Symposium: Accomplishments in Child Nutrition
during the 20th Century
Feeding the Premature Infant in the 20th Century1
Frank R. Greer
Departments of Pediatrics and Nutritional Sciences, University of Wisconsin, Madison, WI 53715
ABSTRACT This article reviews the historical development of feeding the premature infant in the 20th century. It
describes the early work determining the energy requirements of the preterm infant, the evolution of the use of
human milk and its fortification for these infants, the development of special formulas for very-low-birth-weight
infants and the various techniques/methods utilized including total parenteral nutrition. J. Nutr. 131: 426S– 430S,
2001.
KEY WORDS: ● premature infants ● history ● feeding
“In feeding the premature infant, only one food is to be
considered, i.e., breast milk. Any attempt to feed these infants
artificially is practically certain to meet with failure. This is so
true that only success with food other than breast milk may be
regarded as the result of good luck rather than good judge-
ment” (Grulee 1912).
At the beginning of the 20th century, the care of the
premature infant was in its infancy. Breast milk was the
feeding of choice and the common practice was to begin the
feeding of premature infants very soon after birth. This was
largely a result of the work and teachings of Stephane Tarnier
(1828 –1897) and his even better known student Pierre Budin
(1846 –1907) at L’Hôpital Maternité in Paris. Although ob-
stetricians by training, they were the first clinicians to cham-
pion the care of the premature infant, or “weakling,” as they
were known at the time. Key points of their care, which have
come down to us through the published lectures of Budin were
as follows: warming, protection from infection and nutrition
(Budin 1907). In addition to advocating the use of breast milk,
it was Tarnier who popularized the technique of gavage feed-
ings in premature infants who were too weak to receive breast
milk from a syringe, spoon or the breast (Berthod 1887).
Surprisingly enough, the basic energy requirements for in-
fants were determined more or less during the late 19th cen-
tury because it was relatively easy to place infants in the
“closed systems” (bell jars) used to measure oxygen consump-
tion and carbon dioxide production during this period (Ni-
chols 1993). After Heubner determined the energy content of
human milk in 1897, the energy quotient for premature infants
was reported by a number of investigators between the years
1907 and 1920. The range was 95–160 kcal/(kg 䡠 d) (Nichols
1
Presented at the symposium, Accomplishments in Child Nutrition during the
20th Century, given at Experimental Biology 2000, April 15–19, 2000 in San Diego,
CA. This symposium was sponsored by the American Society for Nutritional
Sciences. The proceedings of this symposium are published as a supplement to
The Journal of Nutrition. Guest editors for the supplement publication were
Buford L. Nichols, Baylor College of Medicine, Houston, TX and Frank R. Greer,
University of Wisconsin, Madison, WI.
0022-3166/01 $3.00 © 2001 American Society for Nutritional Sciences.
426S
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1993). It was the practice to provide these infants with high
energy intakes of 150 –200 kcal/(kg 䡠 d) because it was the
common belief that a high energy intake was not only required
but that more rapid weight gain was beneficial. Gordon and
Levine restudied the energy issue in the 1930s using a combi-
nation of closed (2 infants) and open circuit (9 infants)
calorimetry. These premature infants ranged in birth weight
from 1130 to 2220 g and were studied between 10 and 44 d
after birth. The daily energy requirement was determined to be
120 kcal/(kg 䡠 d) [68 kcal(kg 䡠 d) for catabolism, 18 kcal/
(kg 䡠 d) lost in feces and 34 kcal/(kg 䡠 d) stored as energy].
Average weight gain was 16 g/(kg 䡠 d) (Gordon et al. 1940).
These energy requirements for growing premature infants have
withstood the test of time.
It was in 1913 that Julius H. Hess (1876 –1955) began the
first continuously operated center for premature infants in the
United States at Michael Reese Hospital in Chicago. Dr Hess,
who had spent several years in Europe visiting centers caring
for premature infants, also published the first book ever written
dealing with the subject of the premature infant, [Hess
(1922)]. Hess also advocated that human milk was the choice
of feeding for the premature infant and that artificial milk
preparations were a poor substitute, which resulted in an
increased mortality rate. He advocated beginning feedings of
breast milk in the second 12 h of life with the milk supplied by
a wet nurse. During the first 3 wk of life, breast milk intake was
progressively increased from 140 to 200 mL/(kg 䡠 d). His text-
book had elaborate guidelines for “Hygiene of the Wet Nurse”
and breast feeding the premature infant. He also favored
gavage feeding with gravimetric flow for infants unable to
nurse at the breast (Fig. 1). Even for breast-fed infants, he
advocated water or a 1% lactose solution up to one sixth of the
infant’s body weight, to be administered daily to “compensate
for the loss of body fluids through the kidneys, bowels, lungs
and skin.” If “artificial feeding” had to be used of necessity, he
recommended a buttermilk and skim milk mixture with the
addition of sugar (low fat, high carbohydrate) or boiled milk
with the addition of water and sugar. Artificially fed infants
 FEEDING THE PREMATURE INFANT
FIGURE 1 Early 20th century demonstration of the gavage feed-
ing technique for premature infants (Hess 1922).
were to be fed orange juice by wk 3 (2– 4 mL/d) to counteract
the effects of boiling. Small amounts of cod-liver oil were
introduced at 4 wk and increased to 2 mL/d by 8 wk. He also
recommended daily supplements of iron by wk 4. Solid foods
were not instituted until mo 5, beginning with well-cooked
cereal (Hess l922).
Twenty years later in the second version of his textbook,
Hess still advocated the use of breast milk for premature
infants, but his guidelines now reflected the beginning of the
dark period of the 20th century in the nutritional support of
the premature infant (Hess and Lundeen 1941). This practice,
to delay feedings for up to as long as 4 d in the smallest, sickest
premature infants, originated in the United States. Budin’s
earlier advice was ignored: “The path of pleasure for adults is
drinking. May it not be the same for weaklings?” (Budin 1907).
Hess wrote in his 1941 textbook: “It has been our experience
that too early feeding may often be the cause of aspiration
pneumonia and is, therefore, to be avoided . . .. Small prema-
ture babies (those weighing under 1200 g) were not fed for
24 – 48 h . . .. During this time the premature baby receives
physiologic salt solution, subcutaneously in the thighs, one to
three times daily.” He also recommended that infants ⬍1000
g should not receive food by mouth for 24 – 48 h. This trend of
427S
delaying early feedings persisted as mainstream neonatal prac-
tice for 25 y. Not only was it thought that delayed feedings
prevented aspiration pneumonia but also there was a growing
belief that many premature infants were retaining an excessive
amount of extracellular fluid so that early feeding was stressful
to the infant’s kidneys (Hansen and Smith 1953). There were
reports of severe weight loss (⬎20% of birth weight),
hemoconcentration, hyperosmolality and hyperbilirubinemia
in these infants during this period; because these were quickly
reversed, however, when feedings were begun, clinicians ob-
viously believed that premature infants could tolerate these
initial periods of starvation without long-term adverse affects
(Davies 1978, Hansen and Smith 1953). The 1958 version of
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Hess’s textbook had the following to say about initiating early
feedings in the premature infant: “The average premature
infant does better if it is not fed for at least 12 h after birth, and
babies weighing ⬍1200 g at birth are not fed for 36 to 72 h.
All feedings are withheld for at least 48 h in any baby having
marked generalized edema or respiratory embarrassment”
(Lundeen and Kunstadter 1958). To be sure there were a few
“voices in the wilderness during this period,” and in 1955 it
was reported that there was a 28% lower mortality rate in
premature infants who were fed between 12 and 24 h of life
compared with a 41% rate when feedings were delayed until
36 h of life (Gleiss 1955).
Another major change in the 1940s resulted from the work
of Gordon and co-workers (1947). These investigators re-
ported that premature infants fed a diluted “half-skimmed
cow’s milk formula” gained weight more rapidly than those fed
breast milk. In this study, 122 premature infants (birth weight
1022–1996 g) were fed three different diets supplying 120
kcal/(kg 䡠 d). The three diets were human milk, evaporated
cow’s milk formula and partially skimmed cow’s milk formula.
The milk used in the two last-mentioned diets was diluted
with water and Dextri-Maltose was added. For the 16 infants
fed human milk, the average weight gain was 12.5 g/(kg 䡠 d),
compared with 14.1 g/(kg 䡠 d) for the 39 infants fed evaporated
milk and 15.7 g/(kg 䡠 d) for the 67 infants fed half-skimmed
milk (Fig. 2). The differences between these three groups were
significant. Differences were even more striking for the 49
infants with birth weights between 1000 and 1600 g. The
FIGURE 2 Comparison of mean weight gains in premature infants
fed three different diets (Gordon et al. 1947).
428S
implications were that it was the increased protein in the cow’s
milk– based feedings that promoted the increased weight gain
in these infants, and this study led to the widespread use of
such feedings in the premature infant. Furthermore, in 1943,
Benjamin et al. (1943) compared premature infants fed human
milk with infants fed a mixture of skimmed-milk and olive oil,
and demonstrated that human milk, even in the presence of
added vitamin D, was not the food of choice for the formation
of the skeleton of premature infants unless supplemented with
calcium and phosphorus. No wonder the 1958 revision of
Hess’s textbook toned down the promotion of breast milk for
premature infants and included an expanded section on “arti-
ficial feeding” (Lundeen and Kunstadter 1958).
It was not until the 1960s that the issues of fluid restriction
and breast-milk feeding were revisited. First, after reports that
delayed feedings resulted in long-term neurological develop-
mental delays, and that early feedings prevented severe weight
loss and reduced the incidence of hypoglycemia, hypernatre-
mia and hyperbilirubinemia, early feedings of premature in-
fants was gradually reintroduced (Davies 1978). It was also
pointed out that infants fed early did not have an increased
incidence of aspiration pneumonia and that much of the
edema reported in these infants previously could be attributed
to tissue catabolism from starvation (Davies 1978).
Second, it was demonstrated that some of the weight gain
attributed to artificial formulas for premature infants was sec-
ondary to the increased electrolyte intake and water retention
with such formulas. Kagan et al. (1972) noted that both total
body water and extracellular fluid volume of infants fed high
protein, high solute load intakes were greater than those
observed in patients receiving low solute formulas and human
milk. The increase in dry weight (total weight gain minus
increase in total body water) was similar with protein intakes
ranging from 2 to 6 g/(kg 䡠 d). However, Babson and Bramhall
(1969) reported no increase in dry weight gain when only
minerals were added to a formula providing 1.5 g protein/100
mL. Their study also found that higher protein intakes from
formula containing 3.5 g protein/100 mL did not lead to
greater weight gains unless accompanied by higher solute
intakes, although the increase in protein intake (regardless of
solute load) did result in greater increase in length. They
suggested that changes in length were a better indicator of
nutritional adequacy of high protein/high solute load formulas.
Finally, in the 1970s, Raiha and colleagues (1976) pointed
out that protein quality, not quantity, played an important role
in the feeding of the premature infant. In these studies, infants
were randomly assigned to pooled (banked) human milk (pro-
tein content 1.0 g/dL) or one of four isocaloric cow’s milk–
based formulas differing in protein quantity (1.5 vs. 3.0 g/dL)
and quality (ratio of whey proteins to casein of 60:40 or
18:82). Although the weight gain was highest in the infants
receiving the high protein formula [protein intake of 4.5
g/(kg 䡠 d)], some of these infants developed azotemia, hyper-
ammonemia and metabolic acidosis. The intrauterine rate of
weight gain was not achieved in any group. This study sug-
gested that human milk was as adequate for low-birth-weight
(LBW)2 infants as currently available formulas. Another study
from the early 1980s clearly established that LBW infants fed
their own mother’s milk had an improved growth rate com-
pared with premature infants fed pooled, mature, donor milk
(Gross 1983). This was largely thought to be due the higher
protein content of preterm breast milk compared with milk
2
Abbreviations used: AAP, American Academy of Pediatrics; LBW, low birth
weight; TPN, total parenteral nutrition; VLBW, very-low-birth-weight.
SUPPLEMENT
from term mothers during the first few weeks of lactation.
Although this work led to a resurgence in the use of mother’s
own milk for preterm infants, even in Gross’s study, the infants
did not achieve the intrauterine rate of growth.
Since the 1940s, it had been known that human milk was
deficient in protein, calcium, phosphorus, sodium, iron, vita-
mins and trace minerals and would not satisfy the intrauterine
requirements of the growing premature infant. The 1941 edi-
tion of Hess’s textbook recommended supplemental vitamins
for both breast-fed and formula-fed premature infants. Heird
and Anderson (1977) pointed out these deficiencies in their
review on this topic, but also noted that at this time, infants
fed human milk grew as well as those receiving formula, and
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that it remained to be demonstrated that the ideal rate of
weight gain for premature infants ex utero was the in utero rate
of weight gain. Despite this, in 1977, in its first statement on
the nutritional needs of LBW infants, the American Academy
of Pediatrics (AAP) concluded that “the optimal diet for the
LBW infant may be defined as one that supports a rate of
growth approximating that of the third trimester of intrauter-
ine life, without imposing stress on the developing metabolic
or excretory systems” (AAP 1977).
The 1980s saw the commercial development of special
formulas3 for very-low-birth-weight (VLBW) infants (birth
weight ⱕ1000 g ). Compared with standard formulas, these
contained more protein (2.2 g/dL), Na (1.5 mEq/dL), Ca (150
mg/dL), P (80 mg/dL) and vitamins per 100 mL, which more
adequately met the needs of the premature infant who required
smaller total volumes of feedings with higher concentrations of
nutrients compared with larger premature infants. These for-
mulas allowed for the delivery of ⬃3 g/(kg 䡠 d) protein and 6.5
g/(kg 䡠 d) fat with an intake of 150 mL/(kg 䡠 d). They also
contained 50% of the fat as medium-chain triglycerides. Clin-
ical studies with these formulas designed for the needs of the
VLBW infant clearly showed the advantages of improved
growth compared with human milk without the metabolic
abnormalities reported with previous formulations (Cooper et
al. 1984, Greer and McCormick 1988, Gross 1983, Schanler
and Oh 1985, Tyson et al. 1983). In the 1980s and 1990s, with
the development of commercially available human milk for-
tifiers for preterm infants, such fortification of human milk
become the standard of care for the LBW infant. Even so,
comparative studies continued to show that infants fed the
special formulas for VLBW infants grew faster than those fed
fortified human milk (Atkinson et al. 1981, Schanler and
Garza 1987, Schanler et al. 1999). These human milk fortifiers
contain protein, vitamins and minerals that in theory will
meet the intrauterine needs for growth in these infants when
added to human milk.
In the last 25 y, two other clinical issues had a great effect
on the feeding of VLBW infants. The first of these is a disease
of the intestinal tract, necrotizing enterocolitis. Although the
term was first used in the early 1950s by Quaiser (1952), it
really became a clinical problem with the remarkable overall
improvements in neonatal intensive care of the 1960s and
1970s. No other single disease has a greater effect on the
enteral nutrition of premature infants because it is the fear of
this disease by care givers that typically governs when feedings
3
The interest of formula companies in the nutritional requirements of the
premature infant was not new; as early as 1939, the Borden Company produced
a booklet on the care and feeding of premature infants [The Care and Feeding of
Premature Infants (1939), The Borden Company, New York (from the historical
collection of the University of Wisconsin Health Sciences Library)], which pro-
moted an evaporated milk formula “especially suited” for the premature infant
(Biolac) because of its protein content and added vitamins and iron.
 FEEDING THE PREMATURE INFANT
are started, how rapidly they are advanced, what kind of
feeding is used and when they are interrupted. In the 1990s it
was argued that feedings of human milk, even with fortifica-
tion, may decrease the incidence of this disease in LBW
infants (Schanler et al. 1999).
The second issue was the high fluid intakes that were
recommended for VLBW infants in the 1970s, after the long
period of time in which starvation and very low fluid volumes
in the first days of life were the norm. This was the result of
increasing concerns about the very high insensible water loss
rates in VLBW infants. They were treated in overhead warm-
ers to maintain body temperature, often with phototherapy,
and in a relatively low humidity environment. There was also
the need to increase energy intake during a time in which it
was difficult to give concentrated solutions of glucose paren-
terally. Those providing care were also concerned about the
immaturity of the renal glomerulus in which the glomerular
filtration rate was lower in the preterm than the term infant,
and the inability of the premature kidney to concentrate urine.
Others were concerned about the need to increase the renal
excretion of the solute load associated with increasing nutri-
tional intakes. All of this led to a large overestimation of the
water needs of the premature infant, and it was not uncommon
for the total fluid volume to exceed 200 mL/(kg 䡠 d) in the
smallest infants (Roy and Sinclair 1975). These high fluid
intakes compromised administration of other nutrients and
were ultimately associated with an increased incidence of
patent ductus arteriosus, congestive heart failure and even
necrotizing enterocolitis (Bell et al. 1980, Stevenson 1977).
This led to a gradual reduction in the initial fluid rates for
premature infants in the 1980s to reflect more accurately true
fluid needs. Environmental changes were made as well, with
improvements in isolettes and humidification of ventilators,
which lowered insensible water losses.
Any history of the feeding of the premature infant in the
20th century would be incomplete without mentioning the
advances made in total parenteral nutrition (TPN), which
became available with the use of catheters for central fluid
administration only in the 1960s. The technical advancement
of this practice continued into the 1990s, with perfection of
the technique for placing very fine central catheters (28-
gauge) percutaneously through peripheral veins. Dudrick et al.
(1968) were the first to maintain an infant with small bowel
atresia via a hypertonic mixture of protein hydrolysate and
glucose through an indwelling intravenous catheter for 44 d.
The availability of intravenous lipid emulsions for use in LBW
infants in the late 1970s finally permitted adequate growth in
VLBW infants who were given these solutions. Today, it is
routine to manage infants with a birth weight ⬍1500 g with
the use of TPN solutions, which provide necessary energy as
well as vitamins and minerals (AAP 1998). This greatly facil-
itated the ability to approach the “intrauterine requirements
for growth” in these VLBW infants in the early days of life.
Table 1 outlines the major changes in the feeding of the
premature infant in the 20th century. By way of conclusion,
the following statement summarizes the current thinking
about nutrition for the premature infant at the beginning of
the 21st century: “Optimal nutrition is critical in the manage-
ment of small preterm infants. No standard has been set for the
precise nutritional needs of infants born prematurely that is
comparable to the breast milk standard for term infants.
Present recommendations are designed to provide nutrients to
approximate the rate of growth and composition of weight
gain for a normal fetus of the same postconceptional age and
to maintain normal concentrations of blood and tissue nutri-
ents. Initially after birth, the management of acute neonatal
429S
TABLE 1
Timeline: nutrition of the premature infant in the 20th century
1890s (Tarnier and Budin): Lectures on care of the “weakling”; early
feedings of breast milk advocated; popularized gavage feeding
technique (Berthod 1887, Budin 1907).
1913 (Hess): Established unit for premature infants at Michael Reese
Hospital, Chicago (Hess 1922).
1940–1965 (Hess and others): Delayed fluids/feedings for premature
infants up to 96 h of age (Hess and Lundeen 1941).
1930s (Gordon and Levine): Respiratory metabolism studies confirm
energy requirement of 120 kcal/kg/d for growing premature infants
(Gordon et al. 1940).
1943 (Benjamin): Human milk even with added Vitamin D does not
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support skeletal growth for premature infants (Benjamin et al.
1943).
1947 (Gordon and Levine): Premature infants grow faster when fed
“half-skimmed cow’s milk formula” compared with human milk
(Gordon et al. 1947).
1960s: Delayed feedings associated with long-term neurological
developmental delays; concerns with hypoglycemia,
hypernatremia, hyperbilirubinemia and severe weight loss resulting
from delayed feedings. Early provision of fluids/feedings
advocated.
1960s (Kagan and Babson): Some weight gain with the use of cow’s
milk formulas attributable to increased total body water secondary
to electrolyte retention (Babson and Bramhall 1969, Kagan et al.
1972).
1960s (Dudrick): First total parenteral nutrition (TPN) usage in
premature infants (Dudrick et al. 1968).
1970s (Raiha): Importance of protein “quality” not quantity; beginning
of new interest in using breast milk in premature infants (Raiha et
al. 1976).
1980s: Development of special formulas (increased protein, minerals,
vitamins with medium-chain triglycerides) for very-low-birth-weight
(VLBW) infants.
1990s: Development of commercial human milk fortifiers; emphasis
on using mother’s own milk with early institution of “trophic”
feedings.
1990s: TPN becomes standard of care for VLBW infants very early in
life.
illnesses and gradual advancement of feeding to minimize the
risk of feeding-related complications, such as necrotizing en-
terocolitis, may conflict with the nutritional goal of obtaining
rapid growth in preterm infants” (AAP 1998).
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