Feeding The Term Infant: Jatinder Bhatia, Colleen Bucher, and Chantrapa Bunyapen
Feeding The Term Infant: Jatinder Bhatia, Colleen Bucher, and Chantrapa Bunyapen
7
Feeding the Term Infant
Growth
The average weight of a healthy term infant is 3.5 kg. With an anticipated loss of 10% in
body weight in the first week of life, birth weight is regained by two weeks of age in both
breast-fed and formula-fed infants, with the formula-fed infants demonstrating a tendency
to regain birth weight sooner than their breast-fed counterparts.
Body weight should be measured with an electronic scale or a beam balance without
detachable weights, with the balances capable of weighing to the nearest 10 g. Even with
the use of electronic scales, balances should be tared with calibrated weights at least two
times a year. Mean weight and selected centiles for weight are summarized in Table 7.1.
In clinical practice, however, weight and other anthropometric measurements including
length, head circumference, and weight for length are plotted on growth charts (Figures
7.1 and 7.2) adapted from Hamill et al.1 The plotting of growth on these charts will suffice
for monitoring of normal infants; however, a different and more sensitive approach will
be needed for infants with faltering growth. The “reference data” provided by Fomon2
combine data from the University of Iowa and the Fels Longitudinal Study, the latter data
used in the growth charts.
Length
Length should be measured by two examiners using a calibrated length board with a fixed
headpiece and a movable foot board. The head is held by one examiner with the Frankfort
plane (defined as a line that passes through the left porion, the right porion, and the orbits)
TABLE 7.1
Mean Body Weight and Selected Centiles for Males and Females, 0–12 Months of Age
Age Mean 5th centile (g) 50th centile (g) 95th centile (g)
Mean body weight and selected centiles for males, 0–12 months of age
Mean body weight and selected centiles for females, 0–12 months of age
in the vertical position, and gentle traction is placed to bring the head into contact with
the headpiece. A second examiner holds the infant’s feet with the toes pointing upwards,
and while applying gentle traction, brings the footpiece to rest firmly against the infant’s
heels. Measurements agreeing to within 0.4 cm are considered adequate, and the impor-
tance of length measurements is underscored, particularly when serial measurements are
made in a longitudinal fashion. It is generally agreed that faltering in length as well as
weight suggests growth faltering of a longer duration than when weight alone is affected.
Head Circumference
Head circumference is measured by a narrow flexible steel or paper tape applied to the
head above the supraorbital ridges and encircling the most prominent parts of the forehead
and the occiput. The maximum of three measurements should be used as the maximal
circumference. Weight-for-length measurements (Figures 7.1 and 7.2) are also available
and are useful in defining obesity as well as leanness.
A variety of other measures to define growth include skin fold thickness, limb length
and circumference, and body mass index. The latter, body mass index, is calculated by
dividing weight in kilograms by length in meters squared, replacing weight for length in
older children. In any case, accurate measurements are essential to the interpretation of
growth charts.
Normal growth is a strong indicator of nutritional sufficiency and overall health of an
infant. Since infancy is a period of rapid growth, particularly early infancy, identifying
growth failure is important and requires prompt medical attention. As we understand
more about the complex interactions between genetic, immunologic, metabolic, physio-
logic, and psychologic factors and their effects on long-term outcomes of infant feeding
decisions, defining appropriate growth becomes a very important issue for health care
providers of children.
Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 40 E
100 95 100
39 90 39 N
38 G
75 38
95 95 T
37 50 37 H
36 25 36
90 90
35 10 35
5
34
85
33
32 38
80 95 17
31
L 30 36
75 90 16
E
N
29
34
G 28
70 75
15
T 27 32
H 26 65 14
25 50 30 W
24 E
60 13
23 25 28 I
G
22 55 12 H
10 26
21 5 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18
16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
T
4
8
3
6
2
lb kg
Birth 3 6 9
FIGURE 7.1
Girls: birth to 36 months: physical growth NCHS percentiles.
Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS) cm in H
E
A
52 52
D
95
20 90 20
50 50 C
75 I
50 R
H 19 19
48 48 C
E 25 U
A 10 M
D 18 46 5 46 18 F
E
R
C 44 44 E
I 17 17 N
R C
C 42 42 E
U 16
M 40 50
F 22 48
E
15 38 21 46
R
E 20 44
N 36 19 42
14
C 95
E 18 40
34 90
17 38
13 75 36
32 16
50 34
12 25
15
30 32
10 14
5 30 W
13 28 E
12 I
26 G
24 11 11 24 H
22 10 10 22 T
20 9 9 20
18 8 8 18
16 7 7 16
W
E 14 14
6 6
I 12
14 12
G 5 5
10 kg lb
H 4 LENGTH
T 8 cm
64 66 68 70 72 74 76 78 80 82 84 86 88 90 92 94 96 98100
6 3
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 in
4 2
Date Age Weight Length Head Circ. Comment
2 1
lb kg
cm 46 48 50 52 54 56 58 60 62
in 18 19 20 21 22 23 24
FIGURE 7.1
Continued.
Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS)
cm in
41 41 L
40 95 40 E
100 90 100 N
39 39
75 G
38 38
95 50 95 T
37 37 H
25
36 36
90 10 90
35 5 35
34
85
33
32 95 38
80 17
31
L 90 36
30
E 75 16
N
29
75
34
G 28
70 15
T 27 32
H 26 50
65 14
25 30 W
24 25 E
60 13
23 28 I
10 G
22 55 12 H
5 26
21 T
20 50 11 24
19
18 45 10 22
17
16 40 9 20
15
8 18
16 16
7 AGE (MONTHS)
kg lb
12 15 18 21 24 27 30 33 36
14
6 Mother’s Stature Gestational
W Father’s Stature Age: Weeks Comment
E 12
Date Age Weight Length Head Circ.
I 5 Birth
G 10
H
T
4
8
3
6
2
lb kg
Birth 3 6 9
FIGURE 7.2
Boys: birth to 36 months: physical growth NHS percentiles.
Birth 3 6 9 12 15 18 21 24 27 30 33 36
in cm AGE (MONTHS) cm in H
E
95 A
52 90 52
D
20 75 20
50 50 C
50
I
25 R
H 19 19
48 48 C
E 10 U
A 5 M
D 18 46 46 18 F
E
R
C 44 44 E
I 17 17 N
R C
C 42 42 E
U 16
M 40 50
F 22 48
E
15 38 21 46
R
E 20 44
N 36 19 42
14
C
E
95
18 40
34 90
17 38
13 75
36
32 50
16
34
12 25 15
30 10 32
5 14
30 W
13 28 E
12 I
26 G
24 11 11 24 H
22 10 10 22 T
20 9 9 20
18 8 8 18
16 7 7 16
W
E 14 14
6 6
I 12
14 12
G 5 5
10 kg lb
H 4 LENGTH
T 8 cm
64 66 68 70 72 74 76 78 80 82 84 86 88 90 92 94 96 98100
6 3
26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 in
4 2
Date Age Weight Length Head Circ. Comment
2 1
lb kg
cm 46 48 50 52 54 56 58 60 62
in 18 19 20 21 22 23 24
CDC
FIGURE 7.2
Continued.
Energy
Energy requirements during infancy may be partitioned into basal metabolism, thermic
effect of feeding, thermoregulation, physical activity, and growth. The energy requirements
for growth relative to maintenance, except in early infancy, are small, and satisfactory
growth can be considered a sensitive indicator that energy requirements are being met.
Energy balance may be defined as gross energy intake = energy excreted + energy
expended + energy stored. Gross energy intake, measured by the heat of combustion, is
greater than energy available when fed because most foods are not completely digested,
and protein oxidation is incomplete. Fat absorption varies widely among infants fed
various formulas, particularly in infancy. Urea and other nitrogenous compounds are
excreted in the urine. Gross intake is calculated as 5.7 kcal/g, 9.4 kcal/g, and 4.1 kcal/g
obtained from protein, fat, and carbohydrate, respectively, and therefore it varies given
the type of diet fed. The term “digestible energy” refers to gross energy intake minus
energy excreted in the feces. Metabolizable energy is defined as digestible energy minus
energy lost in urine. The metabolizable energy values for protein, fat, and carbohydrate
are close to 4, 9, and 4 kcal/g, respectively. Losses of energy, other than feces and urine,
are negligible and are ignored for practical purposes.
The energy intake of normal infants per unit body weight is much greater than in adult
counterparts. Energy requirements for term infants have been estimated by various groups
and vary from 100–116 kcal/kg/d from 0–3 months and decline to about 100 kcal/kg/d
by the end of the first year.3-7 These recommendations are based on the median intake of
thriving infants; the intakes of breast-fed infants are lower than that of formula-fed infants,
with an average of 3–4% lower in the first three months, and 6–7% from three to six
months. As new, more precise estimates of energy expenditure become available, these
recommendations are apt to change, given that current recommendations are higher than
the “gold” standard — the breast-fed infant. Energy intakes of infants from 6 to 12 months
of age have been reported to be between 91 and 100 kcal/kg/d.8-10
Protein
Intakes of protein and essential amino acids are generally sufficient in developed countries,
in contrast to developing countries where protein and protein-energy malnutrition are still
a frequent occurrence. In appropriately fed infants, protein is not a limiting dietary com-
ponent in infancy and is clearly essential for normal growth and development. For the
human infant, histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine,
tryptophan, and valine are considered essential amino acids. The data for cysteine are
conflicting11,12 for the term infant, although the data are clear for the preterm infant.
Conditionally essential amino acids are those that become essential under certain circum-
stances, since they may be produced in inadequate amounts endogenously. An example
of this is taurine, which is now added to formulas based on reports of greater concentrations
of taurine in the plasma and urine of preterm13,14 and term15 infants. The concern about
taurine depletion stems from the observations of growth retardation, abnormal retinal
findings, and impaired bile acid metabolism in taurine-deficient animals and humans.
Recommended dietary intakes of protein are summarized in Table 7.2. In contrast,
intakes recommended by WHO16 are 2.25, 1.86, 1.65, and 1.48 g/100 kcal from 1–2, 3–6,
TABLE 7.2
Recommended Dietary Intakes of Protein
Age Interval Recommended Dietary Intake
(mo) (g · kg–1 · d–1) (g/100 kcal)
0 to 1 2.6 2.2
1 to 2 2.2 2.0
2 to 3 1.8 1.8
3 to 4 1.5 1.6
4 to 5 1.4 1.6
5 to 6 1.4 1.6
6 to 9 1.4 1.5
9 to 12 1.3 1.5
Reproduced with permission from Fomon, S. J.
Pediatric Research 30, 391, 1991.
6–9, and 9–12 months, respectively. Both of these recommendations are generally higher
than the intakes observed in human milk-fed infants.
Fat
The importance of dietary fat is underscored by the fact that 35% of the weight gain of an
infant in early infancy is accounted for by fat.17 Most of the dietary fat is in the form of
triglyceride formed by three fatty acids esterified to a glycerol backbone. In the body, trig-
lycerides are the main form of storage and transport of fatty acids. Phospholipids and
cholesterol are indispensable components of the lipid bi-layer of all cell membranes, and the
amount of different phospholipids and cholesterol, as well as the fatty acid pattern of incor-
porated phospholipids, modulate membrane fluidity, permeability, enzyme and receptor
activity, and signal transduction. Cholesterol is required for the synthesis of steroids and bile
acids, although the majority of the cholesterol pool in tissue and plasma is derived from
endogenous synthesis; dietary cholesterol contributes to the pool, and diet modifies liver
synthesis.18 Fatty acids (4-26 carbon atoms) are either saturated (no double bonds in the
carbon chain), mono-unsaturated (one double bond) or polyunsaturated (two or more double
bonds). Double bonds occur in two isomeric forms: cis and trans; unsaturated fatty acids are
folded at the site of each double bond, cis, and trans-fatty acids have straight carbon chains.
Human milk contains approximately 4% lipids, but the reported variation is between
3.1 and 5.2%,19,20 with 99% of the fat present in the form of triglycerides and the rest in
the form of diglycerides, monoglycerides, free fatty acids, phospholipids, and cholesterol.
The fat content of human milk increases with duration of lactation.19,21 During this period,
the average size of the fat globules increases, and the ratio of phospholipids and cholesterol
to triglycerides decreases.22 The concentration of fat in human milk remains similar regard-
less of maternal diet or nutritional status, although poor nutrition has been shown to
decrease fat content.23 Fatty acid content of human milk has been reported by numerous
investigators and demonstrates a wide range, as summarized by Fomon.2 Fatty acid
content of human milk is also altered by dietary manipulation.24-27 Human milk fat pro-
vides the essential fatty acids linoleic and α-linolenic acids, along with the long-chain
polyunsaturated fatty acids such as arachidonic and docosahexaenoic acids. The decrease
of milk phospholipid content during the first few weeks after birth is accompanied by a
decrease in arachidonic and docosahexaenoic acids.28 Fat content of human milk and
commonly used formulas is summarized in Table 7.3.
227
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2705_frame_C07 Page 228 Wednesday, September 19, 2001 1:15 PM
228
TABLE 7.3 (Continued)
Nutritional Composition of Human Milk and Commonly Used Formulas
Kilocalories/ Protein Fat Carbohydrate Na K Phosphorus Calcium Osmolality
oz. Source gm/dl Source gm/dl Source gm/dl mEq/dl mEq/dl mg/dl mg/dl mOsm/kg water
Babysoy (pwd) 20 Soy protein 2.1 Oleo, coconut, 3.6 Corn syrup 6.9 0.9 1.8 42 60 228
(Wyeth isolate with high-oleic solids, sucrose
Nutritionals, L-methionine (saff. or sun.),
Inc.) soybean oils
Isomil (Ross) 20 Soy protein 1.7 High-oleic 3.7 Corn syrup, 7.0 1.3 1.9 51 71 230
isolate with safflower, sucrose
L-methionine coconut, soy
oils
Isomil DF 20 Soy protein 1.8 Soy, coconut 3.7 Corn syrup, 6.8 1.3 1.9 51 71 240
(Ross) isolate with oils sucrose, soy
L-methionine fiber
ProSobee 20 Soy protein 1.7 Palm olein, soy, 3.7 Corn syrup 7.3 1.0 2.1 56 71 200
(Mead isolate with coconut, solids
Johnson) L-methionine high-oleic
sunflower oils
Alimentum 20 Casein 1.9 MCT 33%, 3.7 Sucrose, 6.9 1.3 2.0 51 71 370
(Ross) hydrolysate safflower, soy modified
229
© 2002 by CRC Press LLC
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Carbohydrate
Carbohydrates generally account for 35 to 42% of the energy intake of breast- or formula-
fed infants, and the usual carbohydrates in infants’ diets are listed in Table 7.4. Carbohy-
drates may be classified as monosaccharides, oligosaccharides, and polysaccharides.
Monosaccharides can be further defined as aldoses (glucose, galactose, xylose, for example)
or ketoses (fructose). Oligosaccharides are consumed in the diet mainly in milk with lactose,
maltose and sucrose being the main sugars present. Polysaccharides are starches, starch
hydrolysates, glycogen, or components of fiber. The major carbohydrate in human milk
is lactose, although small amounts of glucose and other oligosaccharides are also present.
Carbohydrate content of human milk and various formulas is listed in Table 7.3. Carbo-
hydrate malabsorption, apart from genetic causes, is unusual. When the colonic capacity
to ferment carbohydrate is exceeded by the unabsorbed load, symptoms of carbohydrate
intolerance, usually in the form of diarrhea, occur. The diarrhea improves when dietary
carbohydrates are reduced or eliminated from the diet, making the diagnosis of carbohy-
drate intolerance. Normally, electrolytes in the distal gastrointestinal tract and unabsorbed
TABLE 7.4
Usual Carbohydrates and Related Enzymes
Carbohydrate Enzyme
Lactose Lactase
Sucrose Sucrase-isomaltase
Isomaltose Sucrase-isomaltase
Maltose Maltase-glucoamylase
Amylose α-Amylase
Amylopectin β-Amylase
TABLE 7.5
Commonly Used Formulas and Their Indications
Commonly Used Formulas and Their Indications
Formula Carbohydrate Protein Fat Indication
Bovine milk-based Lactose Bovine whey and Vegetable, animal Normal function
casein
Soy-protein-based Sucrose, glucose Soy Soy Lactose intolerance
Hydrolyzed Sucrose, glucose Hydrolyzed whey or Medium chain Cow milk and soy
protein casein triglycerides protein
hypersensitivity;
pancreatic
insufficiency
Casein-based Modified tapioca Casein hydrolysate MCT oil, corn oil Lactase, sucrase and
(modular) starch, added with added amino maltase deficiency,
carbohydrate acids impaired glucose
transport
Elemental Lactose- and sucrose- Hydrolyzed casein Vegetable Cow milk allergy
free, corn syrup
solids, modified
corn starch
“Metabolic” Depends on Corn syrup solids/ Corn oil/ coconut oil Specific metabolic
condition sucrose disorders
carbohydrates (fermented to volatile fatty acids) are rapidly absorbed. Inadequate colonic
salvage results in diarrhea. In young infants and children with disorders of carbohydrate
metabolism, the ultimate goal of carbohydrate digestion and absorption is to render all
available carbohydrates into smaller compounds that the body can use; chiefly, glucose
and fructose. Lactase deficiency is exceedingly rare in newborn infants. Infants usually
develop diet-induced diarrhea following introduction of lactose-containing milk. The
disease, thought to be autosomal recessive, is treated with the elimination or limitation
of lactose in the diet. More commonly, a transient lactose intolerance can occur after acute
or repeated bouts of diarrhea. Sucrase-Isomaltase deficiency is a rare disease that does not
appear until diets containing sucrose, dextrin, or starch are begun. Bouts of diarrhea may
be observed in infants with this deficiency, and management includes eliminating sucrose
and limiting starch in the diet. Older affected children and adults usually tolerate normal
quantities of carbohydrates. Glucose-Galactose deficiency manifests itself with diet-induced
diarrhea soon after birth and responds to withdrawal of these carbohydrates from the
diet. The defect appears to be a specific absence of glucose and galactose transport mech-
anisms, whereas amino acid transport is normal. Fructose transport is normal, and these
infants respond to a diet containing fructose with relief from diarrhea. With age, variable
amounts of starch and milk may be tolerated. Commonly used formulas for various forms
of intolerance are listed in Table 7.5.32
Iron
Iron deficiency is the most common nutritional deficiency in the U.S. and worldwide, with
young children the most susceptible. The increased susceptibility comes from an increased
iron requirement for the rapid growth during this period and inadequate amounts of iron
in the diet unless adequately supplemented.33 According to the third National Health and
Nutrition Examination Survey (NHANES, 1991), ~5% of children between one and two
TABLE 7.6
Stages of Iron Deficiency
Iron Nutritional Status Indices
Adequate stores Normal
Decreased stores Decreased ferritin (10–20 ng/mL), transferrin normal, erythtrocyte
protoporphyrin normal, MCV normal, hemoglobin normal, transferrin
receptor normal
Iron deficiency Decreased ferritin, transferrin saturation decreased, erythrocyte
protoporphyrin increased, MCV normal, hemoglobin normal,
transferrin receptor increased
Iron deficiency anemia Decreased ferritin, transferrin saturation decreased, erythrocyte
protoporphyrin increased, MCV decreased, hemoglobin decreased,
transferrin receptor increased
years of age had evidence of iron deficiency, and about half were also anemic. However,
between the two previously published studies, NHANES II and I, prevalence of iron
deficiency was observed to be decreasing.34 Stages of iron nutritional status are listed in
Table 7.6.
One should distinguish between anemia and iron deficiency anemia, since the latter
occurs when hemoglobin concentration falls below the 90 to 95% range for the same age
and sex.34 A diagnosis of iron deficiency is made when the anemia is accompanied by
evidence of iron deficiency or when there is a rise in hemoglobin following treatment with
iron. In this regard, serum transferrin receptor may offer an advantage for screening for
iron deficiency, since it rises with iron deficiency and is not affected by infection or acute
liver disease.35
Iron deficiency peaks between six and nine months of age and is a consequence of
multiple factors: rapid growth, depleted stores, low iron content of the diet, and early
feeding of cow’s milk.36,37 Since a milk-based diet is the predominant source of energy, at
least in the first six months of life, the iron content and its bioavailability are strong
predictors of iron nutritional status.38 The estimated requirement of absorbed iron from
birth to one year is 0.55 to 0.75 mg/d, thereby underscoring the need for adequate iron
in the diet to meet these needs. Iron concentration in human milk is low (0.3 to 0.5 mg/
L), and although well absorbed, iron content declines between 14 and 183 days of age.39
Therefore, even given the better absorption as milk intake increases and iron content
decreases, it is easy to see that the amount of absorbed iron will be inadequate to meet
the estimated requirements. Therefore, breastfed infants who do not receive iron supple-
ments or iron from other sources are at risk of becoming iron deficient between 6 and 12
months of age.40 Iron-fortified cow’s milk or soy-based formulas are effective in preventing
iron deficiency, and the decline in iron deficiency anemia over the past few decades has
been attributed to their use.34 Systemic manifestations of iron deficiency anemia include
behavioral and cognitive abnormalities expressed as lower scores on tests of psychomotor
development. These effects have to be interpreted keeping the confounding variables of
poor nutrition, environment, and poor socioeconomic background that often coexist. The
studies suggest that infants with iron deficiency anemia, but not iron deficiency without
anemia, have impaired performance of mental and psychomotor development.41-45 These
deficiencies do not improve with iron therapy, and follow-up studies at five to six years
of age still demonstrate poorer scores in the children who were previously anemic.43,44
Strategies to prevent iron deficiency could include the feeding of iron-fortified formulas,
avoidance of non-iron fortified milks and cow’s milk (the latter, at least, till beyond 12
months of age), the feeding of meats and iron-fortified foods, and, if needed, medicinal
iron supplementation in the form of ferrous sulfate.
TABLE 7.7
Unique Constituents of Breast Milk
Unique Constituents of Breast Milk
Docosahexanoic acid Necessary for growth and development of the brain and retina and for
myelinization of nervous tissue
Cholesterol Enhances myelinization of nervous tissue
Taurine Second most abundant amino acid in human milk, important for bile acid
conjugation
Choline May enhance memory
Enzymes Numerous enzymes such as lipases that are important in digestion and
absorption of fat
Lactoferrin Prevents iron from being available to bacteria
Inositol Enhances synthesis and secretion of surfactant in immature lung tissue
Poly- and Oligosaccharides Inhibit bacterial binding to mucosal surfaces
Protein (such as α- Supply amino acids to the infant, help synthesize lactose in the mammary gland,
lactalbumin) and bind calcium and zinc
Bifidobacterium species Predominant bacterial flora in the gastrointestinal tract of breastfed infants,
creates unfavorable pH conditions for the growth of enteric pathogens
Macrophages Macrophages in human colostrum have high concentrations of slgA which is
released during phagocytosis
Epidermal growth factor Promotes cell proliferation in the gastrointestinal mucosa
Breastfeeding
The benefits of breastfeeding to the infant, mother, family, and society are numerous and
impressive, but they must be put into context when making individual decisions about
breast feeding. These include ready availability, possible enhancement of intestinal devel-
opment, resistance to infection, and bonding between mother and infant. It is the preferred
feeding method for the normal infant. Breast milk, in addition to providing the required
nutrients for the healthy infant, has unique constituents, as listed in Table 7.7.
Protein
Approximately 20% of the total nitrogen in human milk is in the form of non-protein
nitrogen compounds such as free amino acids, and urea, which is considerably greater
than the 5% found in bovine milk,46 although there remains a debate about their contri-
bution to nitrogen utilization.47 The quality of the protein differs from that of bovine milk
as well, with the whey-to-casein protein ratios being 70:30 and 18:82 in human and bovine
milk, respectively. These differences in whey-to-casein ratio are reflected in the plasma
amino acid profile of infants and are readily observed within the first three days of age.48
Further, plasma amino acid patterns in human milk-fed infants has been used as a refer-
ence in infant nutrition.49,50 In addition, specific human whey proteins — lactoferrin,
lysozyme, and slgA — are involved in host defense.51,52
Lipids
Lipids in human milk provide 40 to 50% of the energy content and are vehicles for fat
soluble vitamins. The total fat content varies from 2% in colostrum to 2.5–3.0% in transi-
tional milk, and 3.5–4.5% in mature human milk.19 Cholesterol, phospholipids, and essen-
tial fatty acids are highest in colostrum, and more than 98% of human milk fat comes from
11 major fatty acids of 10-20 carbon length. Human milk lipids can inactivate enveloped
viruses including herpes simplex I, measles, and cytomegalovirus, to name a few.
Monoglycerides also exert antiviral activity.
Fat content of human milk is variable, with the fat content rising throughout lactation
but with changes apparent within the course of one day, within feeds and between
women.53 The effects of these differences in thriving infants is not clear, even given that
hind milk has a higher fat content than fore milk. Human milk lipids provide preformed
LC-PUFAs in amounts sufficient to meet nutrient needs. In term infants, plasma concen-
trations of essential fatty acids (arachidonic acid) at two and four weeks of age were
significantly lower in infants fed formula without LC-PUFA compared to breastfed infants.
Docosahexanoic acid concentrations were similarly lower at four and eight weeks of age.
Neuringer and colleagues showed that visual acuity and learning abilities correlate well
with the amount of DHA in the retina and brain phospholipids.54
Nucleotides
Nucleotides represent 2 to 5% of the non-protein nitrogen in human milk.55 Nucleotides
participate in many biological functions such as forming the basis of genetic information
(DNA, RNA) and storing energy (AMP, GMP), and they play roles in immunity as well
as cellular activities. Although they can be produced by the liver, the body’s requirements
vary considerably, especially during infancy.56 The effect of nucleotides on immune func-
tion is not well understood, but infants fed breast milk or nucleotide-supplemented for-
mula have been shown to exhibit increased natural killer cell activity compared to infants
fed unsupplemented formula.57 Infants fed nucleotide formulas had enhanced Haemophi-
lus influenza type B and diphtheria humoral responses compared to non-supplemented
infants.58 Feeding of human milk resulted in significantly higher neutralizing antibody
titers to polio virus at six months of age than were found in control or formula-fed cohorts.
These data suggest that dietary factors play a role in the antibody response to immuni-
zation, and more studies are needed to better understand the mechanisms involved.
Infection
There are several enzymes present in human milk that appear to be important in the
prevention of infection. These include glutathione peroxidase, alkaline phosphatase, and
xanthine oxidase. In addition, other anti-inflammatory agents such as catalase, lactoferrin,
immunoglobulins, and lysozyme are also present in human milk. The antimicrobial activ-
ities of these are generally found at mucosal surfaces, such as the gastrointestinal, urinary,
and respiratory tracts. Specific factors, such as lactoferrin, lysozyme, and slgA, resist
proteolytic degradation and can line the mucosal surfaces, preventing microbial attach-
ment and inhibiting microbial activity. Each of the mammary immune systems is active
against a variety of antigens. Prospective studies in developing countries indicate that
breast milk feeding reduces the incidence or severity of diarrhea,59 lower respiratory tract
infection,60 otitis media,61 bacteremia,62 bacterial meningitis,63 botulism,64 urinary tract
infection,65 and necrotizing enterocolitis.66
Hyperbilirubinemia is more common in breast-fed than formula-fed infants. This is
usually transient, and discontinuation of breast feeding is not recommended unless biliru-
bin values reach excessively high levels or the jaundice persists. Usually, switching to a
formula for one to two days is therapeutic and diagnostic, and breastfeeding can be safely
resumed. Other causes of jaundice should be sought before making a firm diagnosis of
breast-milk jaundice.
Certain chemicals, drugs, foreign proteins, and viruses may be present in human milk.67
However, the risk–benefit ratio of artificial milk needs to be weighed, especially if the
water sources for mixing the milk are contaminated. Breastfeeding is currently contra-
indicated in disease states such as active herpes, tuberculosis, and AIDS.
Formula Feeding
A variety of formulas are available for feeding infants (Table 7.3). The most commonly
used formulas are from bovine milk, and nutrient specifications for infant formulas are
available.68 Commercially available formulas are recommended when breast feeding is
not chosen. Cow’s milk is not recommended in the first year of life due to its nutritional
limitations and inappropriate nutrient concentrations. Cow’s milk has higher concentra-
tions of protein and phosphorus, a lower calcium-to-phosphorus ratio, limited iron, less
essential fatty acids, vitamin C, and zinc than human milk. Increased renal solute load
due to cow’s milk and increased occult blood loss via the gastrointestinal tract leading to
iron deficiency and anemia in infants fed cow’s milk unsupplemented by other nutrients
are additional reasons to discourage the feeding of cow’s milk in early infancy.
1. Isolated soy protein-based formulas are safe and effective alternatives to provide
appropriate nutrition if breast milk or cow milk-based formulas do not meet the
nutritional needs in term infants. However, no advantage is provided over cow’s
milk protein-based formulas as a supplement for breast feeding.
2. Soy protein-based formulas are appropriate for use in infants with galactosemia
and hereditary lactase deficiency.
3. There is no proven value of the routine use of soy-protein based formula in the
prevention or management of infantile colic.
4. There is no proven value of the routine use of soy protein-based formula in the
prevention of atopic disease in healthy or at-risk infants.
5. Infants with documented cow milk protein-induced enteropathy or enterocolitis
should not be given soy protein-based formula routinely.
The nutritional needs of infants zero to six months can be met by breast milk or infant
formulas. Although both groups of infants need to have health surveillance including
growth and development, breastfed infants need to be followed closely over the first few
weeks to assure appropriate feeding practices and resultant growth. Appropriate counsel-
ing for common breast feeding problems needs to be provided, and community support
groups can be involved if needed. Beyond six months, recommendations for infant feeding
are variable, and the recommendations are largely based on extrapolation from data on
younger infants. Nutritional composition of “follow-up” formulas is specified with mini-
mum lower limits for energy (60 kcal/dL), higher minimum limits for protein (2.25 to 3.0
g/100 kcal) and lower minimum limits for fat (3.0 to 4.0 g/100 kcal) compared to formulas
for younger infants. Nonetheless, iron-fortified formulas designed for younger infants may
be safely fed from 6 to 12 months. Infants by this age are physiologically and develop-
mentally ready to accept a variety of dietary items, and feeding practices vary based on
ethnic, cultural, and economic reasons. As stated earlier, feeding of bovine milk is discour-
aged during this period, although a substantial number of infants are indeed fed bovine
milk.70 In addition, there are concerns about the substitution of low-fat or skimmed milks
during this period because of higher intakes of protein and sodium and lower intakes of
iron and essential fatty acids. However, if infants are being fed non-milk foods, the actual
intake of energy may not be lower than of infants fed bovine milk or formula.71
Weaning
The transition from suckling to eating of non-milk foods occurs during the first year of
life based on cultural beliefs and practices, physicians beliefs, mothers’ perceptions of their
infants’ needs, and economic realities. Complementary foods are introduced from before
three months to by six months of age, and a variety of foods are offered.72-74 In the U.S.,
the total transition to beikost usually occurs by the end of the first year of life and continues
during the second year.
The weaning process can be considered in three ways. First, it could be the weaning
from breast feeding to other milks which may replace breast feeding partially or com-
pletely. In the second form, weaning could be considered the transition from liquid to
non-liquid diet. Health concerns may arise during this period if the added foods are too
nutrient dense (protein or energy) or nutrient-deficient (iron, protein), thus altering the
protein:energy ratio or causing deficiency of specific nutrients. The third aspect of weaning
may be the transition from human milk or formula to bovine milk in addition to the
provision of beikost. Since weaning typically occurs during a period of rapid growth,
attention to both nutritional and developmental issues during this period is warranted.
Complementary foods, in addition to providing the required nutrients, are also important
in establishing lifelong patterns of eating.
Failure to Thrive
Growth, as assessed by weight, length (and subsequently height) and head circumference,
is an important part of anticipatory guidance provided in well child care. These anthro-
pometric measurements, especially weight, can be used to detect inadequate attained
growth or reduced growth velocity. The average birth weight of a full term infant is 3300
to 3500 g; after a weight loss of ~10%, infants should regain their birth weight by two
weeks, with formula-fed infants tending to regain their birth weight a little sooner than
their breastfed counterparts. On an average, infants gain about 1 kg per month for the
first three months, 1/2 kilogram per month for the next three months, 1/3 kilogram per
month from 6 to 9 months and 1/4 kilogram per month from 9 to 12 months. Full term
infants double their weight by 4 months and triple their weight by 12 months, while
doubling their length during the same period. Both weight and length gain are slower in
the second year of life, underscoring the anticipatory nutritional guidance needed during
that period. Growth faltering, or failure to thrive, a descriptive term, is then identified by
the following criteria: (1) weight less than 80 to 85% of the 50th percentile on the National
Center for Health Statistics (NCHS) growth charts, (2) weight for age less than the 3 to 5
percentile on the NCHS growth charts, (3) drop in weight that crosses two or more
percentile categories on standard growth charts from previously established pattern of
adequate growth, and (4) a Z-score of –2 SD below the normal 50th percentile. If growth
velocity is used, a decrement of 2 SD over a 90-day period and loss of >1 SD Z score over
90 days is used as a measure of growth faltering.
Since decline in rate of weight gain or growth velocity is more sensitive than decline in
length or head circumference, serial measurements of weight are an important part of the
anticipatory guidance given during well child checks, and provide an early warning of
growth faltering.75,76 The Body Mass Index (BMI), calculated by dividing weight in kilo-
grams by length/height in meters squared, has largely replaced weight for stature. It should
be recognized that there are growth differences between breast and formula-fed infants. As
reported by Nelson et al.,77 mean gains in both weight (g/d) and length (cm/d) were greater
in formula-fed males and females than their breastfed counterparts from 8–122 days of age.
Since the NCHS growth charts were made from data that was cross-sectional and the infants
were fed formulas, attention to growth faltering in the breastfed infant requires both under-
standing of the growth of breastfed infants and the early recognition of decrease in weight
or growth velocity.78 There are numerous organic and non-organic causes of growth failure
or faltering which need to be addressed during such an evaluation. It is important to realize
that failure to thrive or malnutrition may occur in hospitalized infants and children, as well,
and efforts to recognize and nourish these infants and children should be made.
Summary
In summary, the period of infancy is one of rapid changes in growth and attainment of
developmental milestones. This period imposes unique nutritional needs and challenges
for the health care provider. Understanding nutritional needs, ways of meeting these needs
(Table 7.8), deviations in growth and their causes, and providing nutrition in age-appro-
TABLE 7.8
Recommendations for Feeding Healthy Full-Term Infants
Breastfeeding is strongly recommended.
Infant formulas that meet AAP guidelines are recommended when breastfeeding is not chosen or breast milk
is not available.
Breast milk or infant formula is the preferred feeding in the first year of life.
Adequate intakes of human milk or formula meet all nutrient requirements for the first 6 months of life (exception
may be vitamin D in dark-skinned, sun deprived breast fed infants). Infant formula or “follow-up” formula
may be fed in the second 6 months of life.
Introduction of complementary foods should be based on growth, developmental, cultural, social, psychological
and economic considerations. As a general rule, when an infant is consuming 32 ounces of milk per day and
appears to want more, supplemental feedings may be indicated. This usually occurs between 4 and 6 months
of age.
priate, culturally and ethnically sensitive ways while addressing economic issues is the
task of the health care team. Ideally, the infant’s nutritional need (expressed as hunger),
developmental progress (as observed in attainment of feeding skills), and mother’s and
care provider’s beliefs within the context of the family will guide the infant’s feeding
experience and transition to the next phase in life.
Acknowledgment
The authors thank Tina Corbin for her tireless secretarial support in the preparation of
this manuscript.
References
1. Hamill P. V., Drizd T. A., Johnson C. L., et al. Am J Clin Nutr 32: 607; 1979.
2. Fomon S. J., Nelson S. E. Size and growth: In Nutrition of Normal Infants, CV Mosby, 1993, 36,
p. 155.
3. Butte N. F. Eur J Clin Nutr 50: 24S; 1996.
4. Health and Welfare Canada. Nutrition Recommendations. The report of the scientific review
committee, Ottawa, Canada: Supply and Services, 1990.
5. Dewey K. G., Lonnerdal B. J Pediatr Gastroenterol Nutr 2: 497; 1983.
6. Dewey K. G., Heinig M. J., Nommsen L. A., et al. J Pediatr 119: 538; 1991.
7. Whitehead R. G., Paul A. A., Cole T. J. Acta Paediatr Scand 299: 43S; 1982.
8. Kylberg H., Hofvander Y., Sjolin S. Acta Paediatr Scand 75: 932; 1986.
9. Persson L. A., Johansson E., Samuelson G. Human Nutrition — Applied Nutrition 38: 247; 1984.
10. Heinig M. J., Nommsen L. A., Peerson J. M., et al. Am J Clin Nutr 58: 152; 1993.
11. Zlotkin S. H., Anderson G. H. Pediatr Res 16: 65; 1982.
12. Pohlandt P. Acta Paediatr Scand 63: 801; 1974.
13. Gaull G. E., Rassin D. K., Raiha N. C., et al. J Pediatr 90: 348; 1977.
14. Rassin D. K., Gaull G. E., Jarvenpaa A. L., et al. Pediatrics 71: 179; 1983.
15. Jarvenpaa A. L., Rassin D. K., Raiha N. C., et al. Pediatrics 70: 221; 1982.
16. World Health Organization. Energy and protein requirements. WHO Technical Report Series
No. 742, Geneva, WHO. 98, 1985.
17. Fomon S. J., Haschke F., Ziegler E. E., Nelson S. E. Am J Clin Nutr 34(5): 1169S; 1982.
18. Wong W. W., Hachey D. L., Insull W., et al. J Lipid Res 34: 1403; 1993.
19. Bitman J., Wood L., Hamosh M., et al. Am J Clin Nutr 38: 300; 1983.
20. Harzer G., Haug M., Dieterich I., et al. Am J Clin Nutr 37: 612; 1983.
21. Hibberd C. M., Brooke O. G., Carter N. G., et al. Arch Dis Child 57: 658; 1982.
22. Jensen R. G. The Lipids of Human Milk. Boca Raton: CRC Press, 1989.
23. Prentice A., Prentice A. M., Whitehead R. G. Br J Nutr 45: 495; 1981.
24. Hachey D. L., Thomas M. R., Emken E. A., et al. J Lipid Res 28: 1185; 1987.
25. Hachey D. L., Silber G. H., Wong W. W., Garza C. Pediatr Res 25: 63; 1989.
26. Koletzko B., Thiel I., Abiodun P. O. Z Ernahrungwiss 30: 289; 1991.
27. Harris W. S., Conner W. E., Lindsey S. Am J Clin Nutr 40: 780; 1984.
28. Genzel-Boroviczeny O., Wahle J., Koletzko B. Eur J Paediatr 156: 142; 1997.
29. Joint FAO/WHO Codex Alimentarius Commission, 1984; Food and Drug Administration 1985;
Commission of European Communities, 1991.
30. Lifshitz F., Moses N. Am J Dis Child 143: 537; 1989.
31. Michaelsen K. F., Jorgensen M. H. Eur J Clin Nutr 49: 467; 1995.
32. Bhatia J., Bucher C., Bunyapen C. Pediatr Ann 27: 525; 1998.
33. Dallman P. R., Siimes M. A., Stekel A. Am J Clin Nutr 33: 86; 1980.
34. Yip R. In Dietary Iron: Birth to Two Years. (Filer L. J. Jr., Ed): New York: Raven Press, 1989, pg 37.
35. Ferguson B. J., Skikne B. S., Simpson K. M., et al. J Lab Clin Med 119: 385; 1992.
36. Ziegler E. E., Fomon S. J., Nelson S. E., et al. J Pediatr 116: 11; 1990.
37. Fomon S. J., Ziegler E. E., Nelson S. E., et al. J Pediatr 98: 540; 1981.
38. Pizarro F., Yip R., Dallman P. R., et al. J Pediatr 118: 687; 1991.
39. Siimes M. A., Vuori E., Kuitunen P. Acta Paediatr Scand 68: 29; 1979.
40. Haschke F., Vanura H., Male C., et al. J Pediatr Gastroenterol Nutr 16: 151; 1993.
41. Lozoff B., Brittenham G. M., Viteri F. E., et al. J Pediatr 100: 351; 1982.
42. Lozoff B., Brittenham G. M., Wolf A. W., et al. Pediatrics 79: 981; 1987.
43. Lozoff B., Jiminez W., Wolf A. W. N Eng J Med 325: 687; 1991.
44. Walter T. In: Nutritional Anemias. (Fomon S. J., Zlotkin S., Eds) Nestle Nutrition Workshop
Series, 30. New York: Raven Press; 1990, pg 81.
45. Pollitt E. Ann Rev Nutr 13: 521; 1993.
46. Hambraeus L. Pediatr Clin N Am 24: 17; 1977.
47. Fomon S. J., Bier D. M., Mathews D. E., et al. J Pediatr 113: 515; 1988.
48. Cho F., Bhatia J., Rassin D. K. Nutrition 6: 449; 1990.
49. Lindblad B. S., Alfven G., Zetterstrom R. Acta Paediatr Scand 67: 659; 1978.
50. Rassin D. K. In: Protein Requirements in the Term Infant. (Barness L., Ed) Princeton: Excerpta
Medica: 1988, pg 3.
51. Goldman A. S., Cheda S., Keeny S. E., et al. Sem Perinatol 18: 495; 1994.
52. Hanson L. A., Ahlstedt S., Andersson B., et al. Pediatrics 75: 172; 1985.
53. Neville M. C., Keller R. P., Seacat J., et al. Am J Clin Nutr 40: 635; 1984.
54. Neuringer M., Conner W. E., Van Patten C., et al. J Clin Invest 73: 272; 1984.
55. Uauy R., Quan R., Gil A. J Nutr 124(8): 1436S; 1994.
56. Jyonouchi H. J Nutr 124(1): 138S; 1994.
57. Carver J. D. J Nutr 124(1): 144S; 1994.
58. Pickering L. K., Granoff D. M., Erickson J. R., et al. Pediatrics 101: 242; 1998.
59. Dewey K. G., Heinig M. J., Nommsen-Rivers L. A. J Pediatr 126: 696; 1995.
60. Wright A. L., Holberg C. J., Taussig L. M., et al. Arch Pediatr Adolesc Med 149: 758; 1995.
61. Kovar M. G., Serdula M. K., Marks J. S., et al. Pediatrics 74: 615; 1984.
62. Takala A. K., Eskola J., Palmgren J., et al. J Pediatr 115: 694: 1989.
63. Cochi S. L., Fleming D. W., Hightower A. W., et al. J Pediatr 108: 887; 1986.
64. Arnon S. S. Rev Infect Dis 6, 193S.
65. Pisacane A., Graziano L., Mazzarella G., et al. J Pediatr 120: 87; 1992.
66. Lucas A., Cole T. J. Lancet 336: 1519; 1990.
67. Goldfarb J. Clin Perinatol 20: 225; 1985.
68. Food and Drug Administration: Rules and regulations. Nutrient requirements for infant for-
mulas (21 CFR part 107), Fed Reg 50:45106, 1985.
69. American Academy of Pediatrics, Committee on Nutrition. Pediatrics 101: 148; 1998.
70. American Academy of Pediatrics, Committee on Nutrition. AAP News 8: 18; 1992.
71. Martinez G. A., Ryan A. S., Malec D. J. Am J Dis Child 139: 1010; 1985.
72. Anderson T. A., Ziegler E. E. In: Weaning, Why, What and When? ( Ballabriga A., Ray J., Eds)
Nestle Nutrition Workshop Series, 10, New York: Raven Press, 1987, pg 153.
73. Ballabriga A., Schmidt E. In: Weaning, Why, What and When? (Ballabriga A., Ray J., Eds) Nestle
Nutrition Workshop Series, 10, Raven Press, New York, 1987, pg 129.
74. Ahmad A. In: Weaning, Why, What and When? (Ballabriga A., Ray J., Eds) Nestle Nutrition
Workshop Series, 10, New York: Raven Press, 1987, pg 197.
75. Zumrawi F. Y., Min Y., Marshall T. Ann Human Biol 19: 165; 1992.
76. Healy M. J. R., Yang M., Tanner J. M., Zumrawi F. Y. In: Linear Growth Retardation in Less
Developed Countries. (Waterlow, J. C., Ed) New York: Raven Press, 41, 1988.
77. Nelson S. E., Rogers R. R., Ziegler E. E., et al. Early Hum Devel 19: 223; 1989.
78. Garza C., Frongillo E., Dewey K. G. Acta Paediatr 404: 4S; 1994.