© 2001 The American Society for Nutritional Sciences
J. Nutr. 131:3012S-3015S, November 2001
Symposium: Human Lactogenesis II: Mechanisms, Determinants and Consequences
Maternal and Fetal Stress Are Associated with Impaired Lactogenesis in Humans1
Kathryn G. Dewey2
Department of Nutrition, University of California, Davis, CA 95616-8669
2To whom correspondence should be addressed. E-mail: kgdewey{at}ucdavis.edu
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ABSTRACT
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Studies in animals indicate that various types of stressful stimuli can
depress lactation, but there is much less information in humans.
Experimental studies in breastfeeding women have shown that acute
physical and mental stress can impair the milk ejection reflex by
reducing the release of oxytocin during a feed. If this occurs
repeatedly, it could reduce milk production by preventing full emptying
of the breast at each feed. Prospective observational studies indicate
that both maternal and fetal stress during labor and delivery (e.g.,
urgent Cesarean sections or long duration of labor in vaginal
deliveries) are associated with delayed onset of lactation. The effects
of chronic emotional stress on lactation are not known. Mothers who
experience high levels of stress during and after childbirth should
receive additional lactation guidance during the first week or two
postpartum.
KEY WORDS: lactation breastfeeding stress anxiety oxytocin
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INTRODUCTION
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There are numerous factors potentially associated with lactogenesis in
humans (1
) (Table 1
). On the maternal side, biological factors include parity, mode of
delivery, labor experience, body mass index, smoking, breast or nipple
abnormalities or surgery, illness, anxiety and stress. Behavioral
factors are equally important and include motivation to breastfeed,
social support, nursing frequency, the use of supplements such as
glucose water or formula, pacifier use and breastfeeding experience. It
is important to recognize that the characteristics of the infant also
play a role in the establishment of lactation. Biological factors, such
as the infants birth weight, gestational age and suckling ability,
are major determinants of the ability to latch on to the breast
effectively and extract milk, thereby stimulating continued milk
production. Several factors listed on the maternal side, such as labor
medications, may influence lactogenesis via infant suckling ability, in
particular, the infants alertness and ability to orient
(1
). Behavioral characteristics of the infant, such as
temperament (e.g., irritability vs. passivity, amount of crying) and
suckling style (e.g., gentle vs. firm latch, amplitude and frequency of
suckling bouts during a feed) may also play a role, by eliciting
different responses from the mother, affecting the efficiency of milk
transfer and potentially causing trauma to the nipple.
It is in this context that this article will address the effects of
maternal and fetal stress on lactogenesis. Anxiety and stress are
listed in Table 1
as biological factors because they have physiological
components, but they are clearly related to several of the factors
listed as behavioral. Because there are complex inter-relationships
among the various maternal and infant factors that may affect
lactogenesis, it is often not possible to separate the effects of
stress from those of other variables. For example, the mode of delivery
(vaginal vs. Cesarean section; elective or urgent Cesarean section),
duration and difficulty of labor and use of labor medications are
strongly associated with one another (Fig. 1
). Maternal and/or fetal stress may trigger or be caused by any of these
three variables, which in turn are related to the timing of the first
breastfeed and the infants suckling ability. When lactogenesis is
impaired, leading to delayed onset of milk production and/or
insufficient milk volume, it may be due to the combined result of all
of these factors. Although the majority of difficulties with
lactogenesis can be resolved given sufficient motivation by the mother
and appropriate breastfeeding management, many mothers do not have
access to adequate lactation guidance and support to help them through
this period. For this reason, problems encountered during the
initiation of lactation may result in long-term use of supplemental
feedings or complete abandonment of breastfeeding. Thus, it is
important to understand the role of stress during the period of
lactogenesis.
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Potential mechanisms underlying the association of stress with
lactogenesis
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A certain amount of stress is normal when considering the events
surrounding childbirth and the onset of lactation and is unlikely to
have any detrimental effects. However, women and infants whose
experience is at the high end of the range for stress may be at greater
risk for adverse outcomes. Stress can be categorized as primarily
physical or physiological (e.g., pain and exhaustion) or as emotional
(e.g., anxiety). It is unknown whether the bodys response to these
two types of stress has different effects on lactation.
At least two potential mechanisms can be hypothesized for the
relationship between stress and lactogenesis. First, as will be
discussed in the next section, maternal stress seems to interfere with
the release of oxytocin, the hormone that is responsible for the milk
ejection reflex. If the milk ejection reflex is impaired often, the
resulting incomplete removal of milk from the breast eventually will
lead to down-regulation of milk synthesis. Although milk removal is
not necessary to trigger lactogenesis stage II, it may be related to
the timing of onset of full milk production or the volume of milk
produced (2
, 3
). It is likely that maternal stress affects
levels of other hormones involved in lactation, such as prolactin
(4
), but there is little evidence on this issue in humans
(3
).
Second, a newborn who experienced stress during labor and delivery may
be too weak or too sleepy to latch on and suckle effectively at the
breast. Even if the lactational capacity of the mother is not
compromised, this could lead to impaired lactogenesis if milk removal
is not adequate.
It should also be recognized that the causal pathway between maternal
stress and lactogenesis could be reversed, i.e., mothers who experience
delayed onset of milk production are likely to become stressed as a
result. In observational studies it is often difficult to determine the
temporal relationship between cause and effect.
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Maternal stress and the milk ejection reflex
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Animal studies have demonstrated suppression of lactation after
exposure to certain types of stressful stimuli (4
). Most
of these studies were performed during established lactation, not
during lactogenesis. In humans, several studies have examined whether
maternal stress affects the milk ejection reflex or the amount of milk
transferred during a feed. The first was a unique experiment by Newton
and Newton (5
) in 1948, which involved three different
types of distractions imposed during the first morning feed on a mother
at 7 mo postpartum: immersion of her feet in ice water for 10 s of
every 30 s; verbal math problems, accompanied by mild electric
shocks if the mother got the wrong answer or took too long in
answering, and intermittent pulling of the mothers big toes, causing
sharp pain. On days with one of these distractions, the mother was
injected with either saline solution or pitocin (oxytocin) 2 min before
the infant began to nurse. Despite the fact that the study included
only one woman, the novel design of the experiment provided useful
information. Milk intake by the infant at the first morning feed was
measured on 8 control days and 12 distraction days (4 d for each of the
three treatments). Intake on control days was quite consistent, ranging
from 142 to 209 g (mean, 168 g). When saline preceded the
distraction, milk intake decreased noticeably (to an average of 99 g), particularly with the ice water treatment (Fig. 2
). However, when pitocin was injected before the distraction, milk
intake (average, 153 g) was similar to that of the control days.
The authors concluded that the distractions had interfered with the
milk ejection reflex, because milk transfer was restored when pitocin
was administered.

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Figure 2. Effects of distraction on milk volume transferred during the morning
feed in a single mother-infant pair. For the three distractions
(ice water, math and electric shock, toe pull), feeds were preceded by
injecting the mother with either saline (S) or oxytocin (O); no
injection preceded the control feeds. Source: Newton and Newton
(5
).
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The second study (6
) involved mothers of preterm infants
(average gestational age, 31 wk) in the neonatal intensive care unit
who were regularly expressing their milk using an electric breast pump.
Such mothers are typically under a great deal of stress because of the
anxiety and fatigue associated with such situations. The investigators
randomly assigned 55 women at 35 d postpartum to a control or an
intervention group. The intervention group received a 20-min audiotape
that included a progressive relaxation exercise followed by a guided
imagery section. They were encouraged to listen to the tape daily,
especially before milk expression. After 1 wk, the volume of milk
expressed during a pumping session in the hospital was compared between
groups. The average volume was significantly greater in the
intervention group than in the control group (99 ± 60 mL vs. 55
± 48 mL, respectively; P = 0.05). Because milk
volume was measured at only a single pumping session, it is not known
whether a significant difference would have been seen over a 24-h
period. Nonetheless, the results are consistent with the hypothesis
that reduced stress enhances milk production.
The third study was a randomized trial with 22 exclusively
breastfeeding women studied during a single feed at 5 d postpartum
(7
). The women were assigned to one of three groups:
control, mental stress (verbal math problems), or noise stress (the
sound of building construction, at a mean of 70 dB). Blood samples were
collected every 2 min before and after nursing, and milk intake was
measured by weighing the infants before and after the feed. Milk yield
(average, 36 g) and change in plasma prolactin concentration did
not differ significantly among groups. However, the frequency of
oxytocin pulses during the 20-min feed was significantly lower in the
mothers exposed to stress, by 43% in the mental stress group and 52%
in the noise stress group. These results provide additional support for
the conclusion reached by Newton and Newton 46 y earlier: that the
milk ejection reflex is impaired by maternal stress.
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Effects of stress during labor and delivery on lactogenesis
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Data reported in recent years indicate that events during labor
and delivery can have a marked impact on lactogenesis. Chen et al.
(8
) conducted a prospective study of 40 women in which the
lead author observed the labor and delivery of all subjects and took
blood samples during pregnancy, parturition (cord and maternal blood)
and lactation for analysis of stress hormones. Each day during the
first 2 wk postpartum, the mothers collected a milk sample and recorded
breastfeeding frequency. On d 5 and 14 postpartum, 24-h milk volume was
measured by test weighing. Four markers of lactogenesis were examined:
the time postpartum when the subject first felt increased fullness in
the breasts, milk volume on d 5, milk lactose concentration on d 5, and
the day postpartum when casein first appeared in milk (a marker of the
biochemical maturation of the milk). Three of the four markers of
lactogenesis were highly correlated with each other (breast fullness,
milk volume and milk casein appearance), whereas milk lactose
concentration on d 5 was not significantly correlated with any of the
other markers. Multiple regression analysis (excluding women with
Cesarean deliveries) indicated that several markers of both fetal and
maternal stress during labor and delivery (cord glucose concentration,
duration of labor and maternal exhaustion score) were associated with
delayed breast fullness, lower milk volume on d 5 and/or delayed casein
appearance.
Subsequently, Chapman and Perez-Escamilla (9
)
conducted a prospective study of 192 women in which maternal perception
of the onset of lactation was the primary outcome variable. In this
sample, 24% of the mothers chose not to breastfeed. Risk factors for
delayed onset of breast fullness (>72 h postpartum) included exclusive
formula feeding on d 2, birth weight < 8 lb, unscheduled Cesarean
section, prolonged stage II labor (among those with vaginal
deliveries), maternal heavy or obese body build and white/Hispanic
ethnicity (compared with African-American).
Most recently, our team has investigated the incidence of delayed
lactogenesis and insufficient milk intake by the infant in a
community-based sample of 280 mother-infant pairs in Davis, CA
(1
). Mothers were recruited shortly after delivery in five
area hospitals and given lactation guidance by trained professionals in
the hospital and in the home on d 3, 7 and 14 and additionally as
needed. All infants were healthy, single and born at term (>37 wk) and
all mothers planned to breastfeed exclusively for at least 1 mo.
Motivation and social support for breastfeeding in this university
community are very high. For the data reported here, the major outcome
variables were infant suckling ability on d 1 and 3 (assessed using the
Infant Breastfeeding Assessment Tool (10
), infant weight
change by d 3 and the timing of onset of milk production (defined by
when the mother first reported that her breasts were noticeably fuller:
3 on a scale of 5). Delayed onset of milk production (>72 h
postpartum) occurred in 24% of the women, and 12% of infants were
considered to have excessive weight loss (
10% of birth weight) by d
3. The percentage of infants identified as having poor suckling ability
(
10 of 12 points on the Infant Breastfeeding Assessment Tool) was
49% on d 1 and 22% on d 3. Several variables reflecting stress were
examined as potential predictors of these outcomes, including mode of
delivery, duration of labor, pain during labor, exhaustion after
delivery, time without sleep before delivery, infant Apgar scores at 1
and 5 min, infant given oxygen, meconium staining of the amniotic fluid
and maternal pain, fatigue and stress on d 3 postpartum. Of these
variables, duration of labor (both total and stage II), time without
sleep and maternal pain and stress on d 3 were significantly associated
with a longer interval before onset of breast fullness, and duration of
labor and maternal stress on d 3 were also associated with greater
infant weight loss by d 3. However, maternal stress on d 3 could be the
result of delayed lactogenesis, rather than the cause, so it is
difficult to interpret the associations with that variable. In
multivariate models, both mode of delivery (particularly an urgent
Cesarean section) and duration of labor were linked to delayed onset of
breast fullness.
The degree of consistency in the results of these three studies is
remarkable, with two major risk factors standing out for delayed
lactogenesis: long duration of labor (in vaginal deliveries) and urgent
Cesarean section. Both of these are strongly related to the amount of
stress experienced by both the mother and the infant during
parturition.
Several conclusions can be drawn from the studies described above.
First, acute physical and mental stress can impair the milk ejection
reflex by affecting release of oxytocin during a feed. If this occurs
repeatedly, it could reduce milk production by preventing full emptying
of the breast at each feed. Second, both maternal and fetal stress
during labor and delivery are associated with impaired lactogenesis.
Third, emotional stress postpartum may impair lactogenesis but reverse
causation cannot be ruled out. Mothers who experience high levels of
stress should receive additional lactation guidance during the first
week or two postpartum. With such guidance, nearly all such
mother-infant pairs (e.g., those who experience long labor or have
an urgent Cesarean section) can be successful at establishing exclusive
breastfeeding.
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FOOTNOTES
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1 Presented as part of the symposium "Human
Lactogenesis II: Mechanisms, Determinants and Consequences" given at
the Experimental Biology 2001 meeting, Orlando, FL on April 2, 2001.
This symposium was sponsored by the American Society for Nutritional
Sciences and was supported by educational grants from Medela, Ross Labs
and Wyeth Nutrition International. Guest editors for this symposium
publication were Nancy F. Butte, Baylor College of Medicine, Houston,
TX and Rafael Perez-Escamilla, University of Connecticut, Storrs,
CT. 
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LITERATURE CITED
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1. Dewey, K. G., Nommsen-Rivers, L. A., Heinig, M. J. & Cohen, R. J. (2001) Lactogenesis and infant weight change in the first weeks of life. Davis, M. K. Wright, A. L. Isaacs, C. E. Hanson, L. eds. Integrating Population Outcomes, Biological Mechanisms, and Research Methods in the Study of Human Milk and Lactation 2001 Kluwer Academic/Plenum Publishers New York, NY. (in press). .
2. Neville, M. & Morton, J. (2001) Lactogenesis: the transition from pregnancy to lactation. Pediatr. Clin. North Am. 48:35-52.[Medline]
3. Chapman, D.J. & Perez-Escamilla, R. (2000) Lactogenesis stage II: hormonal regulation, determinants and public health consequences. Recent Res. Dev. Nutr. 3:43-63.
4. Lau, C. (2001) Effects of stress on lactation. Pediatr. Clin. North Am. 48:221-234.[Medline]
5. Newton, M. & Newton, N. R. (1948) The let-down reflex in human lactation. J. Pediatr. 33:698-704.[Medline]
6. Feher, S.D.K., Berger, L. R., Johnson, J. D. & Wilde, J. B. (1989) Increasing breast milk production for premature infants with a relaxation/imagery audiotape. Pediatrics 83:57-60.[Abstract/Free Full Text]
7. Ueda, T., Yokoyama, Y., Irahara, M. & Aono, T. (1994) Influence of psychological stress on suckling-induced pulsatile oxytocin release. Obstet. Gynecol. 84:259-262.[Abstract/Free Full Text]
8. Chen, D. C., Nommsen-Rivers, L., Dewey, K. G. & Lonnerdal, B. (1998) Stress during labor and delivery and early lactation performance. Am. J. Clin. Nutr. 68:335-344.[Abstract]
9. Chapman, D. J. & Perez-Escamilla, R. (1999) Identification of risk factors for delayed onset of lactation. J. Am. Diet. Assoc. 99:450-454.[Medline]
10. Matthews, M. K. (1988) Developing an instrument to assess infant breastfeeding behavior in the early neonatal period. Midwifery 4:154-165.[Medline]
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