Original
Article
& & & & & & & & & &
Breastfeeding and Jaundice
Lawrence M. Gartner, MD
In the breastfed infant, prolongation of unconjugated hyperbilirubinemia
into the third and later weeks of life in the healthy newborn is a normal and
regularly occurring extension of physiologic jaundice. This is known as
breastmilk jaundice. A factor in human milk increases the enterohepatic
circulation of bilirubin. Insufficient caloric intake resulting from maternal
and / or infant breastfeeding difficulties may also increase serum
unconjugated bilirubin concentrations. This is the infantile equivalent of
adult starvation jaundice. It is known as breastfeeding jaundice or
‘‘breast - nonfeeding jaundice.’’ This increase in severity of physiologic
jaundice of the newborn also results from increased enterohepatic
circulation of bilirubin, but not because of a factor in human milk. In
extreme cases, it may place the infant at risk for development of bilirubin
encephalopathy. Optimal breastfeeding practices, which result in minimal
initial weight loss and early onset of weight gain, are associated with both
reduced breastfeeding jaundice and minimization of the intensity of
breastmilk jaundice.
Journal of Perinatology 2001; 21:S25 – S29.
BREASTMILK JAUNDICE
Nearly 40 years ago, the association between breastfeeding and
prolongation of unconjugated hyperbilirubinemia in the newborn
was recognized simultaneously by two separate groups of
investigators.1,2 Initially, it was thought to be a relatively rare clinical
situation, which occurred in only 1% of all breastfed neonates. Later
studies in both England and in the United States demonstrated that
at least one third of all breastfed infants are clinically jaundiced in
the third week of life and that two thirds have significant
unconjugated hyperbilirubinemia in the third week. This contrasts to
the absence of hyperbilirubinemia in the third week in full-term
artificially fed infants3 – 5 (Figure 1). What was once thought to be a
clinical disorder has now been recognized to be a normally occurring
extension of physiologic jaundice of the newborn.
The optimally breastfed infant does not differ from the artificially
fed infant in serum bilirubin concentrations during the first 5 days of
Departments of Pediatrics and Obstetrics / Gynecology, The University of Chicago, Chicago, IL.
Address correspondence to Lawrence M. Gartner, MD, MedWord, 28398 Alamar Road, Valley
Center, CA 92082 - 6452.
Journal of Perinatology 2001; 21:S25 – S29
# 2001 Nature Publishing Group All rights reserved. 0743-8346/01 $17
www.nature.com/jp
& & & &
life. Optimal breastfeeding management includes initiation of
breastfeeding in the first hour, followed by at least 10 to 12
breastfeeds per day for the first 1 to 2 weeks without any water or
other food supplementation, using good positioning that assures
effective milk transfer to the infant, and weight loss from birth of less
than 8%.6 After the fifth day, the great majority of breastfed infants
either maintain a stable, but elevated serum bilirubin level, or have a
second rise in bilirubin, which generally peaks on about the 10th to
15th days of life7 (Figure 2). In some infants, these elevated levels
may continue for many weeks, whereas in others, the levels decline
during the third and fourth weeks. During the third week of life,
among the two thirds or more with elevated levels, the serum
bilirubin concentrations may range from just over the upper limit of
adult normal, 25 M/l (1.5 mg/dl), to more than 250 M/l
(15 mg/dl) (Figure 3). Rarely do the levels in healthy, term
infants rise beyond 25 mg/dl (425 M/l) or place the infant at
risk for bilirubin encephalopathy. Ultimately, serum bilirubin
levels return to normal in all infants with breastmilk jaundice.
Persistence of hyperbilirubinemia beyond 3 months would suggest
an etiology other than breastmilk.
The mechanism of breastmilk jaundice has generated a vast
array of hypotheses, ranging from our own original concept that
human milk contained an inhibitor of hepatic glucuronyl
transferase, the enzyme promoting the conjugation of bilirubin
with glucuronic acid, and that blockage at the step of bilirubin
conjugation was responsible for the ‘‘disorder.’’ This concept was
supported by the detection of an unusual metabolite of
progesterone, pregnane-3(alpha),20(beta)-diol, which was shown
to be an inhibitor of hepatic glucuronyl transferase in vitro.1 The
presence of this metabolite in milk and maternal urine was
confirmed by some, but not all, subsequent investigators. The
inhibitory effect of milk on the conjugating enzyme in vitro did
not correlate closely with the time course of hyperbilirubinemia in
the infants, although it was postulated that the effect of the
inhibitor diminished as the children aged.8 Administration of the
pure metabolite to two anicteric, normal term infants at 6 and
8 days of age was associated with a significant increase in serum
unconjugated bilirubin concentrations to 87 M/l (5.1 mg/dl) and
146 M/l (8.6 mg/dl), respectively.8 Subsequent attempts by other
investigators to demonstrate that the steroid metabolite would
produce clinical jaundice, or an increase in serum bilirubin
concentrations in infants were unsuccessful, however. Now that we
recognize the universality of breastmilk jaundice in all populations
and in the great majority of infants, it appears less likely that
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 Gartner Breastfeeding and Jaundice

Figure 1. ARTIFICIALLY-FED NEWBORNS

Figure 2. OPTIMALLY BREASTFED NEWBORN
120
160

100 140
Total Serum Bilirubin (uM/L)

120

Total Serum Bilirubin (uM/L)

80

100

60
80

40 60

40
20

20

0
0
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
Days of Life
Days of Life

Figure 1. Total serum bilirubin concentrations in full -term, healthy

artificially fed newborns during the first 22 days of life [ redrawn from Figure 3. Percent distribution of total serum bilirubin concentrations in
Gartner LM, Lee KS, Vaisman S, Lane D, Zarafu I. J Pediatr 1977;90:513 – 36 full -term, healthy exclusively breastfed infants 12 to 21 days of age
531 ] .5 [redrawn from Alonso EM, Whitington PF, Whitington SH, et al. J Pediatr
1991;118:425 – 430 ].4

pregnanediol is the primary etiologic agent of the jaundice, although

of the dose in 5 hours and no further absorption thereafter.14 The
it may play some contributory role.
addition of cow’s milk and some human milk to the test dose of
A wide range of other hypotheses rapidly followed this initial
bilirubin completely inhibited intestinal absorption of bilirubin.
one. Most of them also focused on inhibition of conjugation as the
However, milk from mothers of infants with classical breastmilk
likely mechanism, but suggested other inhibitors, most prominently
jaundice inhibited intestinal absorption of bilirubin only for the first
increased free fatty acid concentrations resulting from excessive
2 hours and was then followed by a dramatic increase in absorption,
lipase activity in milk.9,10 Other putative agents include excessive
which continued for at least an additional 14 hours and resulted in a
taurine through its effect on bile acid metabolism and excessive
total absorption of 60% of the intestinal bilirubin dose. A subsequent
 -glucuronidase activity in milk, promoting increased bilirubin
study by other investigators confirmed the role of human milk
glucuronide hydrolysis and an increase in the enterohepatic
enhancement of intestinal bilirubin absorption and demonstrated a
circulation of bilirubin.11,12 None of these etiologies for breastmilk
significant positive correlation between the degree of enhancement
jaundice has stood the test of time, however.4,13
of bilirubin absorption in the rat model by the human mother’s
The most attractive and convincing evidence regarding the
milk and the infant’s serum bilirubin elevation. They found no
mechanism of breastmilk jaundice has come from studies of the
evidence for the effect of human milk inhibition of glucuronide
effect of human milk on the intestinal absorption of bilirubin with
conjugation of bilirubin, or for the roles of  -glucuronidase or
resultant increase in enterohepatic circulation of bilirubin. Using an
free fatty acids in the etiology of breastmilk jaundice.4 The factor
adult rat model, administration of 17 M (1.0 mg) of unconjugated
in human milk that increases intestinal bilirubin absorption
bilirubin into the duodenum resulted in intestinal absorption of 25%
remains unidentified. Breastmilk jaundice does not present in the
first 5 days of life, apparently because the factor in human milk
inducing an increase in intestinal absorption of bilirubin does not
Figure 3. BREASTFED NEWBORNS - 12 - 21 DAYS OF AGE
appear until the transition from colostrum to mature milk. We
45
have concluded that breastmilk jaundice is neither a disease nor a
40
syndrome, but rather a normal developmental phenomenon in the
35
breastfed infant. It is an extension of physiologic jaundice of the
30 newborn.
Percent Distribution

25

20

15
DIAGNOSIS OF BREASTMILK JAUNDICE
10 Recognition that at least two thirds of all breastfed infants will have
5 serum bilirubin concentrations in the third week of life that are
0
significantly higher than the adult normal value is an important
0 - 25 26 - 50 51 - 100 101 - 150 151 - 200 201- 300
Total Serum Bilirubin (uM/L) foundation for diagnosis. Breastmilk jaundice is a normal, regularly
Figure 2. Typical pattern of total serum bilirubin concentrations in a occurring prolongation of physiologic jaundice of the newborn. For
healthy, full - term, optimally breastfed infant during the first 22 days of life. the healthy, full-term infant, elevations of serum unconjugated

S26 Journal of Perinatology 2001; 21:S25 – S29

Breastfeeding and Jaundice
bilirubin to 340 or 425 M/l (20 or 25 mg/dl), the highest levels
seen with breastmilk jaundice, are not a cause for alarm, although
they indicate a need for investigation to rule out pathologic causes of
exaggerated hyperbilirubinemia. Elevations to this level are rare,
occurring in fewer than 1% of all thriving breastfed infants. The great
majority of infants with breastmilk jaundice will have much lower
levels (Figure 3).4 Only one third has levels greater than 100 M/l
(6 mg/dl) and the great majority of breastfed infants with elevated
bilirubin concentrations have less than 150 M/l (9 mg/dl).4 The
recent report by Maruo et al.15 from Japan provides strong evidence
that most of the breastfed infants with these very high levels have a
genetic factor which contributes to their extreme hyperbilirubinemia
by restricting the hepatic conjugation of bilirubin. The diagnosis of
breastmilk jaundice can usually be made in the healthy, thriving
breastfed infant with good weight gain in whom hemolysis and other
pathologic causes of jaundice have been ruled out by clinical or
laboratory study.
CLINICAL MANAGEMENT OF BREASTMILK JAUNDICE
Clinical management of the infant with breastmilk jaundice is of
considerable interest and importance. The full-term infant with
breastmilk jaundice of less than 340 M/l (20 mg/dl) requires no
intervention, and breastfeeding should be continued without
interruption.16 For those full-term, healthy infants with breastmilk
jaundice and serum bilirubin levels between 340 and 425 M/l (20
and 25 mg/dl), closer observation of bilirubin concentrations is
indicated. Some clinicians may wish to observe, whereas others may
choose to complement breastfeeding with formula for 24 to 48 hours,
which will reduce intestinal bilirubin absorption, or initiation of
phototherapy. When serum bilirubin concentrations rise toward
425 M/l (25 mg/dl), the use of phototherapy while continuing
breastfeeding, or the interruption of breastfeeding for 24 hours,
substituting formula, may be indicated. Those infants with
breastmilk jaundice who have developed kernicterus may have
additional factors of hemolysis, infection, or a genetic alteration in
bilirubin metabolism. The great majority of full-term breastfed
infants who developed kernicterus had excessive weight loss of more
than 10%, suggesting a period of lethargy and poor feeding, possibly
secondary to the rising serum bilirubin.17 These infants may have
both breastmilk jaundice and breast-nonfeeding jaundice (see
below). Thus, breastmilk jaundice may be a contributor to
kernicterus, but probably only in combination with other factors.
Early recognition of the breastfed infant with poor intake is essential
to insure preservation of breastfeeding and to avoid excessive rises in
bilirubin due to starvation. It is for this reason that breastfed infants
should be examined by a well-trained clinician 2 to 3 days after
hospital discharge to assess nutritional adequacy, as well as jaundice.
Unlike the full-term infant, the premature infant poses an
interesting dilemma. Breastmilk, whether given directly from the
breast or by cup, bottle, or tube, has been shown to provide significant
protection against a variety of infections and to promote improved
Journal of Perinatology 2001; 21:S25 – S29
Gartner
growth and development in the preterm infant.18,19 Human milk
feeding increases serum bilirubin concentrations in premature
infants by about 3 mg/dl over at least the first 50 days of life
compared with formula-fed infants.20 Whether this degree of increase
places the breastfed premature infant at greater risk of kernicterus is
unknown. There may be compensation or protection against
kernicterus by prevention of infection, a factor known to increase risk
for kernicterus.21
BREASTFEEDING (NONFEEDING) JAUNDICE
Although the optimally breastfed infant has serum bilirubin
concentrations which are identical with that of the artificially fed
infant during the first 5 days of life, many breastfed infants develop
higher bilirubin levels during this early period of physiologic
jaundice. While some authors have considered this higher level of
bilirubin in the breastfed infant to be normal and expected, there is
ample evidence that these elevations are, in fact, abnormal.22,23
Terminology is often the cause of confusion among both authors and
readers. The term ‘‘breastmilk jaundice’’ should be reserved for the
normally occurring prolonged unconjugated bilirubin, which has its
onset after the fifth day of life. The increase in serum unconjugated
bilirubin concentration seen in the first 5 days of life in some
breastfed infants should be called ‘‘breastfeeding jaundice’’ or, more
precisely, ‘‘breast-nonfeeding jaundice.’’
In addition to confusion in the terminology describing the
relationship between human milk feeding and jaundice, there is also
confusion in the literature regarding the precise definition of
breastfeeding. Many papers, particularly in the earlier literature,
failed to include descriptions of the breastfeeding techniques used in
the study population. It is now well recognized that the volume of
milk produced by the lactating mother is intimately linked to the
time of onset of breastfeeding, the frequency of the breastfeeding, the
completeness of emptying of the breast at each feeding, the position
of the infant during nursing, and the ability of the infant to suckle
effectively. Administration of water or other feeds prior to or in
addition to nursing will also adversely affect the volume of milk that
the breastfeeding mother will produce.24 – 27 This is especially critical
during the early days of life when lactation is being established.
Reduced volume of milk transfer to the infant will limit the caloric
intake of the infant, producing a state of partial starvation. I use the
term ‘‘starvation’’ because there is a well-described entity in the
adult human and other adult mammals known as starvation
jaundice. This increase of 17 to 35 M/l (1 to 2 mg/dl) in
unconjugated serum bilirubin, which occurs in virtually all adults
after 24 hours of fasting despite adequate water intake, has been
shown to be due to an enhancement of the enterohepatic circulation
of bilirubin.11,28 Studies in newborn rhesus monkeys demonstrated a
five-fold increase in intestinal bilirubin absorption even with normal
feeding regimens.29 Starvation — even partial starvation — can
be expected to further increase the intestinal absorption of bilirubin
in the newborn.
S27
 Gartner
The presence of large amounts of bilirubin in meconium and
delay in emptying of meconium have been shown to contribute
to an increase in serum bilirubin levels in the early days of life,
further increasing intestinal bilirubin absorption.30,31 Neither
breastfeeding nor reduced caloric intake increases bilirubin
synthesis as measured by expired carbon monoxide.32 Thus, the
most likely explanation for the observed excessive increase in
serum bilirubin in the first 5 days of life in breastfed infants in
some studies is the inadequacy of milk intake due to poor
breastfeeding practices and hospital policies. Support for this is
found in the studies demonstrating that lower serum bilirubin
concentrations in breastfed infants are associated with weight
gains comparable to or better than those of artificially fed
infants.33,34 Elevated bilirubin concentrations have been observed
with greater losses from birth weight.35 Breastfeeding frequencies
of at least 11 times per day, starting with the first day, have
been associated with the lowest serum bilirubin concentrations
on the third to sixth days of life.36,37 Delay in initiation of
breastfeeding beyond the first hour of life, and administration of
water to infants either before initiation of breastfeeding or in
addition to breastfeeding significantly reduce the frequency of
breastfeeding and increase serum bilirubin concentrations.38 While
these negative effects on breastfeeding and increases in jaundice
are seen primarily in the first 5 days of life, reduced caloric
intake later in the newborn period can also produce marked
increases in jaundice, often accompanied by dramatic weight
loss, dehydration, and even kernicterus.17 Many clinicians have
observed the development of lethargy and poor feeding with high
levels of bilirubin. This may further suppress caloric intake and
continue a vicious cycle of increasing serum bilirubin
concentration.
RELATIONSHIP OF BREAST-NONFEEDING JAUNDICE
AND BREASTMILK JAUNDICE
Whereas the two entities of breastmilk jaundice and breast-
nonfeeding jaundice are separate phenomena, they can have an
interactive effect on each other. Infants with breastmilk jaundice
who manifest higher levels of bilirubin in the second and third weeks
of life, often over 255 M/l (15 mg/dl), have been noted to have
had relatively high serum bilirubin concentrations during the first 3
to 5 days of life due to either breast-nonfeeding jaundice,
hemolysis, or unknown etiology. It has been postulated that these
early, elevated bilirubin levels produce an enlarged bilirubin pool in
the body. With the ingestion of mature milk and a consequent
enhancement of the enterohepatic circulation, this bilirubin pool
enlarges still further.
MANAGEMENT OF BREAST-NONFEEDING JAUNDICE
The great majority of breastfed infants with increased serum bilirubin
levels due to breast-nonfeeding jaundice can be managed by careful
S28
Breastfeeding and Jaundice
evaluation of the breastfeeding and correction of the problems to
insure adequate milk production and intake. Some may require
temporary supplemental feeding by cup or bottle. In the full-term
healthy infant, phototherapy and complementary or substitution
feedings with infant formula are not needed until serum levels exceed
300 to 340 M/l (18 to 20 mg/dl). Even when slightly greater than
340 M/l (20 mg/dl), but not rising rapidly, further observation
and assurance of good breastmilk intake may be all that is required.
Hemolysis and other pathologic causes of hyperbilirubinemia must
be ruled out, of course.
Whereas some degree of hyperbilirubinemia is normal and to be
expected in the newborn period and even to be prolonged for weeks in
the breastfed infant, excessive levels that place the infant at risk for
bilirubin encephalopathy are certainly to be avoided, while also
making every effort to preserve the breastfeeding. This can often be
achieved by practicing good lactation techniques that assure an
optimal milk volume and caloric intake. Thus, initiation of
breastfeeding in the first hour, followed by at least 10 to 12
breastfeeds per day for the first week or two without any water or
other food supplementation, and using good positioning that assures
effective milk transfer to the infant will minimize weight loss to less
than 7% and maintain serum bilirubin levels well under those that
would cause concern about risk for kernicterus.
FUTURE RESEARCH
Future research is needed to identify the factor in mature human
milk that promotes the enterohepatic circulation of bilirubin and
to achieve an improved understanding of how bilirubin moves
from the intestinal lumen into the mucosa. This might lead to
therapeutic techniques that would allow continuation of
breastfeeding while minimizing bilirubin elevations in those
occasional infants whose bilirubin concentrations rise to threat-
ening levels.
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