THE RELATIONSHIP BETWEEN SYMPATHETIC NERVOUS SYSTEM ATTUNEMENT
AND INTIMATE PARTNER VIOLENCE IN MOTHER-INFANT DYADS
By
Nicola K. Bernard

A THESIS
Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of
Psychology – Master of Arts
2015

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ABSTRACT
THE RELATIONSHIP BETWEEN SYMPATHETIC NERVOUS SYSTEM ATTUNEMENT
AND INTIMATE PARTNER VIOLENCE IN MOTHER-INFANT DYADS
By
Nicola K. Bernard
When mothers and infants interact socially, they also interact on a physiological level,
which can lead them to have attuned physiological reactions. However, studies have shown that
chronic stressors may negatively affect attunement. One such stressor is intimate partner
violence (IPV). In physiological attunement, the negative effect of a stressor like IPV may be
seen in the dysregulated or exaggerated sympathetic nervous system (SNS) responses of mothers
and their infants, which may make it more difficult for them to attune to one another. This study
hypothesized that IPV would negatively affect SNS attunement such that dyads who experienced
IPV both pre- and postnatally (chronic IPV) would be less attuned than dyads who did not. In
addition, it was hypothesized that maternal warmth would have a positive relationship with
attunement in dyads who experienced chronic IPV. IPV, maternal warmth and SNS reactivity
(via salivary alpha amylase: sAA) were assessed during a laboratory stress task in 182 motherinfant dyads. IPV was assessed for both the pre- and postnatal periods. The attunement literature
operationalizes and analyses attunement in several ways. Therefore, three multilevel modeling
(MLM) analyses that correspond to three common conceptualizations of attunement were run to
test each hypothesis. Overall, the results did not support the hypotheses, suggesting that IPV
does not influence mother-infant SNS attunement. The results also suggest that the way in which
attunement is conceptualized and analyzed may differentially affect results, which may help to
explain the variation in outcomes in the mother-infant physiological attunement literature.

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ACKNOWLEDGMENTS

I would like to thank my advisor, Dr. Alytia Levendosky for her guidance, support, and wisdom
over the past year. Thank you to my committee members Drs. G. Anne Bogat, Joseph Lonstein,
and Deborah Kashy for their support and help with the analyses and interpretations of this study.
Lastly, thank you to my parents for their love and support.

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TABLE OF CONTENTS

LIST OF TABLES ...........................................................................................................................v
LIST OF FIGURES ....................................................................................................................... vi
INTRODUCTION ...........................................................................................................................1
Attunement ...........................................................................................................................3
Maternal Warmth .................................................................................................................6
Sympathetic Nervous System ..............................................................................................7
Salivary Alpha Amylase ......................................................................................................9
Stress Effects on the SNS ..................................................................................................12
Hypothesis 1.......................................................................................................................16
Hypothesis 2.......................................................................................................................18
METHODS ....................................................................................................................................20
Participants .........................................................................................................................20
Procedures ..........................................................................................................................20
Measures ............................................................................................................................21
Proposed Analyses .............................................................................................................23
Exploratory Post-Hoc Analyses .........................................................................................24
RESULTS ......................................................................................................................................25
Missing Data ......................................................................................................................25
Hypothesis 1.......................................................................................................................25
Correlated Growth Analysis ..................................................................................26
Cross-Lagged Analysis ..........................................................................................27
MLM – Mom Predicts Baby Analysis ...................................................................29
Brief Summary of Results ......................................................................................29
Hypothesis 2.......................................................................................................................31
Correlated Growth Analysis ..................................................................................31
Cross-Lagged Analysis ..........................................................................................32
MLM – Mom Predicts Baby Analysis ...................................................................32
Brief Summary of Results ......................................................................................32
DISCUSSION ................................................................................................................................34
APPENDICES ...............................................................................................................................41
APPENDIX A TABLES ....................................................................................................42
APPENDIX B FIGURES ..................................................................................................51
REFERENCES ..............................................................................................................................53

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LIST OF TABLES

Table 1. sAA Means and Standard Deviations for Mothers and Infants ......................................43
Table 2. Fixed Effects of the Correlated Growth Model ..............................................................44
Table 3. Random Effects of the Correlated Growth Model ..........................................................45
Table 4. Fixed Effects of the Cross-Lagged Analysis ..................................................................46
Table 5. Fixed and Random Effects for Maternal sAA Predicting Infant sAA ............................47
Table 6. Fixed Effects of the Correlated Growth Model ..............................................................48
Table 7. Fixed Effects for the Cross-Lagged Analysis .................................................................49
Table 8. Fixed Effects for Maternal sAA, Maternal Warmth, and IPV as Predictors ..................50

v

LIST OF FIGURES

Figure 1. Cross-lagged Model .......................................................................................................52

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INTRODUCTION
When mothers and infants interact with one another, their actions, facial expressions, and
vocalizations are often complementary. This continuous and reciprocal exchange of
physiological, behavioral and affective signals brings mother and infant into attunement, which
serves to promote infant well-being and social-emotional growth (Bornstein, 2007). This
attunement helps a mother respond appropriately to her child’s needs and aids in the
development of infant self-regulation (Feldman, 2007; Middlemiss, Granger, Goldberg, &
Nathans, 2012). Attunement between mother and infant begins at a critical time in infant
development in which physiological/biological systems, affect, and the environment are
integrated to form the basis of lasting patterns in the infant’s personality, emotional expression,
self-regulation, and stress responsivity (Bornstein, 2014; Fogel, 1993). Although physiological
responses are important to the infant’s developing experiential framework, physiological
attunement in human infants has not yet been well-studied (Van Bakel & Riksen-Walraven,
2008). One type of physiological attunement is attunement of the sympathetic nervous system
(SNS), which is one of the body’s stress response systems (Laurent, Ablow, & Measelle, 2012).
In SNS attunement, mother and infant may show similar response patterns in indicators
of SNS activation (e.g., increases in heart rate, skin conductance, norepinephrine or adrenaline).
SNS attunement can also be measured using sAA, a salivary analyte that is indicative of SNS
activation (Chatterton, Vogelson, Lu, Ellman, & Hudgens, 1996). When an infant feels
distressed, this can activate the infant’s SNS and increase the concentration of sAA in the
infant’s saliva (Granger et al., 2006). An attuned and emotionally well-regulated mother would
theoretically also experience distress, SNS innervation, and sAA increases, but to a lesser extent
than the baby. This would allow the mother to be empathic to her baby’s distress but also help
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her to calm the infant by modeling self-regulation. If the infant is able to attune to the mother, the
infant’s stress response and sAA will decrease as the baby mirrors the decreasing distress of the
mother (Pally, 2010). Attunement may be a concurrent process, in which mother and infant
experience physiological changes at about the same time and in the same direction; a reciprocal
and lagged process, in which mothers’ and infants’ physiological arousal influences the others’
subsequent physiological response; or it may be led by the mother, such that a mother’s
physiological response is predictive of her infant’s response and the process is not reciprocal.
Regardless of how attunement is conceptualized, mother-infant attunement likely plays a role in
the development of adaptive infant emotional self-regulation.
Physiological attunement may be negatively influenced by stressors that elicit strong,
maladaptive physiological responses and/or lead to emotional dysregulation in the mother, in the
infant, or in both. One such stressor is intimate partner violence (IPV: defined here as sexual,
physical, or psychological violence perpetrated by a male towards a female partner). With a
lifetime prevalence rate of around 25% (Tjaden & Thoennes, 2000), IPV is a common stressor
that many women face. Four to eight percent of women report experiencing IPV during
pregnancy (Gazmararian et al., 2000), and this percentage may be even higher among ethnic
minority and low income women (Charles & Perreira, 2007). IPV is also more common in young
adults and typically decreases with age (O’Leary, 1999). Young adults often have young
children, and each year millions of children are exposed to IPV (McDonald, Jouriles, RamisettyMikler, Caetano, Green, & 2006). IPV may affect SNS attunement prenatally or postnatally by
differentially influencing the maternal and/or infant SNS response (Diego et al., 2004) or by
affecting the mother’s parenting and mental health (Kessler, Molnar, Feurer, & Applebaum,
2001; Leung & Slep, 2006; Levendosky, Leahy, Bogat, Davidson, & von Eye, 2006). However,

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the negative effect of IPV on mother-infant attunement and infant outcomes may be moderated
by maternal warmth. Indeed, Skopp and colleagues (2007) found that when mothers were warm
(i.e. responding sensitively to their infants and being encouraging), children developed fewer
problematic behaviors despite being exposed to IPV.
No published studies have explored whether IPV could negatively impact a child’s
development by influencing mother-infant SNS attunement using sAA. This kind of research
may be important to better understand whether attunement is one of the mechanisms through
which IPV influences the mother-infant relationship. Moreover, studying physiological
attunement and maternal warmth may help to create new testable hypotheses as to why some
mothers and infants who are exposed to IPV have better outcomes than others. The aim of the
current study is to examine the effects of IPV on mother-infant SNS attunement in response to a
laboratory stressor. This study had four a priori IPV groups – a control group with no IPV, a
prenatal IPV only group, a postnatal IPV only group, and a pre and postnatal IPV group.
Exploring the effect of IPV on mother-infant sAA attunement by IPV grouping would allow for
the examination of which time period (i.e. pre- or post-natal) might have the greatest effect on
mother-infant SNS attunement.
Attunement
From birth onwards, infants depend on a primary attachment figure, most often the
mother, to attune to their needs and respond appropriately (Bowlby, 1969; Leerkes, Blankson, &
O’Brien, 2009). Bornstein (2007) defined attunement as a dyadic process in which one or both
parties are sensitive to the needs and emotions of the other person and respond by mirroring, coregulating, harmonizing, and synchronizing. Attunement can be behavioral, in which the mother
and child mirror one another’s behaviors; affective, in which the mother and infant express

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similar emotions; or biological/physiological, in which the mother and infant have similar
physiological response patterns (Feldman, 2007). Attunement can be intentional or unintentional
and can occur during both stressful and nonstressful situations. Attunement may be concurrent,
reciprocal and delayed, or mother-led and non-reciprocal (Laurent et al., 2012; Sethre-Hofstad,
Stansbury, & Rice, 2002; Stenius et al., 2008). This attunement of behavior, affect, and
physiology between mother and infant occurs at a time in which patterns of personality, intellect,
social functioning, and stress reactivity begin to develop that are evident across the infant’s life
(Bornstein, 2014; Meaney, 2001). These early social and environmental conditions may also
modify gene expression and influence physiological regulatory mechanisms. Therefore, it is not
surprising that mother-infant attunement affects infant self-regulatory behaviors, attachment,
cognition, and social-emotional development (Feldman, 2007; Middlemiss et al., 2012). A lack
of attunement over an extended time period with an attachment figure can lead to a disruption in
infant development as evidenced by physiological dysregulation, depression, and reduced
responsiveness (Field, 1985). Thus, attunement is a vital component of normative infant
development and the mother-infant relationship, and it has been found to be predictive of infant
outcomes, such as attachment security (Isabella & Belsky, 1991).
Initially, the mother must adapt to her infant’s affective state to achieve attunement; by
the age of 9 months, however, infants also adapt to their mothers’ affect to achieve attunement
(Feldman, Greenbaum, & Yirmiya, 1999). Thus, attunement becomes a dyadic process and may
indicate shared emotional and physiological states. Conversely, when a mother and her infant are
not attuned, this may indicate, that at that moment, the mother is unable to attend to her child’s
needs and promote the infant’s emotional regulation and/or the infant is unable to match the
mother’s emotional state, leading to discordant or mismatched affective states. Across the
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attunement literature, attunement has been conceptualized in different ways. It can be seen as a
reciprocal and lagged process in which each member of the dyad influences the other member’s
subsequent response, or as a concurrent process in which both members of the dyad respond
similarly and contemporaneously. In addition, some researchers have specified that the mother
leads the attunement process, while other researchers have indicated that either mother or infant
can lead.
Mother-infant attunement may be important in the development of infant self-regulation.
Feldman et al. (1999) found evidence for the relationship between affective attunement and the
transition from mutual mother-infant affective regulation to infant self-regulation. The
researchers speculated that dyadic attunement provided the infants with a “contained” context in
which to feel increased levels of arousal without fear of dysregulation. Pally (2010) noted that in
this contained context, when the baby shows distress, the mother can attune to the baby’s
feelings and reflect back the baby’s emotions in a toned-down way. This simultaneously helps
the baby to feel understood while also providing the baby with a model for down-regulating
emotional distress. Field (1982) found that when mothers were less attentive to their infants’
behavioral signals, the infants who were already at higher risk of hyper-arousal and disturbed
interactions were more likely to avoid eye contact with their mothers and experience higher
arousal. Thus, both the mother and the infant demonstrated an inability to attune to the other and
consequently the babies were more aroused. However, an additional consideration is whether
attunement is always advantageous or adaptive (Laurent et al., 2012). If an infant attunes to his
mother when the mother is insensitive to the infant’s distress or impaired by her own distress, the
infant may become more avoidant of his emotions or become increasingly distressed and
dysregulated without the modeling and boundaries provided by a sensitive mother (Waters,
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West, & Mendes, 2014). In other words, mother and infant may be attuned behaviorally,
affectively and/or physiologically, but this attunement may be based on maladaptive responses.
Thus, attunement does not always reflect an adaptive response because the response may be
inappropriate given the context or the infant’s needs (Laurent et al., 2012).
Maternal Warmth
Maternal warmth may also play an important role in the mother-infant relationship. When
a mother is affectionate and displays positive affect toward her child, she gives the child an
opportunity to learn and practice appropriate affect expression and regulation (Isley, O’Neil,
Clatfelter, & Parke, 1999). In this way, maternal warmth may promote attunement by fostering
an environment in which attunement may be likely to occur. When a mother is warm and
attentive towards her child, her child may be better able to attend and respond to his or her
mother. Maternal warmth may also have developmental implications. Maternal warmth in
infancy is associated with better later relationships with peers (Davidov & Grusec, 2006), a
greater ability to express emotions appropriately (Isley et al., 1999), higher self-esteem (Clark &
Symons, 2000), better emotional self-regulation during a frustration task (Gilliom, Shaw, Beck,
Schonberg, & Lukon, 2002), and higher IQ at age 4 (Pearson et al., 2011).
Maternal warmth has also been studied in the context of IPV and was found to moderate
the relationship between IPV and children’s externalizing behaviors, such that IPV and
externalizing behaviors were positively related at low levels, but not at high levels, of maternal
warmth (Skopp et al., 2007). This suggests that increased maternal warmth may decrease the
negative effects of IPV on child outcomes. If maternal warmth moderates the relationship
between IPV and child outcomes – outcomes which are also related to disruptions in the mother-

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child relationship (Johnson & Lieberman, 2007) – and if IPV negatively impacts mother-infant
attunement (as hypothesized in this study), it stands to reason that maternal warmth may also
moderate the effect of IPV on attunement. Whereas IPV may disrupt attunement, maternal
warmth may foster it, thereby lessening the strength of the hypothesized relationship between
IPV and attunement.
Sympathetic Nervous System
The nervous system is responsible for carrying out voluntary and involuntary actions in
response to internal and external cues. As outlined by Moore et al. (1988), the human nervous
system begins to develop during gestation and is composed of the central (CNS) and the
peripheral nervous system (PNS). The CNS is made up of the brain and spinal cord while the
PNS consists of the remaining nerves outside of the brain and spinal cord. The PNS is further
subdivided into the autonomic and somatic nervous systems. The autonomic nervous system
(ANS) has two main components and controls homeostasis, stress responses and arousal by
influencing heart rate, sweating, respiration, pupil dilation and digestion. The sympathetic
nervous system (SNS), the “activating” portion of the ANS, is one of the main components of the
mammalian biological stress system. The SNS controls the body’s “fight or flight” response by
releasing two catecholamines, epinephrine and norepinephrine. These hormones activate the
body’s stress response by increasing heart rate, increasing blood flow to muscles, and dilating
pupils, which better enable the organism to confront or escape a stressor (Cannon, 1914). The
SNS is complemented by another component of the ANS, the parasympathetic nervous system
(PSNS). The PSNS slows the heart rate, promotes digestion, and increases salivation. It is often
referred to as the “rest and digest” division of the ANS.

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The SNS can be activated by both physical and psychological stress, from exercise
(Chatterton et al., 1996) and submersion in cold water (Speirs, Herring, Cooper, Hardy, & Hind,
1974), to the Trier Social Stress Test (Kirschbaum, Pirke, & Hellhammer, 1993) and exposure to
audio recordings of interadult conflict in children (El-Sheikh & Harger, 2001). The development
of the SNS begins during gestation and continues after birth (Brodal, 2004). During the final
months of pregnancy and into the first year of life, the SNS must adjust quickly to allow the fetus
or infant to adapt to the immediate environment (Porges & Furman, 2011; Young & Morrison,
1998). There is evidence of prenatal programming, which may occur when changes to the fetus
in the prenatal period contribute to postnatal outcomes of the SNS. Maternal hormones released
during an SNS stress response may affect placental blood flow and influence the development of
the fetus and the fetal SNS (Giannakoulopoulos, Teixeira, Fisk, & Glover, 1999). These
developmental influences may still be apparent in the postnatal period. Indeed, studies have
found that women with higher levels of these hormones during pregnancy tend to have infants
who showed elevated postnatal levels (Diego et al., 2004; Field et al., 2004). This prenatal
programming of the SNS will be discussed further as it relates to SNS indicators, intimate
partner violence as a specific stressor, and the mother-infant relationship.
Although this study examines the SNS, there are two primary stress response systems: the
SNS and the hypothalamic-pituitary-adrenal (HPA) axis. Both systems are responsible for
maintaining and reinstating homeostasis (Chrousos, 2009). Research suggests that both systems
are interrelated, although it is unclear whether they interact or have an additive effect on one
another (Granger, Kivlighan, El-Sheikh, Gordis, & Stroud, 2007). However, they are associated
with different stress reaction profiles (Chrousos & Gold, 1992) and may also be sensitive to
different kinds of stress (Allwood, Handwerger, Kivlighan, Granger, & Stroud, 2011). Still, the

8

HPA axis has been more extensively studied in the physiological attunement literature, and as
such, this paper will cite several studies that measured HPA axis activity in the discussion of
physiological attunement.
Salivary Alpha Amylase
Indicators of physiological reactivity can be found in saliva, which has long been seen as
an informative “diagnostic fluid” (see review in Malamud & Rodriguez-Chavez, 2011). Recently
it was found that a known salivary analyte, alpha amylase (sAA), reflects SNS activity
(Chatterton et al., 1996). Multiple studies have found a positive correlation between sAA
increases and other SNS indicators, and a negative correlation between sAA and PSNS indicators
(Bosch, De Geus, Veerman, Hoogstraten, & Nieuw Amerongen, 2003; El-Sheikh, Erath,
Buckhalt, Granger, & Mize, 2008; Granger et al., 2006; Nater et al., 2006), leading Nater and
Rohleder (2009) to conclude that “the pathways that lead to the secretion of sAA are clearly
sympathetic/parasympathetic in nature” (p.492). An increase in SNS activity leads to higher
levels of alpha-amylase production, which can be measured by examining saliva samples
(Granger et al., 2007). sAA levels in saliva peak within 5-10 minutes of SNS activation and
return to baseline within about 20 minutes (Davis & Granger, 2009). Thus, samples can be
collected quickly and easily, which is ideal for use with infants and children. Although
newborns experience SNS innervation and release norepinephrine, SNS activity cannot be
measured using sAA until several months after birth. Newborns do not yet have sAA in their oral
mucosa because it begins to develop shortly after birth. By 6 months of age, however, an
increase in sAA due to stress can already be measured; between 5 and 6 years of age, sAA
activity has reached the maximum level (Davis & Granger, 2009).

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Multiple studies have examined the relationship between norepinephrine and sAA
because both are associated with SNS activation. However, the results have been inconsistent.
Batzri et al. (1971) found that catecholamines (including norepinephrine) were associated with
sAA secretion in rat salivary glands, and Speirs et al. (1974) conducted a similar experiment in
several humans with comparable results. Chatterton and colleagues (1996) concluded that the
concentration of alpha amylase in saliva was predictive of blood plasma levels of norepinephrine
in 47 males who underwent either a physical or a psychological stressor. In contrast, Nater et al.
(2006) examined 30 men and did not find plasma catecholamines to be associated with sAA
concentrations. However, in a 2012 study, Thoma and colleagues examined 66 men and women
and found a significant relationship between norepinephrine and sAA following a Trier Social
Stress Test. Moreover, the relationship was stronger between norepinephrine and sAA than
between norepinephrine and epinephrine. Thus, sAA and norepinephrine were more correlated
than two already well-established indicators of the SNS. In sum, the literature generally supports
sAA as a valid indicator of the SNS and an association between sAA and norepinephrine.
As a biomarker of the SNS stress response, sAA can be used to measure physiological
attunement of the SNS in mothers and their infants. Although mothers and their infants can be
attuned during day-to-day activities, physiological attunement may be particularly important for
the development of infant emotional self-regulation during distressing situations. When infants
are upset and experience an increase in SNS activity, they may need their mothers to attune to
their physiological state. This allows the mother to understand her infant’s distress and model
self-regulatory behavior by helping the infant to downregulate his or her stress response. Several
studies have examined physiological attunement during stressful situations by activating the SNS
with a frustrating or alarming laboratory task. In a study by Laurent et al. (2012), mothers and
10

their infants from a high-risk, low SES sample showed greater sAA synchrony during a cleanup
task and an emotion battery (Lab-TAB) task than during the Strange Situation, showing the
importance of stressor type on the level of physiological SNS attunement. Shea et al. (2006)
used a burst of noise and infant arm restraint to elicit a stress response from mothers and infants.
The researchers found that sAA levels in mothers and infants were positively related. Gordis et
al. (2010) found that mothers and their adolescent children displayed sAA attunement at baseline
and when discussing interparental conflict except when the family had a history of interparental
aggression. Mothers and their children were not attuned during the discussion in families with
interparental aggression. Thus, the degree of physiological attunement depended on two potential
stressors: the type of discussion (neutral/negative) and the amount of conflict present in each
family (absent/present). These results suggest that mother, child, or both were unable to attend to
physiological changes in the other due to the stress caused by the discussion. These studies
suggest that mother-child SNS attunement is greatly affected by the type of stressor and the
quality of the mother-child relationship (especially in high-risk samples).
Past research on stress responses has often relied on measuring increases in salivary
cortisol, an indicator of the HPA axis stress response system. While salivary cortisol has proven
to be a reliable indicator of HPA activation, several studies have found that it does not
adequately encapsulate a person’s stress response to all types of stressors, especially when
looking at attunement. For example, Laurent et al. (2012) found that mother-infant dyads had
greater cortisol attunement after an attachment stressor, but greater sAA attunement after a
challenge task. Moreover, a study by Allwood et al. (2011) found results suggesting that sAA is
more reactive to laboratory stressors (performance or peer rejection tasks) than cortisol. These
studies suggest that the HPA axis and the SNS respond differentially to different types of
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stressors. Researchers have hypothesized that the HPA axis is more reactive to threatening
stressors while the SNS is responsive to a wider range of stressors to enable an immediate
response to a challenge (Frankenhauser, 1982; Nigg, 2006). Thus, the SNS is more likely to
respond to both a stressor like IPV and a stressful lab task. This study will therefore examine the
SNS response because the lab challenge used in this study is more likely to elicit frustration and
activate the SNS than it is to feel threatening and activate the HPA axis of mothers and their
infants.
Stress Effects on the SNS
Psychological factors, such as the physical and emotional stress caused by IPV, have the
potential to influence infant SNS development pre- and postnatally, which could lead to
maladaptive changes in SNS functioning (Young, 2002). Indeed, Field et al. (2004) found that
changes in maternal norepinephrine levels were predictive of changes in fetal and neonate
norepinephrine levels. Diego and colleagues (2004) had a similar finding when they looked at
the effect of pre- and postpartum maternal depression on norepinephrine dysregulation. They
found that depressed women had higher levels of norepinephrine and their infants did as well.
The effect of maternal depression on infant SNS activity was greatest when mothers had both
pre-and postpartum depression. These results suggest that an emotional response (here, maternal
depression) to a stressor that increases norepinephrine release can influence the development of
the fetal norepinephrine response. Because norepinephrine and sAA are both associated with
SNS activity, higher plasma norepinephrine may be indicative of greater SNS sensitivity to stress
and thus may also be related to increased sAA responsivity. Thus, increased maternal
norepinephrine may lead to prenatal programming of the child’s SNS, which may be associated
with greater stress reactivity postpartum (Phillips & Barker, 1997; Phillips & Jones, 2006).
12

Moreover, the results also indicate that the chronicity or the timing of the stressor may be
important. The authors speculate that the effect of increased maternal SNS activity on fetal SNS
development may be indirect. Maternal norepinephrine can restrict uterine blood flow, which in
turn precipitates the activation of the fetal stress response (Giannakoulopoulos et al., 1999).
Thus, the effect of a stress-induced increase in maternal SNS activity during pregnancy may be
critical to the development of the infant’s SNS during and after parturition. It may also lead to
lasting changes in the child’s SNS reactivity. Moreover, these changes in SNS functioning and
norepinephrine levels may be accompanied by changes in sAA concentrations due to the positive
relationship between SNS activation and sAA levels.
Chronic or more extreme trauma can also have a blunting effect on a person’s SNS.
D’Andrea and colleagues (2013) found that during an acoustic startle paradigm, individuals with
moderate trauma exposure showed increased SNS reactivity, whereas individuals who had more
chronic exposure or worse trauma had blunted SNS reactivity and increased PSNS reactivity.
These results suggest that individuals tend to respond to a stressor with SNS activation. If the
stressor becomes chronic and/or significantly worsens, however, the SNS response may become
blunted and the individual may dissociate and not have a normative physiological response to the
stressor. Thus, women who experience more chronic IPV may have initially responded to a
stressor with SNS hyper-reactivity, but over time, this response may dampen until they no longer
experience SNS arousal when faced with a stressful situation that would normally elicit an SNS
response. If a mother who experienced chronic IPV were to dissociate in the face of a stressful
situation, she may not be able to attend to her baby or respond empathically because she may not
feel the same physiological arousal that the infant is feeling. Therefore, examining the chronicity
of a stressor like IPV may be crucial in understanding the effects on SNS reactivity and the
13

implications for dyadic attunement. Importantly, the existing mother-infant physiological
attunement literature has not yet examined the effect of chronic versus non-chronic trauma on
attunement. However, research on the effects of duration of trauma on the SNS would suggest
that differentiating between chronic and non-chronic trauma in studies of trauma and attunement
may be important.
IPV could disrupt the nascent mother-infant bond during this important developmental
stage in the infant’s life. Women who are victims of IPV are at a greater risk of developing
mental health problems, such as depression, posttraumatic stress disorder, suicidality, and
anxiety (Kessler et al., 2001; Pico-Alfonso et al., 2006). They are also more likely to endorse
physical and mental health problems (Coker et al., 2002). These negative mental health outcomes
are associated with harsh parenting and less sensitive caregiving (Leung & Slep, 2006). For
example, depressed mothers tend to be less warm and consistent in their caregiving (Holmes,
2013; Leung & Slep, 2006) and are less likely to perceive their parental role as being positive
(Black et al., 2002). Furthermore, if a mother is herself emotionally dysregulated, she may be
less able to model adaptive self-regulatory behaviors to her child (Low & Stocker, 2005). IPV
specifically is associated with inconsistent parenting, less physical affection, more hostile
parenting, and child abuse (Casanueva & Martin, 2007; Levendosky et al., 2006; Ritchie &
Holden, 1998; Rossman & Rea, 2005). Moreover, women who have experienced IPV are more
likely to have distorted, incomplete, and unrealistic views of their children (Sokolowski, Hans,
Bernstein, & Cox, 2007), and this distorted representation is associated with insecure infant
attachment (Huth-Bocks, Levendosky, Theran, & Bogat, 2004). Thus, IPV may negatively
influence maternal warmth and caregiving, which in turn may reduce a mother’s sensitivity to
her infant’s needs and disrupt mother-infant attunement. Conversely, Levendosky and colleagues
14

(2003) found that some women who experience IPV “compensate” by being more warm and
attentive parents. In this case, IPV may be associated with increased mother-infant attunement
due to more sensitive caregiving.
The effect of IPV on mother-infant physiological attunement has not been well studied,
especially in infants aged one or younger. Still, given the relationship between IPV and parenting
problems and between IPV and distorted maternal representations of their infants, it seems
feasible that IPV would be associated with changes in attunement. In light of the research that
suggests that younger children may be more affected by IPV, the relationship between IPV and
mother-infant attunement difficulties may be stronger in infants. An important thing to consider
is that this relationship may vary in mother-infant dyads depending on the type of behavioral,
emotional or physiological response - women who have experienced IPV may be more able to
attune to their infants if the infant is expressing a positive behavior or emotion because this
would not alarm the mother and she would be less likely to respond with harsh parenting or
become distracted by her own response. If the infant is distressed, however, there may be a
greater difference in the quality of the subsequent mother-infant attunement between women
who have and have not experienced IPV.
There is a paucity of research studying physiological attunement, IPV, and maternal
factors. Johnson & Lieberman (2007) examined affective attunement in mothers and their
preschool-aged children who had been exposed to IPV and found that IPV was not related to
affective attunement. In a study by Hibel and colleagues (2009), the authors studied
physiological attunement in mother-infant dyads, some of whom had experienced IPV. Mothers
and infants from IPV-exposed dyads showed more physiological attunement during an arm
restraint task than did dyads not exposed to IPV, which suggests that the context of the early
15

mother-infant relationship may affect the coordination between the mother’s and the infant’s
stress response. However, physiological attunement in this study was measured by using cortisol
as a marker of HPA reactivity, which means that the results cannot be applied to physiological
attunement as measured by sAA as a marker of the SNS. Despite the fact that the relationship
between IPV, physiological attunement, and maternal factors has not been well studied, this area
of research may be important for understanding one pathway through which IPV influences
infant development and the mother-infant relationship. The goal of the present study is to explore
how IPV and maternal warmth influence mother-infant attunement. This information may help to
inform intervention efforts that aim to minimize the negative effects of IPV on child outcomes
by adding to pre-existing knowledge of protective and risk factors.
This study is designed to address several of the limitations of the existing attunement
literature that have been reviewed here. Firstly, this study aims to not only examine the effect of
trauma on mother-infant physiological attunement, but also to explore whether the effect differs
between chronic and non-chronic trauma. In addition, to address the problem of differing
definitions and analyses of physiological attunement, the data in this study will be analyzed
using three different analyses, which correspond to three often-used conceptualizations of
attunement, to examine whether the different conceptualizations of attunement would
significantly influence and differentiate the results.
Hypothesis 1
The first hypothesis is that there will be differences in patterns of mother-infant
attunement across the four IPV groups.

16

The control group is expected to show the greatest attunement because mothers will be
most able to model resilience and regulate their own emotions due to not having experienced
recent and/or ongoing IPV and infants will be most able to attune to their mothers because they
have not been prenatally programmed and/or postnatally exposed to IPV. Mothers and infants
will be able to implement adaptive self-regulatory strategies that reduce the infant’s negative
emotions and increase positive emotions (Schore, 2005).
Mothers and infants in the prenatal IPV only group are predicted to be less attuned than
the control group. While mothers may not have any difficulty modeling self-regulation because
their experience of IPV is not recent, infants in this group may be prenatally programmed to
over-react to a stressor. This prenatal programming may make it more difficult for infants to
attend to their mothers.
The postnatal IPV only group is also hypothesized to be less attuned than the control
group. The recency of IPV may lead to hyper-arousal of the SNS, particularly in the mothers.
These mothers may react more strongly to a perceived threat and have greater difficulty reducing
their distress. Consequently, they may not have been able to help their infants self-regulate in the
past. Thus, the infants may react more strongly to the in-lab stress task and be less capable of
self-soothing. Although the mothers may be aware of the infants’ distress, they may be distracted
by their own physiological response to the stressful environment and the infants’ crying. As a
result, they may not be able to attune to the child. Therefore, the dysregulation of the stress
response of both dyad members will result in less physiological attunement.
Mother-infant dyads in the prenatal/postnatal (chronic) IPV group are hypothesized to be
the least attuned. Due to the chronicity of IPV, mothers may be less reactive to stress as a whole
and have a delayed and attenuated physiological response. Like the infants in the prenatal IPV
17

only group, the infants in this group may have also been prenatally programmed, which is
associated with an increased stress response. Thus, the infants in this group may react more
strongly to a stressor, while their mothers do not. Moreover, because the mothers may be less
reactive to stressors, they may also be less reactive and sensitive to their infants’ needs or
distress. If this is the case, these mothers may have been unable to show their infants how to
regulate emotions during previous distressing situations. These mothers would then also be less
able to attune to their infants during the lab stress task. Consequently, mothers and infants in this
group may be less attuned because mothers may have a blunted response to stress while infants
may react more strongly to stress due to prenatal programming and an inability to self-regulate.
Alternatively, the postnatal IPV group and the chronic IPV group may have the most
attuned mothers and infants because they may have more shared stressful situations at home,
causing them to react similarly to a stressful laboratory task. Dyads without postnatal IPV may
not react in a similar way to a stress task because they did not have the same kind of shared
stressful experiences to base their responses on.
Hypothesis 2
The relationship between maternal warmth and attunement is hypothesized to be stronger
in dyads with prenatal/postnatal IPV compared to dyads with no IPV, prenatal IPV only, or
postnatal IPV only. Infants in dyads with more chronic IPV may respond more strongly to stress
due to both prenatal programming and the stressful postnatal environment, and thus may be more
dependent on their mothers to help with self-regulation and adaptation. Mothers from these
dyads may tend to have a blunted SNS stress response, making it more difficult for them to
respond warmly and appropriately to their distressed infant and model adaptive self-regulatory

18

behaviors. However, when mothers are warm, they may be able to attend to their babies’ needs
in spite of the IPV exposure, causing the dyad to be attuned. In dyads with prenatal/postnatal
IPV, maternal warmth may be more crucial for attunement to occur because the child may be
predisposed to an over-reactive stress response and there are more distressing moments in which
the child can become dysregulated emotionally and physiologically. In dyads with no IPV,
prenatal IPV only or postnatal IPV only, mother and infant may be less prone to responding
inappropriately to a stressor, so they may be more likely to respond in an attuned way regardless
of whether the mother is high in warmth or not. Thus, the relationship between maternal warmth
and attunement is expected to be strongest in the prenatal/postnatal IPV group.

19

METHODS
Participants
182 mother-infant dyads participated in the study. They were recruited from three
counties in Michigan using fliers, Craigslist, and Facebook. These fliers were posted in stores,
restaurants, libraries, medical offices (pediatrician and OBGYN), daycares, and preschools. To
recruit IPV-exposed dyads, fliers were also placed in domestic violence shelters and given to
agencies that help victims of domestic violence. The study planned to recruit 40 women for each
group (prenatal IPV, postnatal IPV, pre- and postnatal IPV and control) who were matched on
demographic measures. In total, 914 women were screened, of whom 182 were eligible for the
study.
Procedures
Women were first screened over the phone for eligibility. In order to be included in the
study, they needed to be (1) English speakers, (2) between the ages of 18 and 34 years old, (3)
not currently pregnant, (4) fine with not breastfeeding their child for 2 hours before the
assessment, (5) free from endocrine disorders, cancer, or currently receiving treatment for
cancer, (6) in a heterosexual romantic relationship for at least 6 weeks during the pregnancy, and
(7) their children were not born prematurely before 37 weeks gestation.
Because of the difficulty in finding women who had experienced postnatal IPV only and
prenatal IPV only, the number of participants in each group varied. The control group had 58
women (31.9%), the prenatal IPV only group had 34 women (18.7%), the postnatal IPV only
group had 12 women (6.6%), and the pre- and postnatal group had 78 women (42.9%).
Mothers and their infants were interviewed when infants were around one year old, and
20

all interviews were conducted in the afternoon to minimize the effect of sampling time on the
diurnal rhythm of salivary alpha amylase (see Nater, Rohleder, Schlotz, Ehlert, & Kirschbaum,
2007). Mothers were asked not to drink alcohol 12 hours prior to the visit, not to brush their
teeth, chew gum or consume a large meal 1 hour before the visit, and not to ingest sugary or
acidic foods 20 minutes before the visit. The interviews were conducted by two undergraduate
students. Interviewers inquired about maternal and infant health and took forehead temperatures
to confirm that mother and infant were not ill. Then they collected a pre-task saliva sample from
both mother and infant. Mothers were asked to “chew” to collect saliva and then pass the saliva
into a cryogenic vial. Saliva was obtained from infants by placing two microsponge devices
under the infant’s tongue for 60-90 seconds. These microsponges were transferred to cryogenic
vials. Then the Modified Lab-TAB Arm Restraint task was completed to assess sympathetic
nervous system activation and regulation. Five minutes after the task, when sAA normally peaks,
saliva was collected again from mothers and infants. Then mothers filled out non-stressful
questionnaires (so as not to influence sAA levels). 20 minutes after the task, when sAA usually
returns to baseline or near-baseline levels (recovery), saliva was collected from mothers and
infants. After saliva was collected, mothers filled out the remaining questionnaires and were
compensated for their participation. Infants received a stuffed animal.
Measures
Intimate Partner Violence: Women were first assessed during the telephone screening
using questions 9-19 of the Conflict Tactics Scale (CTS; Straus, 1979) to determine the timing of
IPV and preliminarily place women in one of the four groups. When women came in for the inperson interview, the Severity of Violence Against Women Scales (SVAWS; Marshall, 1992) was
given to determine the final classification of women into the IPV groups. The SVAWS is a 4621

item measure that assesses psychological, physical, and sexual violence on a 4-point scale.
Women also indicated how distressing each item was on a scale of 1 to 3. Women were asked to
complete the SVAWS twice: once for prenatal IPV experiences and once for postnatal IPV
experiences. Women were grouped based on their responses to #14 and higher (these items
assess minor, moderate, serious and sexual violence). They were also asked to indicate whether
any violence had occurred in the past 48 hours and if their infants had witnessed or heard any of
the violence. In the present sample, for the prenatal SVAWS, α = .978, and for the postnatal
SVAWS, α = .975.
Parenting Behavior Checklist (PBC; Fox, 1992): The PBC is a 50-item parenting selfreport measure used for women with children ages 1-4. There are 3 subscales: Expectations,
Discipline, and Nurturing. Only the nurturing subscale (α = .826) was used in this study, and it
measures how much mothers stimulate and encourage the psychological growth of their children
(maternal warmth).
Challenged Salivary Alpha Amylase: The Modified Lab-TAB Arm Restraint task
(Goldsmith & Rothbart, 1999) was used to assess mother and infant stress responses and
regulation via sympathetic nervous system activation. In the Arm Restraint task, which is used to
assess child temperament, an infant sits in a highchair and is given a toy to play with. Usually the
mother holds the child’s arms, but in the modified version used for this study, the interviewer
restrained the child’s arms gently after 2 minutes of play. The interviewer sat directly behind the
child and the mother sat behind and to the left of the infant. The infant could see neither the
interviewer nor the mother, but the mother could see the child. The interviewer held the infant’s
arms at the infant’s sides for 2 minutes or until the infant cried hard for 20 seconds. The mother
was told beforehand that if the infant became too upset by the task, the interviewer would stop.
22

The mother could also stop the task at any time. After the task, the infant was taken out of the
chair and given back to his or her mother.
Mother and infant saliva samples were collected pre-task, 5 minutes after the task, and 20
minutes after the task. The saliva samples were kept in a freezer until they could be assayed and
analyzed. Commercially available kinetic reaction assays were used. Saliva samples were
analyzed by pipetting samples (8 ul diluted 1:200) onto 96-well plates. These plates contained 2chloro-p-nitrophenol and maltotriose, which react spectrophotometrically with sAA such that the
amount of sAA in the sample was proportional to the optical density of the product. The intraassay variation was computed using the mean of 30 replicate tests and was less than 7.5%. The
inter-assay variation was calculated using the mean of average duplicates of 16 runs and was less
than 6%.
Proposed Analyses
Other studies have analyzed physiological attunement data using multiple methods, such

as difference score correlations, regression, and multilevel modeling (MLM). As mentioned
previously, they also had different conceptualizations of attunement. However, the data analytic
strategies in these studies were not always in accordance with the definition of attunement given
in the study (e.g., operationalizing attunement as lagged process but analyzing the data as if it
were concurrent). More recent studies have tended to forgo the more simplistic and flawed
analytical methods (e.g., difference score correlations) in favor of multilevel modeling (MLM),
which is recommended for this kind of data analysis. MLM can be used to analyze data in which
individuals are nested within dyads, and individual data is crossed with time due to the multiple
data collection time points. Therefore, MLM will be used to analyze the present data.

23

Three MLM analyses, which correspond to the aforementioned three conceptualizations
of attunement, will be run for each hypothesis. Firstly, a correlated growth model will be run,
which corresponds to the conceptualization of attunement as concurrent and similar changes in
mother and infant across time. Then, a cross-lagged analysis will be conducted, which
corresponds to the definition of attunement as being a reciprocal and lagged process, in which
both members of the dyad influence the other’s subsequent response. The last analysis will be
one in which maternal values predict infant values over time, which corresponds to the
conceptualization of attunement as a non-reciprocal process.
Exploratory Post-Hoc Examinations
If there are no significant differences among the four a priori groups or if there is not
enough variability within each group to determine whether they are attuned or not, post-hoc
examinations will be done.

24

RESULTS
Missing Data
Of the 182 dyads, 23 had one or more missing sAA values. This may have been due to
mothers and infants not being able to produce enough saliva needed for the measurement at one
or more collection time points, or infants being too upset for a sample to be taken. Missing sAA
values were not imputed because this was not necessary for the planned analyses as MLM is
robust to missing data. There were no missing items for any dyads on the Nurturing subscale of
the PBC or for the pre- and postnatal SVAWS.
To determine whether the absent sAA values were missing at random, each dyad was
coded with either a “0” to indicate no missing data, or a “1” to indicate that 1 or more sAA
values were missing in a dyad. This was then correlated with the other measures that were used
and important demographic variables. IPV grouping, the presence of IPV at any time point
(dichotomously coded), SVAWS scores, maternal warmth, maternal education, maternal age,
infant gender, monthly income, maternal ethnicity, maternal mental health issues (depression,
anxiety, PTSD), and maternal drug and alcohol use were not significantly correlated with the
presence or absence of missing data. Therefore, there does not appear to be a pattern to the
missing data, and the data will be considered to be missing at random (e.g., see Counts, Nigg,
Stawicki, Rappley, & von Eye, 2005).
Hypothesis 1
(1)

Does the timing and duration of IPV exposure affect mother-infant attunement in an

acutely stressful situation?

25

It was hypothesized that there would be differences in mother-infant attunement among
the four a priori IPV groups. Dyads from the control group were expected to show the greatest
attunement, the prenatal IPV only group and the postnatal IPV only group were expected to be
less attuned, and the prenatal/postnatal IPV group was expected to be the least attuned. However,
the four group model would not run because there was not enough variability in the sAA values
across time, particularly among the infants. The model was then simplified by dividing the dyads
into two groups rather than four. Given that chronic IPV was expected to be the most disruptive
to attunement, the IPV groups were then divided to examine the relationship between chronic
versus non-chronic IPV and attunement. The first group was made up of dyads who had either
experienced no IPV, prenatal IPV only, or postnatal IPV only (n = 104) (i.e. no or some IPV).
Dyads with both pre- and postnatal IPV were in the second group (n = 78) (i.e. chronic IPV). The
means and standard deviations are presented below, in Table 1.
Correlated Growth Analysis. The correlated growth analysis evaluates attunement as a
concurrent process. For this analysis, the fixed effects model included separate intercepts and
slopes for mothers and babies. The intercept estimated the person’s average sAA and the slope
measured the linear change in sAA as time increased by one unit. In the random effects part of
the model, different mother and baby intercept and slope variances in each of the two groups
were specified. The model then attempted to estimate the correlation between mother and baby
slopes separately for the two a priori groups. The IPV variable was effects coded (no/some IPV
or chronic IPV). In this model, individuals were nested within dyads, and this was crossed with
time. The fixed effects of the model included separate intercepts and slopes for mothers and
babies, as well as interactions between the intercepts and slopes and the level two IPV variable.
The IPV by intercept interaction would indicate whether there were mean differences in average
26

sAA for the two groups, while the IPV by slope interaction would show whether there were
average differences in the change in sAA over time as a function of IPV. The model also
included separate random effects for the two IPV groups. For each group the model included
variances in the intercepts and slopes of the mothers, variances in the intercepts and slopes of the
infants, the covariance of mother and infant intercepts, the covariance of mother and infant
slopes, and the residual variances.
Results for the fixed effects from the two-grouping growth model showed that there was
a significant mean difference in average maternal sAA for the two IPV groups (β = -.844, p <
.001), but there was no significant mean difference between both IPV groups in average infant
sAA (β = .213, p = .236)
Results for the random effects are presented in the Table 3. They indicated that mothers’
intercepts and slopes varied significantly in both groups. There was significant variance in the
babies’ intercepts in both groups, but variance was not significant in babies’ slopes in both
groups. Mothers’ and babies’ intercepts covaried significantly in both groups such that mothers
who were relatively high in sAA on average had babies who were also relatively high on
average. Mothers’ and infants’ slopes did not covary in either group, suggesting that mothers and
infants were not attuned and that the chronicity of IPV did not have a significant and differential
effect on attunement.
Cross-Lagged Analysis. The reciprocal and lagged definition of attunement can be
tested in a cross-lagged model like the one depicted in Figure 1. The horizontal arrows represent
stability (e.g., a mother’s sAA value at T1 will be related to her sAA value at T2), and the

27

diagonal arrows represent the influence of one member of the dyad’s past response on the other’s
subsequent response (e.g., a baby’s sAA value at T1 is related to the mother’s sAA value at T2).
Mothers and infants were treated as both “actors” and “partners” within the model to test
the reciprocal and lagged influence of mother and infant sAA, while controlling for the effect of
an individual’s past response on that individual’s next response. Actor and partner scores were
grand mean centered, and mother and infant were dummy coded. IPV was effects coded
(no/some IPV or chronic IPV). Dyad ID and time were entered as repeated effects. The
dependent variable was actor sAA. The residual structure was specified as compound
heterogeneous symmetry (CSH), which allowed for unequal variances.
According to the results, a person’s previous sAA was a good predictor of that person’s
subsequent sAA for both mothers and infants (infants: β = .895, p < .001; mothers: β = .824, p <
.001), indicating that there was stability. However, neither mother nor infant sAA values
influenced the other person’s subsequent sAA value (Baby: β = -.009, p = .646; Mother: β =
.068, p = .156), suggesting that influence was not significant. Moreover, IPV did not moderate
the relationship between actor and partner sAA, nor was IPV related to maternal or infant sAA
across time. Thus, IPV did not significantly affect the stability or influence of maternal or infant
sAA values.
Thus, the results suggest that mother and infant sAA values were stable, such that a
person’s past sAA value significantly predicted the person’s subsequent sAA value. However,
mothers’ previous sAA values did not predict infants’ subsequent sAA values, and infants’
previous sAA values did not predict subsequent maternal sAA values. This partner effect
remained nonsignificant even when IPV was added as a moderator. In addition, IPV did not
affect maternal or infant sAA values across time.

28

MLM – Mom Predicts Baby Analysis. The conceptualization of attunement as nonreciprocal can be examined with a mixed model analysis in SPSS, in which the values of one
dyad member are predictors of the values of the other dyad member. Here, maternal sAA was the
predictor, and infant sAA was the dependent variable. Thus, this analysis examined whether a
mother’s sAA at a particular time point predicted her infant’s sAA at that same time point.
In this model, the intercept, maternal sAA, IPV group, and the maternal sAA x IPV
interaction were entered as fixed effects predicting the infant’s sAA. The intercept and maternal
sAA were also entered as random effects. The fixed effects indicated whether mothers and
infants were similarly high or low at specific time points; the random effects gave measures of
intercept, residual and maternal sAA variance. Maternal sAA was centered and IPV was effects
coded (no/some IPV and chronic IPV). The residual structure was specified as variance
components (VC), which specifies variances for intercepts and for the effect of maternal sAA on
infant sAA and residual, but fixes the covariances between these parameters to zero.
Results of this analysis suggested that maternal sAA predicted infant sAA, such that if the
mother had high sAA at a time point, the baby tended to have high sAA at that time point (β =
.09, p = .007). IPV did not predict infant sAA (β = .257, p = .142), and the strength of the
relationship between maternal sAA and infant sAA was not significantly changed by the
presence or absence of chronic IPV (β = -.021, p = .521). However, the estimate of maternal sAA
variance suggested that the degree to which a mother’s sAA predicted her baby’s sAA differed
from family to family (β = .039, p = .005).
Brief Summary of Results. The results of all three analyses suggest that IPV did not
moderate mother-infant attunement in this sample. There was slight variation in the results from
each. The correlated growth model indicated that the change in maternal sAA over time differed

29

between the no/some IPV group and the chronic IPV group, suggesting a blunting of the
maternal SNS response in the chronic IPV group which was a prediction of this hypothesis. This
is consistent with research that suggests that chronic trauma is associated with a decreased SNS
stress response. However, infants’ sAA did not differ between both groups and also did not
significantly vary across time, and so dyads did not have attuned stress responses in either group.
The cross-lagged analysis only indicated that mother and infant sAA values across time were
stable. Maternal and infant past sAA values did not significantly influence the other’s subsequent
response, suggesting that mothers and infants were not attuned. Stability and influence did not
differ between both IPV groups, indicating that IPV did not have a significant effect on sAA
values. In the analysis in which maternal sAA was examined as a predictor of infant sAA,
maternal sAA was a significant predictor of infant sAA, and the strength of maternal sAA as a
predictor varied from dyad to dyad. However, this variance was not accounted for by the
presence or absence of chronic IPV. The results of the last analysis may have differed from the
other results because it was not a dyadic or lagged measure of attunement and did not treat the
mother and infant SNS responses as reciprocal.
Because the arm restraint task was terminated early if an infant cried hard for 20 seconds,
a regression was run to determine whether the lack of results was due in part to the infants of one
IPV group becoming significantly more distressed and needing to end the arm restraint task
early. The regression suggested that IPV grouping did not predict early termination of the arm
restraint task (β = .082, p = .274). Therefore, the lack of a significant difference between infants
of both IPV groups is likely not a function of early task termination due to excessive infant
distress.

30

Hypothesis 2
(2) Does maternal warmth influence the relationship between the maternal SNS stress response
and the infant SNS stress response? Does the relationship differ in the context of exposure to
both pre- and postnatal IPV?
It was hypothesized that in dyads with both prenatal and postnatal (chronic) IPV, higher
levels of maternal warmth would be associated with increased mother-infant attunement; in
dyads with no IPV, prenatal IPV only, or postnatal IPV only, the relationship between maternal
warmth and mother-infant attunement was not expected to be as strong. Given that there was not
enough variability in sAA within the a priori groups, and that some of the groups were too small,
the original analyses that were planned to test this hypothesis were not possible. Instead, the data
were examined using the three analyses from the first hypothesis. All analyses were run in SPSS.
Correlated Growth Analysis. The first analysis was a correlated growth model. IPV was
effects coded (1 = chronic IPV, -1 = no/some IPV), and time and maternal warmth were both
grand-mean centered. IPV, time, maternal warmth, maternal sAA, infant sAA, and their
interactions were entered as fixed effects into the model. The mom by time (centered) interaction
and the baby by time (centered) interaction were entered as random effects. The dependent
variable was a person’s sAA. Dyad ID by time was entered as a repeated effect. The covariance
structure was specified as CSH. For more information about the model, please see Hypothesis 1.
Maternal warmth was not a significant predictor of maternal or infant average sAA
values or sAA slopes across time, even when the chronicity of IPV was taken into account.
These values are presented in Table 6.

31

Cross-Lagged Analysis. As mentioned in the first hypothesis, in the cross-lagged model,
mothers and infants were entered as both “actors” and “partners” into the model. For this
analysis, maternal warmth was also entered into the model as a fixed effect. Actor and partner
scores were grand mean centered, as was maternal warmth. Mother and infant were dummy
coded, and IPV was effects coded (1 = chronic IPV, -1 = no/some IPV). Dyad ID by time was
entered as a repeated effect. The dependent variable was actor sAA. The residual structure was
specified as CSH.
The relationship between a partner’s past sAA and the actor’s present sAA (which could
indicate attunement) remained nonsignificant when maternal warmth and IPV were included in
the model (mother as partner, β = -.005, p = .40 and baby as partner, β = -.002, p = .46). The
estimates of all fixed effects in this analysis are presented in Table 7.
MLM – Mom Predicts Baby Analysis. In this analysis, maternal sAA, maternal
warmth, and IPV were examined as predictors of infant sAA. The maternal variables, IPV and
their interactions were entered as fixed effects, and infant sAA was specified as the dependent
variable. The intercept and maternal sAA were entered as random effects. Maternal sAA and
maternal warmth were grand-mean centered. IPV was effects coded to indicate the presence of
chronic or no/some IPV. The residual structure was VC. For additional details, please see the
corresponding analysis for the first hypothesis.
Maternal warmth, IPV, and their interactions with maternal sAA were not predictors of
infant sAA. The estimates of the fixed effects are presented in Table 8.
Brief Summary of Results. All three analyses indicated that maternal warmth did not
significantly influence mother-infant attunement in the presence or absence of chronic IPV.

32

Moreover, maternal warmth was not significantly related to maternal or infant sAA over the
course of the laboratory stress task.

33

DISCUSSION
The present study examined the relationship between IPV, mother-infant physiological
attunement, and maternal warmth using six MLM analyses. This was the first study to explore
mother-infant sympathetic nervous system attunement in an IPV-exposed population and the first
to examine the association between maternal warmth and mother-infant attunement in the
context of IPV. In addition, given the multiple conceptualizations of attunement within the
literature and the variability within the analyses used to determine attunement, this study was an
important step towards examining whether differences within the conceptualization and analysis
of attunement lead to different results.
This study had two research questions. Specifically, it aimed to examine the relationship
between the timing and duration of IPV exposure and mother-infant physiological attunement
during a stressful situation; and to examine the relationship between maternal warmth and
mother-infant physiological attunement during a stressful situation, and whether this relationship
differed depending on the IPV experiences of a dyad.
It was hypothesized that IPV would be related to mother-infant physiological attunement
during a stressful situation that was unrelated to IPV. However, the initially planned analyses
could not be run using the four group model. Instead, the dyads were split into two groups: a
group who had experienced either no IPV or IPV during only one time period, and a group who
had experienced IPV during both the pre- and postnatal periods. Three analyses were run that
corresponded to the three main conceptualizations of attunement from the physiological
attunement literature. Overall, the findings from all three analyses did not support this
hypothesis. The final analysis did suggest a relationship between the maternal stress response

34

and the infant stress response, although this relationship did not vary between both IPV groups as
hypothesized. It did vary between dyads, suggesting that other intra-family factors may account
for attunement differences.
Due to the lack of research in this area, a null finding is difficult to interpret. It could be
that the null finding is valid and that the results are real or it could also be that the lack of
findings is due to a methodological issue. Both possibilities will be explored more in depth here.
Mothers and infants who had experienced IPV were expected to be less physiologically
attuned when stressed, particularly if the IPV exposure was both prenatal and postnatal.
However, the results indicated that attunement was not related to IPV exposure. If these results
are valid, they suggest that IPV may not influence mother-infant physiological attunement. The
presence or absence of chronic IPV did not differentiate infants in the study, but mothers who
experienced chronic IPV had lower levels of sAA than mothers who did not. This suggests that
there may be important differences between mothers and infants that leaves mothers more
vulnerable to SNS changes following exposure to chronic IPV. This may be because the mothers
were the direct targets of the IPV, whereas the infants may have experienced the IPV more
indirectly. There may also be age-related differences in the effect of IPV on SNS reactivity.
Perhaps IPV does not affect SNS reactivity in infants (via prenatal programming and postnatal
exposure) but does affect reactivity in adults. However, potential reasons for this are unclear
given that prenatal programming of the infant SNS has been found in another study that
examined the effect of prenatal exposure to a stressor on postnatal SNS responsivity. This
inconsistency suggests that prenatal programming of the SNS should be further studied.

35

The null finding for the effect of IPV on attunement is inconsistent with attunement
findings in a similar sample when the HPA axis was the stress system of interest. Hibel and
colleagues (2009) found that IPV affected HPA axis attunement in exposed mother-infant dyads.
Thus, it may be that IPV only influences mother-infant physiological attunement of the HPA axis
and not of the SNS stress response. This may be because sAA responsivity varies based on age.
Granger and colleagues (2006) found differences among infants, school-aged children,
adolescents, and adults in sAA responsivity to social stressors. The infants and children did not
show an increase in sAA in response to a stressor while the adolescents and adults did. These
results are similar to the findings of this study: infants did not show significant variability in their
sAA reactivity, while the mothers showed more variability. Thus, the null findings may be
attributable in part to infant sAA not yet being significantly responsive to a short social stressor
(arm restraint).
However, it is also possible that the lack of findings is due to a methodological issue. For
example, there may have been problems with the activation or measurement of SNS reactivity.
There was not enough variability in sAA, which could mean that the arm-restraint task was not
stressful enough to elicit a sufficient stress response from both mother and infant. While the task
itself was not expected to be directly stressful for mothers, it was thought that the task might be
indirectly stressful via the infants’ response to the task. However, the infants may have felt more
irritated by the arm restraint than threatened, which in turn may not have been sufficiently
stressful to elicit the mothers’ stress responses. Thus, the arm restraint task may not have been
stressful enough for a one-year-old to increase the amount of sAA in the infant’s oral mucosa.
The lack of sAA variability in infants in this study is consistent with the results of Granger and
colleagues (2006), who also did not find changes in sAA following stressful lab tasks (including
36

the arm restraint task) in infants six to ten months of age. Laurent and colleagues (2012) used
multiple Lab-TAB tasks to elicit an SNS stress response, suggesting that perhaps the one task
used in this study was insufficient. Still, it is important to note that in this sample, the arm
restraint task was stressful enough to activate the infant HPA axis stress response. This finding is
difficult to explain, given that the SNS is typically more easily activated and responds to a wider
range of stressors than the HPA axis.
The lack of findings may also have been due to the sample. Firstly, it was a high risk
sample, which means that dyads within the a priori groups may not have been significantly
different in terms of overall stress that they experienced, which was not controlled for. Secondly,
the a priori group sizes did not turn out as initially planned. They were unequal in size and two
of the groups were smaller than had been initially planned. Specifically, it was difficult to find
women who had experienced IPV only during the prenatal period or only during the postnatal
period. In relationships plagued by IPV, it is less common for IPV to suddenly end or suddenly
begin when pregnancy is over unless a woman leaves or begins a relationship with an abusive
partner around that time. Consequently, it was difficult to recruit an equal and sufficient number
of women for each IPV group. If there had been enough women in each group, the initially
planned analyses might have run, and this study may have been better able to illuminate how the
timing and duration of IPV is related to mother-infant physiological attunement. As this was not
the case, this study could not explore whether the timing of IPV (pre- or postnatal) was
differentially related to mother-infant attunement.
The second hypothesis of the study was that maternal warmth would be associated with
mother-infant physiological attunement, and that the strength of this association would be related
to IPV. The same three analyses from the first hypothesis were also run here. None of the
37

analyses showed an association between maternal warmth and mother-infant physiological
attunement, regardless of whether the dyad had experienced chronic IPV or not.
The results of this analysis may be an accurate reflection of the relationship (or lack
thereof) among physiological attunement, IPV and maternal warmth. If the results are valid, they
could suggest that warm and nurturing parenting is not related to mother-infant physiological
attunement and that this relationship is not influenced by the presence or absence of chronic IPV.
However, these results may not be valid and the lack of findings may be due to
methodological issues. Firstly, the measurement of maternal warmth was a self-report measure,
and thus it may not have captured maternal warmth in the same way that an objective measure
would have. Secondly, this hypothesis builds off of the first hypothesis. Thus, if the null findings
for the first hypothesis were due to a methodological issue, this would have a direct impact on
the findings for the second hypothesis.
The limitations addressed here provide direction for future research, which may create a
context within which to understand the results of this study. Given the lack of consensus in the
physiological attunement literature as to how to define and determine attunement, this study
aimed to examine not only whether mother-infant dyads were attuned, but also whether the
results stayed the same across different conceptualizations and analyses of attunement. Although
the results of this study were similar across the three types of analyses used, the analyses should
be replicated in other samples. Until then, studies that conceptualize and analyze attunement
differently cannot necessarily be compared because they may be measuring different things or
using analyses that treat the data differently.

38

Additionally, future studies could break up the prenatal and postnatal periods. The effect
of IPV on fetal and infant SNS development and on mother-infant attunement may differ
depending on when during development the IPV occurs. There may be windows during
pregnancy, for example, where the fetus is more susceptible to prenatal programming such that if
IPV were to take place during that time, the development of the fetus would be more likely to be
altered. While several studies have suggested different sensitive periods during gestation for
specific psychological outcomes in later life, research has not yet examined sensitive periods for
infant SNS development or mother-infant attunement.
This study did not find evidence for or against prenatal programming of the SNS because
the initially planned analyses could not be run. However, other studies have found evidence in
support of prenatal programming, although the mechanisms by which the fetal SNS may be
prenatally programmed are unclear since maternal SNS hormones do not pass into the placenta.
It has been suggested that maternal norepinephrine restricts blood flow to the fetus, which could
activate and program the fetal SNS stress response. Future research should continue to explore
this potential mechanism and others to better understand prenatal programming of the SNS.
Despite the limitations of this study, it represents a contribution to the nascent literature
on mother-infant physiological attunement in IPV-exposed dyads and may help to inform the
methodology used in future research. Previous research has examined physiological attunement
via the HPA axis in IPV-affected mother-infant pairs, but this is the first study to examine
attunement in this population using the SNS. Moreover, it is also one of the first to address the
issues of multiple definitions of attunement and multiple analytical approaches that muddle the
physiological attunement literature. Although further research is needed to examine the potential

39

differential effects of timing and chronicity of IPV exposure on mother-infant attunement, this is
one of the first studies to propose and attempt to do so.

40

APPENDICES

41

APPENDIX A

TABLES

42

Table 1. sAA Means and Standard Deviations for Mothers and Infants
Total

No/Some IPV

Chronic IPV

Mother sAA Time 1

7.253 (3.82)

8.036 (4.10)

6.216 (3.15)

Mother sAA Time 2

7.248 (3.77)

8.065 (3.86)

6.179 (3.40)

Mother sAA Time 3

7.345 (3.78)

7.989 (3.71)

6.494 (3.76)

Infant sAA Time 1

6.200 (2.49)

6.011 (2.68)

6.457 (2.19)

Infant sAA Time 2

6.29 (2.58)

6.110 (2.64)

6.532 (2.49)

Infant sAA Time 3

6.375 (2.55)

6.213 (2.67)

6.582 (2.37)

43

Table 2. Fixed Effects of the Correlated Growth Model
Role: Mother

Role: Infant

Estimate

t

Estimate

t

Intercept

7.156**

28.500

6.268**

35.030

IPV Status

-.844**

-3.360

.213

1.190

Time

.061

.580

.055

1.050

IPV x Time

.054

.510

-.018

-.350

**p < .001

44

Table 3. Random Effects of the Correlated Growth Model
No/Some IPV

Chronic IPV

Estimate

Z-Value

Estimate

Z-Value

12.849**

6.81

8.764**

5.79

Infant Intercept Variance

6.194**

6.84

4.771**

5.92

Maternal Slope Variance

.470*

2.03

1.344**

3.41

Infant Slope Variance

.078

1.08

.132

1.51

Maternal/Infant Intercept

2.891*

2.98

1.605*

2.00

.023

.24

.177

1.34

Maternal Intercept
Variance

Covariance
Maternal/Infant Slope
Covariance
**p < .001, *p < .05

45

Table 4. Fixed Effects of the Cross-Lagged Analysis
Role: Mother

Role: Infant

Estimate

t

Estimate

t

Role

6.958**

57.144

6.778**

96.932

Actor Previous sAA x Role

.824**

24.614

.895**

31.875

Partner Previous sAA x Role

.0684

1.423

-.009

-.459

IPV x Role

-.097

-.798

.0004

.006

Actor Previous sAA x IPV x

.001

.028

-.008

-.299

.033

.688

-.013

-.650

Role
Partner Previous sAA x IPV x
Role
**p < .001, *p < .05

46

Table 5. Fixed and Random Effects for Maternal sAA Predicting Infant sAA
Estimate

Standard Error

df

t

Intercept

6.272**

.174

170.815

35.986

Maternal sAA

.090*

.033

127.145

2.747

IPV

.257

.174

170.815

1.478

Maternal sAA x

-.021

.032

127.145

-.644

Intercept Variance

4.609**

.577

-

-

Maternal sAA

.039*

.014

-

-

IPV

Variance
**p < .001, *p < .05

47

Table 6: Fixed Effects of the Correlated Growth Model
Role: Mother

Role: Infant

Estimate

t

Estimate

t

Intercept

7.150**

27.433

6.287**

34.311

IPV

-.825*

-3.166

.193

1.053

Time

.059

.570

.058

1.110

IPV x Time

.065

.631

-.021

-.409

Maternal Warmth

.025

.847

-.024

-1.152

Time x Maternal Warmth

.013

1.123

-.005

-.803

IPV x Maternal Warmth

-.008

-.264

.025

1.216

IPV x Time x Maternal

-.003

-.248

.004

.597

Warmth
**p < .001, *p < .05

48

Table 7. Fixed Effects for the Cross-Lagged Analysis
Role: Mother

Role: Infant

Estimate

t

Estimate

t

Intercept

6.976**

56.490

6.783**

95.578

Actor Previous sAA

.821**

23.299

.906**

30.017

Partner Previous sAA

.079

1.544

-.010

-.475

IPV

-.130

-1.050

.005

.071

Maternal Warmth

.021

1.470

-.008

-.952

Actor Previous sAA x IPV

-.003

-.074

.015

.511

Partner Previous sAA x IPV

.018

.360

-.023

-1.142

Actor Previous sAA x

-.001

-2.34

.003

1.040

.007

1.265

-.003

-1.347

Maternal Warmth x IPV

-.016

-1.141

.009

1.122

Actor Previous sAA x

.004

1.168

.003

1.080

-.005

-.844

-.002

-.745

Maternal Warmth
Partner Previous sAA x
Maternal Warmth

Maternal Warmth x IPV
Partner Previous sAA x
Maternal Warmth x Postnatal
IPV
**p < .001

49

Table 8. Fixed Effects for Maternal sAA, Maternal Warmth, and IPV as Predictors
Estimate

t

Intercept

6.286**

35.955

Maternal sAA

.102*

3.145

Maternal Warmth

-.018

-.922

IPV

.244

1.395

Maternal sAA x Maternal

.003

.936

Maternal sAA x IPV

-.014

-.433

Maternal Warmth x IPV

.023

1.184

Maternal sAA x Maternal

.006

1.888

Warmth

Warmth x IPV
**p < .001, *p < .05

50

APPENDIX B

FIGURES

51

Figure 1. Cross-Lagged Model

Mother T1

Mother T2

Mother T3

Baby T1

Baby T2

Baby T3

52

REFERENCES

53

REFERENCES

Allwood, M. A., Handwerger, K., Kivlighan, K. T., Granger, D. A., & Stroud, L. R. (2011).
Direct and moderating links of salivary alpha-amylase and cortisol stress-reactivity to
youth behavioral and emotional adjustment. Biological psychology, 88(1), 57-64.
Batzri, S., Selinger, Z., & Schramm, M. (1971). Potassium ion release and enzyme secretion:
adrenergic regulation by α-and β-receptors. Science, 174(4013), 1029-1031.
Black, M. M., Papas, M. A., Hussey, J. M., Dubowitz, H., Kotch, J. B., & Starr, R. H. (2002).
Behavior problems among preschool children born to adolescent mothers: Effects of
maternal depression and perceptions of partner relationships. Journal of Clinical Child
and Adolescent Psychology, 31(1), 16-26.
Bornstein, M. H. (2007). On the significance of social relationships in the development of
children’s earliest symbolic play: An ecological perspective. Play and development.
Mahwah: Erlbaum, 101-29.
Bornstein, M. H. (2014). Human Infancy… and the Rest of the Lifespan. Annual review of
psychology, 65, 121-158.
Bosch, J.A., De Geus, E.J., Veerman, E.C., Hoogstraten, J., Nieuw Amerongen, A.V., 2003.
Innate secretory immunity in response to laboratory stressors that evoke distinct patterns
of cardiac autonomic activity. Psychosom. Med. 65, 245—258.
Bowlby, J. (1969). Attachment and loss (Vol. 1). New York: Basic Books.
Brodal, P. (2004). The central nervous system: structure and function. Oxford University Press.
Cannon, W. B. (1914). The interrelations of emotions as suggested by recent physiological
researches. The American Journal of Psychology, 256-282.
Casanueva, C. E., & Martin, S. L. (2007). Intimate partner violence during pregnancy and
mothers' child abuse potential. Journal of interpersonal violence, 22(5), 603-622.
Charles, P., & Perreira, K. M. (2007). Intimate partner violence during pregnancy and 1-year
post-partum. Journal of Family Violence, 22(7), 609-619.
Chatterton, R. T., Vogelsong, K. M., Lu, Y. C., Ellman, A. B., & Hudgens, G. A. (1996).
Salivary α-amylase as a measure of endogenous adrenergic activity. Clinical Physiology,
16(4), 433-448.
Chrousos, G. P. (2009). Stress and disorders of the stress system. Nature Reviews
Endocrinology, 5(7), 374-381.
54

Chrousos, G. P., & Gold, P. W. (1992). The concepts of stress and stress system disorders:
overview of physical and behavioral homeostasis. Jama, 267(9), 1244-1252.
Clark, S. E., & Symons, D. K. (2000). A longitudinal study of Q-sort attachment security and
self-processes at age 5. Infant and Child Development, 9(2), 91-104.
Coker, A. L., Davis, K. E., Arias, I., Desai, S., Sanderson, M., Brandt, H. M., & Smith, P. H.
(2002). Physical and mental health effects of intimate partner violence for men and
women. American journal of preventive medicine, 23(4), 260-268.
Counts, C. A., Nigg, J. T., Stawicki, J. A., Rappley, M. D., & Von Eye, A. (2005). Family
adversity in DSM-IV ADHD combined and inattentive subtypes and associated
disruptive behavior problems. Journal of the American Academy of Child & Adolescent
Psychiatry, 44(7), 690-698.
D'Andrea, W., Pole, N., DePierro, J., Freed, S., & Wallace, D. B. (2013). Heterogeneity of
defensive responses after exposure to trauma: Blunted autonomic reactivity in response to
startling sounds. International journal of psychophysiology, 90(1), 80-89.
Davidov, M., & Grusec, J. E. (2006). Untangling the links of parental responsiveness to distress
and warmth to child outcomes. Child development, 77(1), 44-58.
Davis, E. P., & Granger, D. A. (2009). Developmental differences in infant salivary alphaamylase and cortisol responses to stress. Psychoneuroendocrinology, 34(6), 795-804.
Diego, M. A., Field, T., Hernandez-Reif, M., Cullen, C., Schanberg, S., & Kuhn, C. (2004).
Prepartum, postpartum, and chronic depression effects on newborns. Psychiatry:
Interpersonal and Biological Processes, 67(1), 63-80.
El-Sheikh, M., Erath, S.A., Buckhalt, J.A., Granger, D.A., Mize, J., 2008. Cortisol and children’s
adjustment: the moderating role of sympathetic nervous system activity. Journal of
Abnormal Child Psychology, 36, 601—611.
El-Sheikh, M., & Harger, J. (2001). Appraisals of marital conflict and children's adjustment,
health, and physiological reactivity. Developmental Psychology, 37(6), 875.
Feldman, R. (2007). Parent–infant synchrony and the construction of shared timing;
physiological precursors, developmental outcomes, and risk conditions. Journal of Child
Psychology and Psychiatry, 48(3-4), 329-354.
Feldman, R., Greenbaum, C. W., & Yirmiya, N. (1999). Mother–infant affect synchrony as an
antecedent of the emergence of self-control. Developmental Psychology, 35(1), 223.
Field, T. (1982). Affective displays of high-risk infants during early interactions. Emotion and
early interaction, 101-125.
55

Field, T. (1985). Attachment as psychobiological attunement: Being on the same
wavelength. The psychobiology of attachment and separation, 415-454.
Field, T., Diego, M., Hernandez-Reif, M., Vera, Y., Gil, K., Schanberg, S., Kuhn, C., GonzalezGarcia, A. (2004). Prenatal maternal biochemistry predicts neonatal
biochemistry. International Journal of Neuroscience, 114(8), 933-945.
Fogel, A. (1993). Developing through relationships. University of Chicago Press.
Fox, R. A. (1992). Development of an instrument to measure the behaviors and expectations of
parents of young children. Journal of pediatric psychology, 17(2), 231-239.
Frankenhauser, M. (1982). Challenge-control interaction as reflected in sympathetic-adrenal and
pituitary-adrenal activity: Comparison between sexes. Scandinavian Journal of
Psychology, 1, 158-164.
Gazmararian, J. A., Petersen, R., Spitz, A. M., Goodwin, M. M., Saltzman, L. E., & Marks, J. S.
(2000). Violence and reproductive health: current knowledge and future research
directions. Maternal and child health journal, 4(2), 79-84.
Giannakoulopoulos, X., Teixeira, J., Fisk, N., & Glover, V. (1999). Human fetal and maternal
noradrenaline responses to invasive procedures. Pediatric Research, 45, 494-499.
Gilliom, M., Shaw, D. S., Beck, J. E., Schonberg, M. A., & Lukon, J. L. (2002). Anger
regulation in disadvantaged preschool boys: strategies, antecedents, and the development
of self-control. Developmental psychology, 38(2), 222.
Goldsmith, H. H., & Rothbart, M. K. (1999). Laboratory temperament assessment battery
(technical manual). University of Wisconsin-Madison, USA.
Gordis, E. B., Margolin, G., Spies, L. A., Susman, E. J., & Granger, D. A. (2010). Interparental
aggression and parent–adolescent salivary alpha amylase symmetry. Physiology &
behavior, 100(3), 225-233.
Granger, D.A., Kivlighan, K.T., Blair, C., El-Sheikh, M., Mize, J., Lisonbee, J.A., Buckhalt,
J.A., Stroud, L.R., Handwerger, K., Schwartz, E.B. (2006). Integrating the measurement
of salivary alpha-amylase into studies of child health, development, and social
relationships. J. Pers. Soc. Relat. 23, 267—290.
Granger, D. A., Kivlighan, K. T., El-Sheikh, M., Gordis, E. B., & Stroud, L. R. (2007). Salivary
α-amylase in biobehavioral research. Annals of the New York Academy of Sciences,
1098(1), 122-144.
Hibel, L. C., Granger, D. A., Blair, C., & Cox, M. J. (2009). Intimate partner violence moderates
the association between mother–infant adrenocortical activity across an emotional
challenge. Journal of Family Psychology, 23(5), 615.
56

Holmes, M. R. (2013). Aggressive behavior of children exposed to intimate partner violence: An
examination of maternal mental health, maternal warmth and child maltreatment. Child
abuse & neglect, 37(8), 520-530.
Huth-Bocks, A. C., Levendosky, A. A., Theran, S. A., & Bogat, G. A. (2004). The impact of
domestic violence on mothers' prenatal representations of their infants. Infant Mental
Health Journal, 25(2), 79-98.
Isabella, R. A., & Belsky, J. (1991). Interactional synchrony and the origins of infant‐ mother
attachment: A replication study. Child development, 62(2), 373-384.
Isley, S. L., O'Neil, R., Clatfelter, D., & Parke, R. D. (1999). Parent and child expressed affect
and children's social competence: Modeling direct and indirect pathways. Developmental
Psychology, 35(2), 547.
Johnson, V. K., & Lieberman, A. F. (2007). Variations in behavior problems of preschoolers
exposed to domestic violence: The role of mothers’ attunement to children’s emotional
experiences. Journal of Family Violence, 22(5), 297-308.
Kessler, R. C., Molnar, B. E., Feurer, I. D., & Appelbaum, M. (2001). Patterns and mental health
predictors of domestic violence in the United States: Results from the National
Comorbidity Survey. International journal of law and psychiatry, 24(4), 487-508.
Kirschbaum, C., Pirke, K. M., & Hellhammer, D. H. (1993). The ‘Trier Social Stress Test’–a tool
for investigating psychobiological stress responses in a laboratory setting.
Neuropsychobiology, 28(1-2), 76-81.
Laurent, H. K., Ablow, J. C., & Measelle, J. (2012). Taking stress response out of the box:
Stability, discontinuity, and temperament effects on HPA and SNS across social stressors
in mother–infant dyads. Developmental psychology, 48(1), 35.
Leerkes, E. M., Blankson, A. N., & O’Brien, M. (2009). Differential Effects of Maternal
Sensitivity to Infant Distress and Nondistress on Social-Emotional Functioning. Child
development, 80(3), 762-775.
Leung, D. W., & Slep, A. M. S. (2006). Predicting inept discipline: The role of parental
depressive symptoms, anger, and attributions. Journal of Consulting and Clinical
Psychology, 74(3), 524.
Levendosky, A. A., Huth-Bocks, A. C., Shapiro, D. L., & Semel, M. A. (2003). The impact of
domestic violence on the maternal-child relationship and preschool-age children's
functioning. Journal of Family Psychology, 17(3), 275.
Levendosky, A. A., Leahy, K. L., Bogat, G. A., Davidson, W. S., & von Eye, A. (2006).
Domestic violence, maternal parenting, maternal mental health, and infant externalizing
behavior. Journal of Family Psychology, 20(4), 544.
57

Low, S. M., & Stocker, C. (2005). Family functioning and children's adjustment: associations
among parents' depressed mood, marital hostility, parent-child hostility, and children's
adjustment. Journal of family psychology, 19(3), 394.
Malamud, D., & Rodriguez-Chavez, I. R. (2011). Saliva as a diagnostic fluid. Dental Clinics of
North America, 55(1), 159-178.
Marshall, L. L. (1992). Development of the severity of violence against women scales. Journal
of family violence, 7(2), 103-121.
McDonald, R., Jouriles, E. N., Ramisetty-Mikler, S., Caetano, R., & Green, C. E. (2006).
Estimating the number of American children living in partner-violent families. Journal of
Family Psychology, 20(1), 137.
Meaney, M. J. (2001). Maternal care, gene expression, and the transmission of individual
differences in stress reactivity across generations. Annual review of neuroscience, 24(1),
1161-1192.
Middlemiss, W., Granger, D. A., Goldberg, W. A., & Nathans, L. (2012). Asynchrony of
mother–infant hypothalamic–pituitary–adrenal axis activity following extinction of infant
crying responses induced during the transition to sleep. Early human development, 88(4),
227-232.
Moore, K. L., Persaud, T. V. N., & Torchia, M. G. (1988). The developing human: clinically
oriented embryology (pp. 417-418). Saunders.
Nater, U. M., La Marca, R., Florin, L., Moses, A., Langhans, W., Koller, M. M., & Ehlert, U.
(2006). Stress-induced changes in human salivary alpha-amylase activity—associations
with adrenergic activity. Psychoneuroendocrinology, 31(1), 49-58.
Nater, U. M., & Rohleder, N. (2009). Salivary alpha-amylase as a non-invasive biomarker for the
sympathetic nervous system: current state of research. Psychoneuroendocrinology, 34(4),
486-496.
Nater, U. M., Rohleder, N., Schlotz, W., Ehlert, U., & Kirschbaum, C. (2007). Determinants of
the diurnal course of salivary alpha-amylase. Psychoneuroendocrinology, 32(4), 392-401.
Nigg, J. T. (2006). Temperament and developmental psychopathology. Journal of Child
Psychology and Psychiatry, 47(3‐4), 395-422.
O'Leary, K. D. (1999). Psychological abuse: A variable deserving critical attention in domestic
violence. Violence and victims, 14(1), 3-23.
Pally, R. (2010). FRONTLINE-The Brain's Shared Circuits of Interpersonal Understanding:
Implications for Psychoanalysis and Psychodynamic Psychotherapy. Journal of the
American Academy of Psychoanalysis and Dynamic Psychiatry, 38(3), 381-411.
58

Pearson, R. M., Heron, J., Melotti, R., Joinson, C., Stein, A., Ramchandani, P. G., & Evans, J.
(2011). The association between observed non-verbal maternal responses at 12 months
and later infant development at 18 months and IQ at 4 years: A longitudinal study. Infant
Behavior and Development, 34(4), 525-533.
Phillips, D. I., & Barker, D. J. (1997). Association between low birthweight and high resting
pulse in adult life: is the sympathetic nervous system involved in programming the
insulin resistance syndrome?. Diabetic Medicine, 14(8), 673-677.
Phillips, D. I., & Jones, A. (2006). Fetal programming of autonomic and HPA function: do
people who were small babies have enhanced stress responses?. The Journal of
physiology, 572(1), 45-50.
Pico-Alfonso, M. A., Garcia-Linares, M. I., Celda-Navarro, N., Blasco-Ros, C., Echeburúa, E.,
& Martinez, M. (2006). The impact of physical, psychological, and sexual intimate male
partner violence on women's mental health: depressive symptoms, posttraumatic stress
disorder, state anxiety, and suicide. Journal of Women's Health, 15(5), 599-611.
Porges, S. W., & Furman, S. A. (2011). The early development of the autonomic nervous system
provides a neural platform for social behaviour: A polyvagal perspective. Infant and child
development, 20(1), 106-118.
Quené, H., & Van den Bergh, H. (2004). On multi-level modeling of data from repeated
measures designs: A tutorial. Speech Communication, 43(1), 103-121.
Ritchie, K. L., & Holden, G. W. (1998). Parenting stress in low income battered and community
women: Effects on parenting behavior. Early Education and Development, 9(1), 97-112.
Rossman, B. R., & Rea, J. G. (2005). The relation of parenting styles and inconsistencies to
adaptive functioning for children in conflictual and violent families. Journal of Family
Violence, 20(5), 261-277.
Schore, A. N. (2005). Back to basics attachment, affect regulation, and the developing right
brain: linking developmental neuroscience to pediatrics. Pediatrics in Review, 26(6), 204217.
Sethre-Hofstad, L., Stansbury, K., & Rice, M. A. (2002). Attunement of maternal and child
adrenocortical response to child challenge. Psychoneuroendocrinology, 27(6), 731-747.
Shea, A. K., Steiner, M., Brennan, P., Walker, E., Newport, D. J., Stowe, Z. N. (2006). Maternal
depression and salivary alpha-amylase response to stress in their infants. Psychosomatic
Medicine, 68, A5.
Skopp, N. A., McDonald, R., Jouriles, E. N., & Rosenfield, D. (2007). Partner aggression and
children's externalizing problems: Maternal and partner warmth as protective factors.
Journal of Family Psychology, 21(3), 459.
59

Sokolowski, M. S., Hans, S. L., Bernstein, V. J., & Cox, S. M. (2007). Mothers' representations
of their infants and parenting behavior: Associations with personal and social-contextual
variables in a high‐ risk sample. Infant Mental Health Journal, 28(3), 344-365.
Speirs, R. L., Herring, J., Cooper, W. D., Hardy, C. C., & Hind, C. R. K. (1974). The influence
of sympathetic activity and isoprenaline on the secretion of amylase from the human
parotid gland. Archives of Oral Biology, 19(9), 747-752.
Stenius, F., Theorell, T., Lilja, G., Scheynius, A., Alm, J., & Lindblad, F. (2008). Comparisons
between salivary cortisol levels in six-months-olds and their
parents. Psychoneuroendocrinology, 33(3), 352-359.
Straus, M. A. (1979). Measuring intrafamily conflict and violence: The conflict tactics (CT)
scales. Journal of Marriage and the Family, 75-88.
Thoma, M. V., Kirschbaum, C., Wolf, J. M., & Rohleder, N. (2012). Acute stress responses in
salivary alpha-amylase predict increases of plasma norepinephrine. Biological
psychology.
Tjaden, P., & Thoennes, N. (2000). Prevalence and consequences of male-to-female and femaleto-male intimate partner violence as measured by the National Violence Against Women
Survey. Violence against women, 6(2), 142-161.
Van Bakel, H. J., & Riksen-Walraven, J. M. (2008). Adrenocortical and behavioral attunement in
parents with 1-year-old infants. Developmental psychobiology, 50(2), 196-201.
Vigil, J. M., Geary, D. C., Granger, D. A., & Flinn, M. V. (2010). Sex Differences in Salivary
Cortisol, Alpha-Amylase, and Psychological Functioning Following Hurricane
Katrina. Child Development, 81(4), 1228-1240.
Waters, S. F., West, T. V., & Mendes, W. B. (2014). Stress Contagion Physiological Covariation
Between Mothers and Infants. Psychological Science, 0956797613518352.
Young, J. B. (2002). Programming of sympathoadrenal function. Trends in Endocrinology &
Metabolism, 13(9), 381-385.
Young, J. B., & Morrison, S. F. (1998). Effects of fetal and neonatal environment on sympathetic
nervous system development. Diabetes Care, 21, B156-60.

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