IRON BALANCE AND REQUIREMENTS IN INFANCY

COMMITTEE ON NUTRITION

134

IRON BALANCE AND REQUIREMENTSIN INFANCY

H UMAN iron requirements and metabo-

lism of iron during the first 18

months of life have been the subjects of a

number of reports, reviews, and commen-

taxies over the past decade.1#{176} Sufficient

knowledge has been accumulated to permit

a clear statement of dietary recommenda-

tions. Implementation of these would assure

a satisfactory iron intake for the majority of

North American infants and minimize the

incidence of serious iron deficiency.

Several official recommendations concern-

ing human iron requirements have been

made.�9 Not all have emphasized clearly

the unique requirements of infants, espe-

cially low birth weight infants. In addition,

they have failed to agree upon dietary re-

quirements during the first year of life and

have not indicated practical ways of achiev-

ing a satisfactory iron intake. The present

memorandum reviews current knowledge

concerning iron needs of infants, attempts to

quantitate iron requirements in relation to

birth weight and age, and examines practi-

cal methods for assuring adequate iron in-

takes. In addition, certain persistent gaps in

our understanding of iron metabolism, sub-

jects of controversy, and areas of investiga-

tive potential are reviewed.

IRON ENDOWMENT OF THE NEWBORN

Data obtained from carcass analysis per-

formed on a small number of stillborn in-

fants indicate that the body of the average

term weight infant contains about 75

mg/kg of iron. There is a considerable

range, however, in the actual values ob-

tained by this measurement.1#{176} The iron con-

tent of the circulating blood can be fairly

accurately estimated from the red cell mass,

and it is evident that more than three quar-

ters of the infant’s iron endowment is in the

red cell. Tissue stores as such probably ac-

count for less than 10 to 20 mg of iron.” No

data are available concerning the effect of

maternal iron depletion upon the extra-he-

moglobin iron stores of the fetus; but, be-

cause of the small size of this iron compart-

ment, its effect on iron endowment must

be minimal. Since iron stores cannot be

measured accurately in living infants, most

attention has centered upon those factors

which influence the initial hemoglobin

mass. In normal newborns, levels of hemo-

globin in cord blood vary from 13.7 to 20.1

gm/ 100 ml” and hematocrits vary from

53% to 79%�13 Differences between these ex-

tremes may constitute differences in body

iron amounting to as much as 50 mg. The

factors which contribute to this variability

are not well defined. Most evidence mdi-

cates that the maternal iron status has little

effect on the infant’s initial hemoglobin

level. Multiparity, low socioeconomic sta-

tus, and racial factors are commonly linked

with a high incidence of iron-deficiency

anemia in the older infant. The frequent as-

sociation of these situations with low birth

weight and with an inadequate postnatal

intake of iron are probably far more impor-

tant than any maternal effects on the in-

fant’s iron endowment�’4”3 Likewise, the

magnitude of the placental transfusion, al-

though important, does not have the deci-

sive effect upon a broad range of neonatal

hemoglobin values.16”7 A systematic study

of the regulation of fetal erythropoiesis is

needed to provide a better understanding

of the causes of variability in the infant’s

iron endowment.

During the 6 to 8 weeks following birth,

erythropoiesis virtually ceases. The concen-

tration of circulating hemoglobin decreases

at a rate which is proportional to the short

life span of fetal red cellsls and to the ex-

panding volume of distribution. The iron

derived from red cell breakdown is retained

and used when hematopoiesis resumes. The

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AMERICAN ACADEMY OF PEDIATRICS 135

size of this reserve and the time and rate at

which it is utilized depends upon the size

of the initial hemoglobin mass.

In addition to low birth weight infants

and those with low initial hemoglobin 1ev-

els, infants who experience various types of

blood loss are at risk for development of

iron deficiency. The iron endowment of an

occasional infant may be reduced by blood

loss in the perinatal period. Massive feto-

maternal hemorrhages during pregnancy,

though unusual, have been documented19

and iron-deficiency anemia due to chronic

transplacental hemorrhage has been recog-

nized at birth. 20.21 Transfusions between

identical twins, energetic diagnostic phle-

botomy, external hemorrhage, and ex-

change transfusions may significantly di-

minish the hemoglobin mass.

The only practical indicators of the new-

born’s iron endowment are body weight

and initial hemoglobin level. Measurement

of hemoglobin or hematocrit should be per-

formed in all infants in the neonatal period

if an assessment of iron endowment is

sought. This may be performed from free

flowing capillary blood on the third or

fourth day of life. When this value is exam-

ined in relation to birth weight, most in-

fants with greater than normal iron require-

ments during the first year will be identi-

fied.

ASSESSMENT OF IRON STATUSOF THE INFANT

A well defined sequence of changes oc-

curs in progressive iron depletion.

1. The storage forms of iron, hemosid-

erin and ferritin, disappear and cannot be

demonstrated in bone marrow and other re-

ticuloendothelial tissues.

2. The level of serum iron decreases and

concomitantly the serum iron-binding ca-

pacity increases, resulting in a decreased

percent iron saturation. A serum iron satu-

ration of less than 15% is indicative of iron

depletion.

3. A slight decrease in the circulating red

cell mass occurs.

4. Changes in red cell morphology, in-

eluding microcytosis and hypochromia, and

poikilocytosis appear.

5. Anemia of a progressive degree of se-

verity supervenes.

6. Decreases of the intracellular iron

content of enzymes ultimately develop, al-

though the point at which this depletion

begins is uncertain.”

During infancy, normal values for the

various measures of iron balance differ con-

siderably from those observed in adults.

Unless appropriate standards based upon

age are used when evaluating infants in the

first 18 months of life, misinterpretations

are unavoidable. Bone marrow hemosid-

erin, a form of storage iron that is easily ac-

cessible to study, is virtually absent after 6

months of age.” Levels of serum iron in

healthy infants are lower than are those of

adults. The ranges of hemoglobin and he-

matocrit values are considerably lower than

those of the adult. The practice of reporting

hemoglobin values of infants as a percent

of an arbitrary adult standard should be

abandoned to avoid an unwarranted diag-

nosis of anemia.

Hemoglobin concentration and hemato-

crit are widely used to assess iron ade-

quacy. Sturgeon4 reported that, when nor-

mal infants were provided with relatively

generous amounts of food or medicinal iron

( between 1 to 2 mg/kg/day), the mean he-

moglobin level at 1 year of age was 11.6

gm/ 100 ml. Administration of parenteral

iron to such infants at 9 months of age in-

creased the mean hemoglobin by less than

1 gm/100 ml (mean, 12.3 gm/100 ml). Be-

tween 3 and 18 months of age, a hemoglo-

bin of about 12 gm/ 100 ml, or a hematocrit

of 36%, may be considered optimal. Since

hemoglobin and hematocrit values will as-

sume a “normal” or Gaussian distribution,

hemoglobin levels as low as 11 gm/100 ml,

and hematocrits as low as 33% will fall

within one and a half standard deviations

of these means and should be considered

“normal.”

The prevalence of iron depletion or iron

deficiency depend upon the criteria em-

ployed for diagnosis. By the time significant


136 IRON IN INFANCY

degrees of anemia develop due to made-

quate hemoglobin synthesis, iron deficiency

is fairly advanced and morphologic abnor-

malities of the red cells are evident. The

need to fulfill at least minimum diagnostic

criteria for iron deficiency anemia must be

emphasized. Minimum criteria include mi-

crocytosis and hypochromia of the red cells

in a smear of peripheral blood and a re-

sponse to specific therapy. A careful history

(including family history), physical exami-

nation, and examination of the blood smear

may suggest other forms of anemia, for

which iron therapy will be ineffectual.

NON-HEMOGLOBIN ASPECTS OFIRON DEFICIENCY

Iron is an important constituent of sev-

eral intracellular oxidative enzymes. The

activities of various iron-containing en-

zymes have been studied in iron-deficient

animals and humans. Activity of some en-

zymes, and cofactors such as cytochrome C

and aconitase, is decreased while activity of

others, such as catalase and cytochrome oxi-

dase, is unchanged.24”5 Whether or not

these decreases have functional signifi-

cance is uncertain. For example, the respi-

ration of leukocytes from iron-deficient pa-

tients is normal’6 and oxygen consumption

by the iron-deficient patient does not differ

from normal.27 On the other hand, oxidative

metabolism in muscle homogenates from se-

verely iron-deficient rats is significantly

impaired.25

An increase in the frequency of respira-

tory infections has been reported in infants

with iron deficiency, as well as a reduced

incidence in such infections in children re-

ceiving iron supplements, even when signif-

icant anemia was absent.28 Confirmation of

such effects would imply previously unsus-

pected metabolic functions of iron in hu�

mans. The proper design and control of

prospective studies to document this obser-

vation are extremely difficult and, at pres-

ent, such effects of iron deficiency or of

therapy must be considered unproven.

Symptoms such as fatigue, weakness, and

pallor, commonly ascribed to iron defi-

ciency, have been shown to be unrelated to

the levels of hemoglobin and hematocrit in

surveys of otherwise healthy individuals.’9

The entire question of tissue effects of iron

depletion is of great interest and demands

imaginative investigation.30

IRON ABSORPTION

Iron is absorbed from both dietary and

medicinal sources even early in life.31’3’

However, in the term infant, only a rela-

tively small amount of absorbed iron is in-

corporated into circulating hemoglobin dur-

ing the first 6 months of life. This point was

demonstrated convincingly by the studies

of Smith and associates,33 who labeled the

hemoglobin of infants in utero with Fe55.

By 6 months of age, the specific activity of

the hemoglobin had decreased by only

about 20%. These data indicate that only a

small amount of postnatally absorbed iron

is incorporated into hemoglobin and sup-

port the observations that iron supplemen-

tation of the diets of full-term infants has a

minimal effect on hemoglobin levels during

the first 4 to 5 months of life.�’8 Iron which

is absorbed in the early weeks of life,

however, may exert a prophylactic effect

against iron deficiency anemia in the later

months of infancy.’8 By contrast, premature

infants incorporate considerable amounts of

dietary iron into hemoglobin by 2 to 4

months of age.34

The efficiency of absorption of various

forms of dietary iron depends to some ex-

tent upon the food in which it is contained.

In most estimates of dietary iron require-

ments, an absorption of 10% is assumed.

This value is merely a convenient approxi-

mation and may not be valid for an individ-

ual patient. Non-anemic infants may absorb

between 5 and 20% of iron from eggs,

meats, and cereals. In contrast, premature

infants have been shown to absorb an aver-

age of 32% of iron contained in fortified

milks.31’34 This is comparable to absorption

of medicinal iron by infants with iron defi-

ciency.35

Dietary constituents such as ascorbic

acid increase absorption of dietary iron ap-



parently by maintaining ionic iron in the

ferrous form.�6 Other substances such as

phosphates and phytates may decrease iron

absorption by forming insoluble complexes,

although the effect of phytates present in

the usual diet is probably not significant.3�

IRON EXCRETION AND BLOOD LOSS

Physiological iron excretion is probably

negligible during infancy,’ but blood loss of

any sort imposes an increased need for iron.

The possibility of blood loss should be con-

sidered in every infant or child with severe

iron deficiency. Wilson and associates have

described a syndrome of chronic blood loss

due to gastrointestinal intolerance to whole

cows milk and believe it to be a common

cause of iron deficiency anemia.38’39 A

lively controversy is now in progress con-

cerning the importance of this condition.

Diamond states that he has recognized it

only once or twice in his large experience40

and believes blood loss is a secondary gas-

trointestinal manifestation of iron defi-

ciency rather than a primary cause. The

prevalence of this syndrome must be deter-

mined in anemic infants before its impor-

tance as a cause of iron deficiency anemia

can be established. In some areas of the

country hookworm infestation may be a

common cause of iron deficiency.

IRON CONTENTS OF FOODS

Human and cows milk contain little iron

(about 1.5 mg/l and 0.5 mg/l, respec-

tively) �41 42 About 15 quarts of cows milk

would have to be consumed each day to

provide enough iron to meet the require-

ments of normal infants during the first

year of life! When milk accounts for a large

proportion of the infant’s calories, the diet

will perforce be grossly deficient in iron.

The most important source of iron in the

diet of American infants is cereal that has

been artificially fortified with reduced iron

or iron-pyrophosphate during processing.

Such cereals contain 8.6 to 22 mg of iron in

each dry ounce. Limited amounts of eggs

and meats are ordinarily consumed during

the first year of life and so usually contrib-

ute a relatively small proportion of the total

iron requirements. Although it is sometimes

believed that the child receiving only

human milk does not become iron deficient,

there is little published data to support this

opinion. In fact, in a small series of pa-

tients, Moe has shown the same incidence

of iron deficiency in babies fed human milk

as in those fed cows milk.’

It has not been widely appreciated that

methods of preparation and cooking affect

the iron content of food. Although Moore

has reported that the iron content of some

acid foods prepared at home in iron utensils

may be increased 30 to 100 times over that

of the same food cooked in glass or alumi-

num utensi1s,�� the effect of cooking vessels

on iron content of ordinary foods is far less

striking.�� In certain geographic regions, a

high iron level in soil or water may increase

the iron content of the diet sufficiently to

invalidate calculations of dietary iron based

only on food composition tables. In fact,

“contamination” of foods by non-food iron

may represent a most significant source of

iron, although the strict sanitary methods

which are used for modern food processing

in fact result in exclusion of much iron from

the diet. A recent study showing a striking

geographic variability in the prevalence of

anemia in preschool American children sup-

ports the thesis that local factors may

appreciably affect iron balance.4�

IRON REQUIREMENTS

The amount of iron which should be pro-

vided by the infant’s diet has been esti-

mated by two different methods with simi-

lar results. The first involves calculations

based upon estimates of the infant’s aver-

age body iron content at birth and at 1 year

of age. The difference between these two

values approximates the net increase in

body iron which must be realized from the

diet during the first year of life. Using this

approach, Schulman’ derived a value of 0.8

mg/day which must be absorbed by infants

to supply the amount needed after the iron

derived from the high concentration of he-

moglobin at birth has been reclaimed for


138 IRON IN INFANCY

hemoglobin synthesis. Thus, he calculated

that the daily diet of the normal term infant

must contain 8 mg of iron by 6 months of

age. The term infant with a low initial iron

endowment requires this amount by 3 to 4

months of age, and the low birth weight in-

fant, requires this amount by 2 months of

age. Gairdner, using similar calculations,

arrived at a comparable requirement.46

The second method of determining di-

etary iron requirements has involved the

administration of various amounts of iron to

groups of infants and observation of effects

on hemoglobin concentration. In extensive

studies of this type Sturgeon4 demonstrated

that highest hemoglobin levels were at-

tained by infants who consistently received

daily iron intake of about 1.0 mg/kg.

Based upon an absorption efficiency of

10%, an intake of 1.0 mg/kg/day to a maxi-

mum of 15 mg, if begun at an appropriate

time with respect to initial iron endowment,

will provide sufficient iron to maintain nor-

mal hemoglobin values in most infants. This

figure allows some leeway for individual

variability in absorption and iron endow-

ment. A somewhat greater allowance ( 2.0

mg/kg/day begun by age 2 months to a

maximum of 15 mg) is advisable for low

birth weight infants, for infants with low

initial hemoglobin values, and for those

who have experienced significant blood

loss. In 1960, the Committee on Nutrition

recommended an iron intake of 1.5

mg/kg/day for all infants.9 Because of the

rather marked differences between the iron

needs of normal term infants and those in-

fants who fall in the foregoing special cate-

gories, it is now believed that the separate

recommendations should be stated.

SPECIFIC DIETARY RECOMMENDATIONS

Food naturally rich in iron such as meats

and eggs are expensive and tend to be re-

stricted especially in the diets of the poorer

segments of the population. Although this

memorandum deals with iron, it is obvious

that nutritional adequacy cannot be assured

by simple iron supplementation, and all ele-

ments of dietary intake must be considered.

Iron content of a diet consisting primarily

of unfortifled milk is always inadequate.

Even when a good mixed diet is consumed,

the intake of iron does not usually exceed

6.0 mg per 1,000 kcal unless foods

artificially enriched with iron are utilized.4�

To meet the recommendations of this mem-

orandum, iron supplemented foods are nec-

essary during infancy.

Iron requirements of normal infants can

be met in a number of ways. Daily con-

sumption of 3� oz dry weight of iron en-

riched baby cereal (2 to 3 dry tablespoons

or 30 to 45 cc of reconstituted cereal ) be-

ginning by 6 weeks of age and progres-

sively increasing to % oz dry weight (5

to 6 dry tablespoons or 60 to 90 cc of recon-

stituted cereal) by 6 months of age assures

an adequate iron intake for all infants ex-

cept those with low initial endowment.

Commercial infant cereals provide 8.6 to 22

mg of iron/ dry ounce of cereal.

Consumption of iron-enriched milk for-

mulas also assures adequate iron intake.

Several studies have indicated that iron-de-

ficiency anemia can be prevented by the use

of cows milk formula to which iron has

been added.’8’47”8

Unfortunately, because of cost or prac-

tice by mothers, these excellent sources are

not regularly utilized. The consumption of

iron-fortified baby cereals decreases

markedly during the second 6 months of

life, so that by 12 months of age most in-

fants no longer receive these cereals.�� In

common usage, few infants continue to re-

ceive proprietary milk formulas after 6

months of age.5#{176}Although experience indi-

cates that many robust infants consuming a

balanced, varied diet with abundant meats

and eggs may not develop iron deficiency

anemia, pediatricians should emphasize the

importance of inclusion in the diet of iron-

supplemented foods for at least 18 months

in order to assure optimal iron intake for

their patients.

This Committee suggests the most effec-

tive way to prevent iron deficiency on a

large scale is to provide an iron-fortified di-

etary staple which can be begun by 6



weeks of age for infant consumption. Milk

or carbohydrate staples ( cereal, bread,

grits, rice ) have been shown to be suitable

for fortification. The most appropriate food

selected for iron enrichment may vary in

different sections of the country and in dif-

ferent ethnic and social groups. At present

such supplemented food staples are not in

general use and efforts to identify and de-

velop suitable vehicles for enrichment are

mandatory if optimal iron nutrition is to be

assured. Research into the most suitable

chemical form of the iron supplement must

be continued, since absorption of several

iron additives may vary considerably.51 The

low birth weight infant and infants with re-

duced iron endowment, as previously de-

scribed, need relatively larger amounts of

iron. It is doubtful that diet alone, even

when iron supplemented cereals are used,

can provide sufficient iron for these greater

requirements. Iron fortified milk or medici-

nal iron should be prescribed in order to as-

sure an iron intake of at least 2 mg/kg/day

to a maximum of 15 mg/day for infants

with reduced iron endowment.

IRON DEFICIENCY AFTER INFANCY

Recent surveys from widely separated

areas in the United States suggest that se-

vere nutritional anemia is not an important

universal problem by 4 to 6 years of age,

even in children from low socioeconomic

backgrounds. For example, in Chicago only

5.5% of such children had hematocrits

below 32%, and the mean hematocrit (36%)

for these children did not differ signifi-

cantly from normal.45 This is in the same lo-

cale where a 25 to 30% incidence of severe

iron deficiency of infancy has been

described.’ Therefore, it seems likely that,

except for anemias secondary to blood loss,

symptomatic problems of iron nutrition in

childhood are largely restricted to the first

2 years of life.

IRON THERAPY

When iron deficiency anemia is diag-

nosed, specific therapy is usually recom-

mended. Oral therapy with simple ferrous

salts ( sulfate, gluconate, fumarate ) pro-

vides an inexpensive and predictably satis-

factory response. There is no evidence that

addition of any trace metal, additional he-

matinic substance or vitamin, increases

appreciably the clinical response to simple

ferrous salts.�� Indeed, absorption of other

iron compounds or chelates may be sub-op-

timal occasionally, and therapeutic “fail-

ures” may result when such compounds are

used.5253

The therapeutic dosage of iron must be

calculated in terms of elemental iron. A

total of 6 mg/kg/day of elemental iron

given in three divided doses between meals

provides an adequate amount of iron for

the stimulated bone marrow to utilize.��

Doses in excess of 6 mg/kg/day will not re-

sult in a more rapid hematologic response

and may, in fact, increase the possibility of

intolerance when administered, although

intolerance to oral iron is extremely rare in

pediatric practice. Decreased absorption of

oral iron has not been convincingly docu-

mented as a cause of iron deficiency or

therapeutic failure.

Only one effective parenteral iron prepa-

ration, iron-dextran ( Imferon ) is currently

available for pediatric use. Oncogenic prop-

erties of this preparation in experimental

animals have not been substantiated in

humans.5� However, there is no proof that

the hematologic response to parenteral iron

is significantly faster or more complete than

that to properly administered oral iron, and

its use for prophylaxis is unwarranted. In

most instances the indication for adminis-

tration of parenteral iron for treatment of

infants and children is a social one; that is,

a parent who for social or intellectual rea-

sons cannot be relied upon to properly ad-

minister oral iron.

Medicinal iron should be continued for a

month or so after normal hemoglobin levels

have been attained to assure replacement of

the child’s iron stores. Although there are

potential harmful effects of iron overload in

the tissues of the body in the normal indi-

vidual, these complications result only after

very prolonged administration of large


140 IRON IN INFANCY

doses of medicinal iron. On the other hand,

in chronic anemias such as thalassemia

major, which are associated with greatly in-

creased iron absorption, medicinal iron may

signfficantly increase the body burden of

iron and contribute to an earlier death.

Acute poisoning due to accidental inges-

tion of medicinal iron is a serious problem.

The importance of keeping containers of

iron medications from the reach of young

children cannot be overemphasized.

SUMMARY

1. The iron endowment of the newborn

is proportional to the initial hemoglobin

mass. This in turn depends upon the birth

weight and initial hemoglobin level. The

presence of low birth weight or decreased

hemoglobin level in the first few days of

life may identify infants with special iron

requirements during the first 18 months of

life.

2. It is recommended that the diet of

normal term infants provide 1.0 mg/kg/day

of iron by 3 months of age to a maximum in-

take of 15 mg/day. This requirement can

be easily met by inclusion in the diet of

appropriate amounts of foods which have

been enriched with iron, such as infant

cereals or milk formulas.

3. Infants with low birth weight and oth-

ers with reduced iron endowment require

as much as 2.0 mg of iron per kilogram per

day beginning by 2 months of age. This

amount of iron will not ordinarily be pro-

vided by the diet, even if iron-supple-

mented cereals are given. Attainment of

these larger amounts requires the use of me-

dicinal iron or iron-supplemented milk for-

mula.

4. Attention should be directed to pro-

viding a variety of iron-enriched dietary

staples to be used routinely for feeding

American infants during the period of life

from 3 to 18 months of age and to more pre-

cisely determining the best form of iron

supplementation. At the present time iron

fortified baby cereals and milk formulas are

the iron supplemented foods most generally

available. These are not utilized by the seg-

ments of the American population which

have the greatest need for them.

Cr�iu�s U. Lowi�, M.D., Chairman

DAVID B. CounslN, M.D.

LLOYD J. FILER, JR., M.D.

FELIX P. HEALD, M.D.

MALCOLM A. HOLLIDAY, M.D.

D0N0uGH O’BRIEN, M.D.

GEORGE M. OWEN, M.D.

How�uw A. PE�uisoN, M.D.

CHARLES R. Saiw�n, M.D.

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142 IRON IN INFANCY

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1969;43;134Pediatrics Holliday, Donough O'Brien, George M. Owen, Howard A. Pearson and Charles R. Scriver

Charles U. Lowe, David B. Coursin, Lloyd J. Filer, JR., Felix P. Heald, Malcolm A.IRON BALANCE AND REQUIREMENTS IN INFANCY

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