breastfed
Nutrition Reviews® Vol. 69(Suppl. 1):S71–S77
Figure 3 Plasma ferritin concentrations of breastfed infants receiving dry cereal fortified with electrolytic iron or
ferrous fumarate. None of the differences were statistically significant. Reproduced with permission from Ziegler et al.13

infants. ID and IDA occurred mostly, though not exclu-
sively, among infants who did not receive supplemental
iron, i.e., infants in the placebo group of the EarlyFe
study, infants in the control group of the FeCereal study,
and infants in most studies before starting interventions
at 4 months of age (N = 291). Data for infants who devel-
oped IDA (N = 8) are summarized in Table 1. The preva-
lence of IDA was 2.75%. Since the 10th centile for plasma
ferritin (PF) was 124 mg/L at age 1 month and 64 mg/L at
age 2 months, all but one infant with IDA had early PF
below the 10th centile and, thus, were born with a low
BIE. The sole exception was infant 9,905 who at 1 month

Table 1 Occurrence of iron-deficiency anemia (IDA) and iron deficiency

(ID) in breastfed infants during the first 6 months of life.
Group and subject no. PF at month 1 or 2 Age (months) PF (mg/L) Hb (g/L)
(mg/L)
IDA
8,325 60 5.5 5 93
10,117* 23 2 6 93
9,905 222† 5.5 5 98
9,950 34 5.5 4 104
10,068 51‡ 5.5 7 99
10,935* 29‡ 4 5 101
10,939 55‡ 4 4 105
10,941 39‡ 4 2 100
ID
9,765 203 5.5 7 116
9,931 229 5.5 9 112
9,938 159 5.5 7 109
10,913 49‡ 4 8 110
10,933 32‡ 4 9 119
10,937 34‡ 4 5 119
10,993 44‡ 5.5 9 107
10,924 65‡ 5.5 7 114
* Siblings.
†
Elevated C-reactive protein.
‡
PF at 2 months of age.
Abbreviations: Hb, hemoglobin; PF, plasma ferritin.

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had a PF of 222 mg/L. However, since this infant had an
elevated C-reactive protein level of 3.2 mg/dL, an acute
reaction may have raised the PF, thereby masking the
presence of low iron stores. Thus, a low BIE seems to be a
prerequisite for IDA in the first 6 months of life. All
infants who developed IDA received treatment with iron.
Non-anemic ID also occurred in the first 6 months of life
(N = 8) and data are summarized in Table 1. The preva-
lence of ID without anemia was 2.75%. Contrary to
infants who developed IDA, these infants did not all have
low PF at 1 or 2 months of age. None of these infants
received iron treatment and none went on to develop
IDA later. During the second 6 months of life, we did not
observe IDA, but non-anemic ID occurred in about 5.6%
of infants. At 12 months, ID was present in 6.8% of
infants.
CONCLUSION
Breastfed infants can develop ID, including IDA, which
represents severe ID. In the three studies reviewed here,
IDA occurred in 2.75% of breastfed infants in the first 6
months of life. All of these infants were born with a low
birth iron endowment. An additional 2.75% of infants
developed ID in the first 6 months of life. In the second 6
months of life, 5.6% of infants developed ID but no infant
developed IDA. Medicinal iron prevented ID and IDA
but had a small yet significant negative effect on growth.
The feeding of iron-fortified cereals, both dry and wet-
pack, almost completely prevented ID. Our data suggest it
is possible to prevent IDA and almost all ID in breastfed
infants.
Acknowledgement
Funding. The studies reviewed here were supported by
the National Institutes of Health (grant HD40315).
Declaration of interest. The authors have no relevant
interests to declare.
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