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The Psychoneuroimmunology of Stress in Pregnancy

Mary E. Coussons-Read
Current Directions in Psychological Science 2012 21: 323
DOI: 10.1177/0963721412453720
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The Psychoneuroimmunology of Stress

in Pregnancy

Current Directions in Psychological

Science
21(5) 323328
The Author(s) 2012
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0963721412453720
http://cdps.sagepub.com

Mary E. Coussons-Read

Department of Psychology, University of Colorado Denver

Abstract
The rate of preterm birth in the United States remains high. In up to 40% of cases of preterm birth, the mothers are
healthy women who have no clear risk factors. Accordingly, research has begun to explore the effect of prenatal stress
on the risk of preterm birth and shortened gestational age at birth. There is increasing evidence that psychosocial stress
throughout gestation increases the risk of preterm birth through changes in maternal endocrine, immune, and inflammatory
activity during pregnancy. In this article, I describe foundational and current research examining the effects and biological
mechanisms of prenatal stress in preterm birth and shortened gestational age at birth. I emphasize psychoneuroimmunologyfocused studies showing that prenatal stress alters inflammatory and endocrine markers during gestation and that these
changes are associated with preterm birth and shortened gestational age at birth.
Keywords
pregnancy, psychosocial stress, inflammatory markers, preterm birth, cytokine balance
Mounting evidence has shown that prenatal stress can have a
profound effect on pregnancy and infants outcomes. Among
the primary findings of research in this area is that stress during gestation is a potentially important factor in preterm birth
(i.e., birth prior to 37 weeks gestation) and other adverse
pregnancy outcomes (Copper et al., 2001; Dole et al., 2003).
Despite improvements in prenatal care, the rate of preterm
birth in the United States remains quite high (11% to 13% of
all births; Centers for Disease Control and Prevention, 2012).
In many cases, the causes of preterm birth are unclear; nearly
40% of preterm deliveries occur in the absence of clear risk
factors (Goldenberg, Culhane, Iams, & Romero, 2008). Studies have shown that prenatal stress is associated with shortened gestational age at birth and an increased risk of preterm
birth1 (Copper et al., 2001; Lobel et al., 2008; Ruiz, Fullerton,
& Dudley, 2003), and attention has begun to turn to the
physiological processes through which these effects occur
(Coussons-Read, 2012; Dunkel Schetter, 2011).
In this review, I focus on psychoneuroimmunologyoriented studies of the biological mechanisms underlying the
adverse effects of prenatal stress on pregnancy outcomes.
Studies from my laboratory and others have shown that exposure to psychosocial stressors may predispose women to
preterm birth and shortened gestational age at birth by disrupting the endocrine, immune, inflammatory, and nervous
system adaptations that normally support healthy pregnancy
(Coussons-Read et al., 2012; Coussons-Read, Okun, &
Nettles, 2007; Coussons-Read, Okun, Schmitt, & Giese, 2005;
DAnna-Hernandez et al., 2012). Although these studies have

clearly pointed to stress-related changes in neural-immune

activity as factors increasing the risk of adverse pregnancy
outcomes, many questions have to be answered before these
relationships are clear and interventional strategies for identifying and alleviating the effects of prenatal stress can become
a routine part of clinical care.

The Psychoneuroimmunology of Stress

and Health
Psychoneuroimmunology studies of how stress affects immunity and health in nonpregnant adults have provided the foundation for research addressing the biological underpinnings of
the effects of prenatal stress in pregnancy. These studies have
shown that psychosocial stressorssuch as changes in ones
social status, personal life, relationships, job status, housing,
and family makeupare connected to alterations in immune
function, elevations in systemic inflammatory activity, and
increased long-term risk for health problems.
These effects occur, at least in part, through the activation
of the bodys biological fight or flight response systems
(Malarkey & Mills, 2007). Exposure to stress activates the
endocrine systems hypothalamic-pituitary-adrenal (HPA) axis

Corresponding Author:
Mary E. Coussons-Read, University of Colorado Denver, 1380 Lawrence St.,
Suite 300, Campus Box 120, Denver, CO 80217-3364
E-mail: mary.coussons-read@ucdenver.edu

324
and the sympathetic nervous system, increasing the production
of stress hormones, such as cortisol and corticotropin-releasing
hormone, as well as catecholamine neurotransmitters to help
deal with the potential threat posed by the stressor. Chronic
activation of this suite of biological systems by prolonged stress
is associated with adverse health effects, such as increased
inflammatory activity, reduced resistance to disease, cardiovascular disease, some cancers, dementia, and increased severity
of viral illnesses (Coe, 2010). These relationships are now
being examined in the context of pregnancy, a time when
not only the health of the mother is potentially at risk, but
the health of her developing infant is as well (de Weerth &
Buitelaar, 2005).

Stress Contributes to Adverse

Pregnancy Outcomes
Many types of stress can contribute to increased risk of preterm birth and shortened gestational age at birth (CoussonsRead, 2012; Dunkel Schetter, 2011). Whereas some studies
have shown that psychosocial stress as described above is
associated with an increased risk of preterm birth, others have
examined how pregnancy outcomes are affected by stressors
that are specifically tied to the experience of being pregnant.
For example, pregnancy-specific distress and anxiety, which
are related to maternal concerns about aspects of the pregnancy itself (e.g., worries about prenatal testing, ones ability
to be a good mother, or life changes after pregnancy) increase
the risk for preterm birth and shortened gestational age at birth
(Dunkel Schetter, 2011; Kramer et al., 2009; Lobel et al.,
2008). Acute and intense stressors, such as the death of a loved
one or a terrorist attack, also increase the incidence of adverse
outcomes, including miscarriage, especially when they are
experienced early in pregnancy (Bruckner, Catalano, & Ahern,
2010; Livingston, Otado, & Warren, 2003). The effects of
prenatal stress are more pronounced in minority women, who
may also experience race- or culture-based stressors during
pregnancy (Dominguez, Dunkel-Schetter, Glynn, Hobel, &
Sandman, 2008; Luecken, Purdom, & Howe, 2009); this finding is especially important given that preterm birth is disproportionately common among African American women
(Giscombe & Lobel, 2005).
Studies of nonpregnant populations have shown that individual differences in lifetime experiences of stress and trauma
and responsiveness to stress can play an important role in how
stress affects health outcomes. For example, firefighters with
stronger coping skills have fewer health challenges associated
with chronic job-related stress (Steffen, Ortiz, Tidler, & Smith,
2012), and children with higher levels of resilience fare better
in the face of a cancer diagnosis (Noeker, 2012). Recent work
has begun to address how these factors may contribute to the
effects of stress on pregnancy (Cowchock et al., 2011; Dunkel
Schetter, 2011). Studies have shown, for example, that trauma
and depression before and during pregnancy contribute to
adverse pregnancy outcomes, may predispose women to the

Coussons-Read
negative biological effects of prenatal stress, and are heightened in minority women who experience race-based stress
(Blackmore et al., 2011; Cassidy-Bushrow, Peters, Johnson, &
Templin, 2012; Christian, Franco, Glaser, & Iams, 2009). As
researchers continue to unravel how different sources of stress,
maternal race and culture, and individual differences interact
to affect pregnancy, other investigators are examining the biological mechanisms through which these factors may translate
into an increased risk of adverse pregnancy outcomes.

Biological Adaptations Support

Healthy Pregnancy
A driving hypothesis behind studies in our laboratory and studies by others working in this area is that prenatal stress increases
the risk of preterm birth and shortened gestational age at birth
by disrupting adaptations in the maternal immune, endocrine,
and nervous systems that support healthy pregnancy (CoussonsRead, 2012; Denney et al., 2011; Wadhwa, Entringer, Buss, &
Lu, 2011). As shown in Figure 1, studies have suggested
that aspects of endocrine, nervous, and immune system activity
are adjusted throughout gestation to support healthy pregnancy
and that these systems can co-regulate one another (Arck,
Knackstedt, & Blois, 2006; Wadhwa et al., 2011).
A key aspect of these adjustments is that the maternal
immune system shifts to favor an anti-inflammatory profile in
pregnancy. Inflammation is one of the first components of the
immune systems response to an infection, and it is focused on
defending the body against a foreign invader, such as a virus or
bacterium. It is thought that during pregnancy, the immune
system shifts away from this tendency because the presence of
paternal immune markers in the fetus could be detected as an
immunologic challenge, such that without this shift, the mothers immune system might reject the embryo (Thornton, 2010).
Evidence of this shift is seen in reduced levels of circulating
inflammatory cytokines, such as interleukin-6 and tumor necrosis factor- (TNF-), relative to levels of anti-inflammatory
cytokines, such as interleukin-10, during normal pregnancy
(Curry et al., 2008) and in a tendency toward expression of antiinflammatory relative to inflammatory cytokines in cultured
immune cells from healthy pregnant women (Denney et al.,
2011). Cytokines are protein substances produced by the
immune system and other cells in the body that regulate the
inflammatory response as well as many other functions. Interestingly, the inflammatory cytokines interleukin-1, interleukin-6,
and TNF- are not only part of the immune systems response to
infection but are also part of the normal process of childbirth.
Levels of inflammatory cytokines increase as the end of pregnancy nears, and these inflammatory cytokines play a role in the
process of cervical ripening and the initiation of normal labor
and delivery (Thornton, 2010).
Adaptations in the immune system during pregnancy are
supported by concurrent reductions in the stress reactivity of
the endocrine and nervous systems. Studies have shown that
during pregnancy, maternal stress and inflammatory responses,

325

The Psychoneuroimmunology of Stress in Pregnancy

Prenatal Stress

Nervous System Activity

Catecholamines
Neurotransmitters
Neuropeptides

Healthy Pregnancy

Endocrine System
Activity
CRH
Cortisol
Hormones

Immune System
Activity
Cytokines
Inflammatory
Mediators

Fig. 1. Stress affects the activity of biological systems that adapt during gestation to support healthy
pregnancy. CRH = corticotropin-releasing hormone.

although down-regulated, are intact; both stress and infection

can strongly activate the stress response and increase the
production of corticotropin-releasing hormone and inflammatory cytokines during gestation (Parker & Douglas, 2010;
Thornton, 2010). Elevations in corticotropin-releasing hormone and inflammatory cytokines are commonly observed in
women who experience preterm birth (Romero et al., 2006).
My research group and others have hypothesized that prenatal
stress stimulates activity of the maternal endocrine and
immune systems, which, in turn, increases the likelihood of
preterm birth or shortened gestational age at birth (CoussonsRead, 2012; Curry et al., 2008; Pearce et al., 2010; Romero
et al., 2006).

Stress-Related Neural-Immune Activity

Affects Pregnancy
An increasing body of work has supported this hypothesis.
Separate studies have shown (a) that elevations in stressrelated markers of HPA-axis activity and inflammation are

associated with preterm birth; (b) that prenatal stress elevates

levels of these markers in pregnant women; and, as previously
discussed in this article, (c) that prenatal stress is associated
with an increased risk of preterm birth and shortened gestational age at birth.
Specifically, elevated levels of corticotropin-releasing
hormone and inflammatory cytokines are predictive of preterm birth (Romero et al., 2006; Wadhwa et al., 2011). Work
from our laboratory has shown that psychosocial stress is
associated with elevated serum levels of inflammatory cytokines (interleukin-6 and TNF-) and reduced levels of antiinflammatory cytokines (interleukin-10) both early and late in
pregnancy (Coussons-Read et al., 2007; Coussons-Read et al.,
2005), and that stimulated immune cells from women reporting moderate or high levels of stress late in pregnancy produce
more inflammatory cytokines (interleukin-6 and interleukin-1)
than do cells from women reporting low levels of stress,
although these data did not address pregnancy outcomes
(Coussons-Read et al., 2007). Finally, as reviewed above,
there is clear evidence that prenatal stress is associated with

326

Coussons-Read

preterm birth (Dunkel Schetter, 2011; Glynn, Dunkel Schetter,

Hobel, & Sandman, 2008). Although findings from these studies support aspects of our hypothesis regarding the effects of
stress on adverse pregnancy outcomes, it has been difficult to
demonstrate complete pathways from prenatal stress through
inflammatory or endocrine mediators to preterm birth and/or
shortened gestational age at birth.
Recent work from our laboratory has, however, provided
initial confirmation of a pathway from prenatal stress to
shortened gestational age at birth via elevated inflammatory
cytokines (Coussons-Read et al., 2012). We examined the
relationships between levels of prenatal stress and inflammatory cytokines early and late in pregnancy and gestational age
at birth in a diverse sample of primarily Caucasian and Latina
women. The effects of early prenatal stress in reducing gestational age at birth are mediated by elevations in serum levels
of TNF- (Fig. 2); similarly, the effects of pregnancy-specific
distress on gestational age at birth are mediated by levels of
interleukin-6 across pregnancy. These are critical findings, as
they demonstrated that prenatal stress can increase the risk of
preterm birth by increasing inflammatory activity during pregnancy, providing the first firm confirmation of this hypothesized pathway.
Work from other laboratories has demonstrated pathways
among stress, HPA-axis activation, and preterm birth. For example, stress- and anxiety-related elevations in corticotropinreleasing hormone and cortisol early in pregnancy have been
shown to be predictive of preterm birth (Dunkel Schetter &
Glynn, 2011; Glynn et al., 2008). In our most recent work, I
and my research group have looked at the combined role of
HPA-axis and inflammatory activity in the effects of stress on
preterm birth in the context of maternal acculturation (i.e., the
degree to which Latina subjects in our sample were connected

to American culture). Although acculturation did not affect

observed relationships among stress, cytokines, and gestational age at birth, high acculturation itself predicted shortened
gestational age at birth, and stress-related increases in cortisol
were related to high acculturation and low infant birth weight
(DAnna-Hernandez et al., 2012). These findings underscore
the need for an examination of the role of factors such as ethnicity and race in the biological pathways that connect stress
to adverse pregnancy outcomes.

Future Directions
Increasingly, epigenetic studies have shown that stressful prenatal events experienced by mothers, such as abuse by ones
intimate partner, poverty, and food insecurity, have enduring
effects on their infants physiology, and that prenatal and
early-childhood stress can set the stage for lasting psychological and health challenges (Bloomfield, 2011; Miller, Chen,
& Parker, 2011). Hence, a key goal of future research is
determining the degree to which stress-related alterations in
prenatal maternal and fetal nervous, endocrine, and inflammatory activity are predictive of poor birth and developmental
outcomes. To date, few studies have conducted the concurrent,
longitudinal assessment of the biological, psychological, obstetric, and neonatal/pediatric variables that would be necessary
to firmly establish the predictive value of these measures in
clinical settings. Critical collaborations are developing to
examine how these relationships affect not only pregnancy
outcomes but also the course of behavioral and immunologic
development in infants and children. Although difficult to execute, such investigations are necessary, given that another goal
of research in this area is to develop screening tools and, eventually, interventions that clinicians can use to identify and

Early TNF-
Early Stress

60

50

40

30

20

10

0
Term

Early Stress

Early TNF- (pg/ml)

Pre Term

Gestational Age at Birth

Fig. 2. Prenatal stress early in pregnancy increases the risk for preterm birth via elevations in
tumor necrosis factor- (TNF-). The data in this graph are derived from Coussons-Read et al.
(2012). Early-stress values reflect mothers scores on a measure of overall stress (an adapted
version of the Denver Maternal Health Assessment); higher scores indicate greater stress.

The Psychoneuroimmunology of Stress in Pregnancy

support women who are at risk for stress-related preterm birth
and other adverse outcomes. An additional research priority is
developing interventions to reduce maternal stress, alleviate
the maladaptive biological changes that may be associated
with it, and, ultimately, improve birth outcomes. Progression
from the current state of knowledge to the development of reliable interventions will take time, but psychological science
and psychoneuroimmunological research are already providing a strong foundation for achieving this goal.
Recommended Reading
Christian, L. M. (2011). Psychoneuroimmunology in pregnancy:
Immune pathways linking stress with maternal health, adverse
pregnancy outcome, and fetal development. Neuroscience &
Biobehavioral Reviews, 36, 350361. A review of the psychoneuroimmunology of stress, maternal health, and fetal development:
Coussons-Read, M. (2012). (See References). A chapter providing a
review of the effects and mechanisms of prenatal stress in pregnancy and infant development.
Dunkel Schetter, C. (2011). (See References). An accessible review
of research examining psychosocial stress in pregnancy.
Giscombe, C. W., & Lobel, M. (2005). (See References). An examination of the role of racism and stress in adverse pregnancy outcomes.

Declaration of Conflicting Interests

The author declared that she had no conflicts of interest with respect
to her authorship or the publication of this article.

Note
1. Preterm birth is defined as birth prior to 37 weeks of gestation,
whereas shortened gestational age is anything less than 40 weeks of
gestation. Thus, shortened gestational age may or may not involve
preterm birth. Studies have shown that even shortened gestational
age can have negative consequences for babies.

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