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dissertation entitled

DIFFERENTIAL EFFECTS OF CLINICAL DIAGNOSES AND
TRAUMA CHARACTERISTICS ON CORTISOL OUTCOMES
IN VICTIMS OF INTIMATE PARTNER VIOLENCE

presented by

ARCHANA BASU

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DIFFERENTIAL EFFECTS OF CLINICAL DIAGNOSES AND TRAUMA
CHARACTERISTICS ON CORTISOL OUTCOMES IN VICTIMS OF INTIMATE
PARTNER VIOLENCE
By

Archana Basu

A DISSERTATION

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY
Psychology

2010

ABSTRACT
DIFFERENTIAL EFFECTS OF CLINICAL DIAGNOSES AND TRAUMA
CHARACTERISTICS ON CORTISOL OUTCOMES IN VICTIMS OF INTIMATE
PARTNER VIOLENCE
By
Archana Basu

The current study sought to understand how hypothalamic adrenal axis
functioning, as assessed through salivary cortisol, may differ across psychological
disorders that are commonly seen in trauma exposed populations. Another study goal was
to address the lack of theoretical integration in the literature by examining how various
theoretically posited trauma related characteristics (Herman, 1992) might account for
variations in cortisol measures.

As intimate partner violence (IPV) tends to be a chronic form of trauma (Griffin,
Resick, & Yehuda, 2005; Jones, Gross, & Becker, 2002) and female survivors of IPV
have often experienced traumatic events in the early stages of their development as well
(Herman, 1992), examining IPV victims can help to assess the role of various trauma
related characteristics (i.e. early vulnerability factors such as childhood abuse, trauma
chronicity, effects of cumulative types of trauma exposure, and role of social support).
Thus, using a sample of adult premenopausal non pregnant female survivors of IPV, this
study examined whether specific diagnostic groups [e.g., posttraumatic stress disorder
(PTSD), PTSD and Major Depressive Disorder (MDD), and subthreshold symptoms of

PTSD/ PTSD and MDD] would differ from each other, and from a control comparison

group with no lifetime diagnosis of PTSD/ MDD or exposure to IPV, with respect to

cortisol measures. The study examined basal cortisol concentrations, diurnal rhythm of
cortisol, and challenged cortisol measures in the context of a cognitive stress task.

This study did not find support for the effects of the aforementioned diagnostic groups or
trauma related characteristics on the cortisol measures assessed in the study. Findings
from the current study indicated that trauma exposed women had significantly higher
levels of dissociative symptoms, which were inversely related to awakening cortisol
concentrations. This finding is consistent with studies in the literature (Simeon, Yehuda,
Knutelska, & Schmeidler, 2008) which suggest that various trauma related
symptomatology (e.g., PTSD, dissociation) may present with different phenomenological
and neurobiological correlates. As a well controlled study, which improved on multiple
methodological limitations in the literature, these findings require further examination.
Findings suggest that low awakening cortisol concentrations may be a marker for
dissociation, which frequently co-occurs with PTSD, which in turn mediates the effects

between trauma exposure and later development of PTSD.

DEDICATION

To my parents,
Shobharani Basu and Ashok Kumar Basu,
For loving me unconditionally,
For encouraging me to pursue my passion,
For supporting me against the currents of life,
For inspiring me by example.

iv

ACKNOWLEDGMENTS

First and foremost I would like to acknowledge my dissertation chair, Dr. Alytia
A. Levendosky, whose support and guidance were critical in bringing this study to its
fruition. It has been my honor and privilege to work with someone as inspiring,
dedicated, and loving as her. Alytia’s mentorship and compassion have been an
invaluable part of my professional and personal development and will continue to
influence me well beyond my tenure as a graduate student.

I am deeply indebted to Dr. Joe Lonstein, who has been a role model in selfless
mentorship and has influenced me greatly in the time that I worked with him. I thank him
for patiently training me in conducting cortisol salivary assays and providing his
scholarly mentorship and laboratory equipment in support of my study. This study would
not have been possible without his generous support.

I would also like to thank Dr. Kathy E. Stansbury who consulted with me on the
methodological and statistical aspects of collecting and analyzing cortisol data. She
generously made herself available prior to starting her tenure at Michigan State
University and while I was on internship. Finally, I would like to thank Dr. Brent
Donnellan for his thoughtful comments on my dissertation proposal and his support of
my research.

I would like to acknowledge the extramural and intramural sources of funding for
this study - Grants in Aid Award, Society for the Psychological Study of Social Issues,
The Graduate School, Michigan State University, and the Department of Psychology,
Michigan State University. Additionally, I would like to acknowledge Ms. Stacie Dubay

and Ms. Susan Shultz from EVE Inc., who allowed me to recruit participants through

EVE Inc. and use their facilities to complete interviews with women living in their shelter
in a safe manner. I am very grateful to the undergraduate and graduate research assistants
who assisted in data collection for the study. Also, while there are far too many people
than I could possibly acknowledge who encouraged me throughout graduate school and
through the course of this study, I would like to acknowledge some who were particularly
instrumental in supporting me - my husband, Koushik Ganguly, and my friends, Dr.
Janeen A. DeMarte, Dr. Mariam R. Mourad, and Dr. Carolyn J. Dayton. Finally, I would
like to thank the women who participated in this study for sharing some of their most
diffith personal experiences, whose stories of strength and survival continually inspire

my research and clinical endeavors.

vi

TABLE OF CONTENTS

LIST OF TABLES ................................................................................... ix
LIST OF FIGURES .................................................................................. x
CHAPTER 1
Introduction ........................................................................................... 1
Problem of IPV .............................................................................. 9
Mental health consequences of IPV ..................................................... 10
CHAPTER 2
Trauma Theory ...................................................................................... 13
Development of PTSD in IPV ............................................................ 13
Early trauma exposure as a vulnerability factor for IPV ............................. 17
Implications of trauma characteristics ................................................... 19
CHAPTER 3
Neurobiological model of PTSD: The HPA axis ................................................ 27
Review of studies examining basal cortisol in PTSD in children .................... 31
Review of studies examining basal cortisol in PTSD in adults ...................... 34
Diurnal rhythm of cortisol ................................................................ 39
Challenged cortisol ........................................................................ 42
Studies examining IPV and cortisol outcomes ......................................... 46
CHAPTER 4
Rationale &
Hypotheses .................................................................................. 50
Basal cortisol ................................................................................ 50
Hypotheses based on diagnostic classification ................................ 50
Hypotheses based on trauma characteristics ................................... 51
Diurnal rhythm of cortisol ................................................................ 51
Hypotheses based on diagnostic classification ................................ 52
Hypotheses based on trauma characteristics .................................. 53
Challenged cortisol ........................................................................ 54
Hypotheses based on diagnostic classification ................................ 54
Hypotheses based on trauma characteristics ................................... 54
CHAPTER 5
Methods .............................................................................................. 56
Participants ................................................................................. 56
Procedures .................................................................................. 56
Measures .................................................................................... 62
CHAPTER 6
Results ................................................................................................ 69

vii

Missing data ................................................................................. 69

Data transformation ........................................................................ 69
Hypotheses testing ......................................................................... 69
CHAPTER 7
Discussion ........................................................................................... 79
Basal and diurnal cortisol findings ...................................................... 79
Challenged cortisol findings .............................................................. 85
Limitations .................................................................................. 87
Conclusion .................................................................................. 88
APPENDICES ...................................................................................... 90
REFERENCES ................................................................................... 130

viii

Table 1:

Table 2:

Table 3:

Table 4:

Table 5:

Table 6:

Table 7:

Table 8:

Table 9:

Table 10:

LIST OF TABLES

Classification of Sample Based on Diagnostic Groups ...................... 91
Age and Income Across Diagnostic Groups ................................... 92
Education Information Across Diagnostic Groups ........................... 93
Ethnicity Information Across Diagnostic Groups ............................ 94

Descriptive Statistics for Cortisol Values Pre and Post Mean
Substitution ........................................................................ 95
Dissociative Symptoms and Daily Hassles Diagnostic Groups ............. 99

Self Perceived Stress Ratings for Cognitive Stress Task across Diagnostic
Groups ............................................................................. 100

AN COVA for Basal Cortisol Concentrations Across Diagnostic
Groups ............................................................................. 101

Repeated Measures AN COVA for Diurnal Cortisol Concentrations Across
Diagnostic Groups ............................................................... 102

Repeated Measures ANCOVA for Challenged Cortisol Concentrations
Across Diagnostic Groups ...................................................... 103

ix

LIST OF FIGURES

Figure l: Basal Cortisol Concentrations Across Diagnostic Groups .................. 105
Figure 2: Diurnal Cortisol Concentrations Across Diagnostic Groups ................ 106
Figure 3: Challenged Cortisol Concentrations Across Diagnostic Groups............ 107

CHAPTER 1
Introduction

Intimate partner violence (IPV: defined here as male physical or sexual violence,
and threats of aggression against female partners) is a significant public health problem
associated with negative mental health consequences. Battered women are at risk for
developing a range of mental health problems, including posttraumatic stress disorder
(PTSD), which refers to a constellation of symptoms typically seen in the aftermath of an
extreme traumatic stressor (e.g., Cascardi & O'Leary, 1992; Kemp, Green, Hovanitz, &
Rawlings, 1995; Kemp, Rawlings, & Green, 1991). Rates of PTSD among battered
women vary between 45% and 81% based on sample characteristics, the definition of
IPV used, and history of prior interpersonal trauma (Houskamp & F oy, 1991; Kemp et
al., 1995; Sharhabani—Arzy, Amir, Kotler, & Liran, 2003; Stein & Kennedy, 2001). In
addition, battered women are also at an increased risk for developing major depressive
disorder (MDD) and other mood-related difficulties (Cascardi, Langhinrichsen, & Vivian,
1992; Cascardi & O'Leary, 1992; Coker, Watkins, Smith, & Brandt, 2003), a range of
anxiety disorders (e. g., generalized anxiety disorder) (Coker et al., 2002; Kemp et al.,
1991; Moore, Pepler, Mae, & Michele, 1989; Olson et al., 2003; Wolfe, Zak, Wilson, &
Jaffe, 1986), dissociative symptoms (Dorahy, Lewis, & Wolfe, 2007), somatization
(Frasier et al., 2004; Lown & Vega, 2001), and substance use related problems (Coker et
al., 2002; Doyle, Frank, Saltzman, McMahon, & Fielding, 1999; Frasier et al., 2004;
Golding, I999; Kaysen et al., 2008; Sullivan & Holt, 2008; Weaver & Etzel, 2003).

Mental health consequences of trauma exposure, including IPV, are associated

with dysfunctions in the neuroendocrine system including the hypothalamic-pituitary-

adrenal (HPA) axis, which regulates multiple bodily processes including responses to
stress. One measure of alterations in the HPA axis is a corticosteroid called cortisol
produced by the adrenal gland, which is involved in the stress response. Evidence for
alterations in cortisol outcomes in women exposed to a variety of interpersonal and
nonpersonal forms of traumas is mixed with studies reporting high (Lemieux & Coe,
1995; Macs et al., 1998; Rasmusson et al., 2001), low (Yehuda, 2002) and comparable
levels of basal cortisol (i.e., diurnal or 24-hour cortisol concentrations) (Meewisse,
Reitsma, de Vries, Gersons, & Olff, 2007) relative to control comparison groups.
Similarly, studies examining challenged cortisol (i.e., changes in cortisol concentrations
after exposure to a psychosocial or chemical challenge) that assess HPA axis reactivity
also present mixed findings with evidence (Mason et al., 2002) for hyperresponsivity
(e.g., Heim et al., 2000; Lindley, Carlson, & Benoit, 2004) and hyporesponsivity levels
(e.g., Stein, Yehuda, Koverola, & Hanna, 1997; Yehuda, Golier, Halligan, Meaney, &
Bierer, 2004). Finally, studies examining circadian rhythms of cortisol outcomes note
alterations at specific times of the day, most consistently in the waking response of
individuals with chronic trauma exposure, relative to control comparison groups (e.g.,
Johnson, Delahanty, & Pinna, 2008).

There are several methodological limitations in the extant literature examining
cortisol outcomes in trauma exposed adults, including small sample sizes, the lack of
appropriate control for diagnostic comorbidity for disorders that tend to co-occur but are
associated with unique alterations in cortisol concentrations such as PTSD and MDD
(Yehuda, 2002), appropriate controls for the effects of medications (e.g., contraceptives,

anxiolytics), substance use, physical health problems such as autoimmune diseases that

may influence cortisol through their direct effects or the impact of the use of medications,
and the timing, frequency, and type of cortisol sampling. In addition, while a handful of
studies have assessed whether and how characteristics of trauma such as chronicity, age
of trauma onset, severity, and latency of trauma are related to alterations in cortisol
concentrations (Griffin et al., 2005; Johnson et al., 2008; Lemieux & Coe, 1995;
Rasmusson et al., 2001; Yehuda, 2002; Yehuda, Halligan, & Grossman, 2001), few
studies have assessed whether trauma characteristics versus diagnostic outcomes provide
a better organizing framework to understand cortisol dysfimction and if there are any
incremental advantages in combining these frameworks (Johnson et al., 2008; Miller,
Chen, & Zhou, 2007; Pico-Alfonso, Garcia-Linares, Celda—Navarro, Herbert, & Martinez,
2004)

One important issue that has received considerable attention in the literature is the
issue of comorbidity. Although PTSD and MDD are both common sequelae of exposure
to traumatic events, including IPV, their associated basal cortisol levels are significantly
different (Yehuda, Halligan, Golier, Grossman, & Bierer, 2004). For instance, while basal
cortisol concentrations in PTSD tend to be low, those diagnosed with MDD tend to have
high levels, compared to controls (Yehuda, 2002). However, these disorders are
frequently comorbid and some studies suggest that individuals with comorbid diagnoses
of PTSD and MDD may represent a subgroup whose neuroendocrine profile is distinct
from those with either one of the diagnoses only or other diagnoses like acute stress
disorder typically seen in the context of trauma exposure (Stein & Kennedy, 2001;
Yehuda, 2002). Some researchers have suggested that these findings could be indicative

of etiological differences in subtypes of MDD, and that one of the subtypes of depression

maybe more closely linked to the development of PTSD (e.g., Constans, Lenhoff, &
McCarthy, 1997). These findings could also have implications for treatment outcome
research in PTSD. For instance, both psychological and pharmacological treatment
models can be informed by the development of an integrative and comprehensive model
of PTSD that incorporates both neuroendocrine and behavioral components (Friedman,
2002; Rabois, Batten, & Keane, 2002). Similarly, to the extent that trauma characteristics
such as chronicity and age of exposure add incrementally to this understanding, a
developmental model of the stages of evolution of PTSD, particularly chronic trauma
exposure is key (Friedman, 2002). Relatedly, it would also be important to examine
whether the neuroendocrine and behavioral components would differ across comorbid
conditiOns, across different stages of chronic PTSD. These findings have important
methodological implications as well and a number of studies examining cortisol
outcomes in trauma exposed populations fail to use appropriate comparison groups or
control for comorbid symptoms resulting in heterogeneous findings of cortisol outcomes
in PTSD populations.

Another important issue with the current research on the neurobiology of trauma
is the lack of integration of a theoretical framework. Trauma theory provides a useful
framework to examine the development of PTSD, particularly in the context of severe
and chronic forms of trauma such as IPV (Herman, 1992). The theory posits mechanisms
through which specific coping mechanisms adopted in the face of overwhelming stress
eventually become dysfunctional and symptomatic of psychopathology. However,
attempts to integrate findings from empirically tested hypotheses to inform theoretical

understanding of the development of PTSD have been negligible (Miller et al., 2007).

Studies examining cortisol outcomes in adults typically do not examine theoretically
derived hypotheses.

However, there is evidence to suggest that theoretically related trauma
characteristics might play an important role. For instance, a recent meta-analysis of 107
studies examining cortisol outcomes in the context of different types of chronic stress
(assault, abuse, bereavement, unemployment, combat-related war, natural disasters, and
caregiving stress) found that a diagnosis of PTSD does not account for the effects of
various trauma characteristics (e.g., timing) (Miller et al., 2007). Also, consistent with
ideas posited by trauma theory that chronic PTSD has a specific course of development,
researchers have suggested that the development of PTSD may involve different stages of
evolution, each of which is likely associated with unique cortisol outcomes and
neuroendocrine functioning, and behavioral and cognitive profiles (Friedman, 2002).
Thus, findings related to neuroendocrine outcomes can inform theoretical development
and treatment outcomes research in addition to building a comprehensive model of
PTSD.

IPV is one form of trauma that tends to be chronic in nature (Griffin et al., 2005;
Jones et al., 2002). In addition, individuals exposed to IPV have often experienced
traumatic events in the early stages of their development as well, which indicates the role
of early vulnerability factors in the outcomes observed in adulthood (e.g., Heim &
Nemeroff, 2001; Seedat, Stein, & F orde, 2005). Thus, examining IPV victims can help to
examine the differential impact of early vulnerability factors such as childhood neglect
and abuse and later traumatic experiences of trauma such as IPV. Outside the realm of a

prospective longitudinal study, such a population provides the opportunity to examine the

differential impact of chronicity and age of trauma exposure. Research examining the
effects of chronicity and age of onset of trauma on cortisol outcomes has been limited but
indicate that these are important characteristics of trauma exposure that need careful
consideration because chronic exposure to trauma is related to lower levels of basal
cortisol concentration (Heim et al., 2000; Resnick, Yehuda, Pittnan, & Foy, 1995; Santa
Ana et al., 2006; Yehuda, 2002; Yehuda, Halligan, & Bierer, 2002) relative to episodic
trauma exposures (Lemieux & Coe, 1995; Maes et al., 1998; Rasmusson et al., 2001;
Resnick et al., 1995). It is notable that among the studies that have examined the impact
of trauma exposure at different developmental stages, the definition of a developmental
stage is neither empirically supported nor theoretically driven (e.g., Heim et al., 2000;
Santa Ana et al., 2006). Thus, the studies lack specificity about the mechanisms
associated with the age of exposure but do suggest differences in neuroendocrine
functioning depending on the age of trauma exposure and chronicity or the cumulative
effects of trauma exposure over time. Finally, other trauma characteristics that have
received limited attention include the relationship of the victim to the perpetrator in
interpersonal forms of trauma (e. g., Ketring & Feinauer, 1999; Leahy et al., 2004;
Lucenko et al., 2000) and the potential moderating impact of social support (e. g., Regehr,
LeBlanc, Jelley, Barath, & Daciuk, 2007).

Despite the possibilities to examine multiple issues related to the development of
PTSD in the context of chronic trauma, and the varied cortisol profiles found within adult
populations with PTSD, only six studies to date have examined cortisol outcomes in
battered women (Griffin et al., 2005; Inslicht et al., 2006; Johnson et al., 2008; Pico-

Alfonso et al., 2004; Seedat, Stein, Kennedy, & Hauger, 2003; Young, Toman,

Witkowski, & Kaplan, 2004). Taken together they yield mixed findings with respect to
cortisol outcomes and whether risk factors such as IPV or childhood abuse provide a
better organizing framework than diagnostic classification.

With respect to studies of challenged cortisol, a number of studies have examined
responses in traumatized samples in response to a chemical challenge i.e., a low dose
dexamethasone test (DST) but only a handful of studies have examined these outcomes in
the context of a psychosocial stressor in adults with trauma exposure (Carpenter et al.,
2007; Elzinga et al., 2008; Heim et al., 2000; Santa Ana et al., 2006) and only, one study
has examined challenged cortisol outcomes in IPV victims, using a low dose DST
(Griffin et al., 2005). Till date no study has examined the effects of a cognitive
psychosocial stressor on HPA reactivity in IPV victims. Examining challenged cortisol
outcomes in IPV victims can help assess HPA reactivity in individuals exposed to
chronic trauma beginning in early developmental stages, compared to those exposed to
IPV in adulthood alone. This would help better understand HPA reactivity at different
stages of the development of PTSD (Friedman, 2002).

The current study sought to address the aforementioned issues in the literature.
First, the study seeks to use diagnoses, typically seen in trauma exposed and IPV
populations, as an organizing framework to examine how differences in diagnoses (i.e.,
PTSD, comorbid PTSD and MDD, subthreshold trauma! trauma and depression
symptoms, and no lifetime exposure to trauma control comparison group) are related to
alterations in cortisol measures. Specific cortisol measures that the study assessed include
basal (defined as the average of four salivary cortisol samples across the diurnal cycle for

the purposes of this study), diurnal trajectories (over four samplings through out the day),

and challenged (defined as changes in cortisol concentrations in the context of a
psychoscocial stress challenge) cortisol. While studies typically include groups meeting
diagnostic criteria only, the current study also seeks to assess whether a diagnostic levels
of symptom severity is necessary to see alterations in cortisol outcomes i.e. if diagnostic
groups (PTSD only and comorbid PTSD and MDD) would differ from a group of
battered women with subthreshold symptoms of anxiety and mood disorders. Another
area which is largely unexplored in the literature is the role of theoretically relevant
variables, if any, in the observed neuroendocrinological differences within trauma
exposed populations. Thus, this is one of a handful of studies which seeks to assess how
alterations in basal cortisol concentrations, diurnal trajectories of cortisol concentrations,
and challenged cortisol measures are accounted for by various trauma related
characteristics. Specifically, the study examines how trauma characteristics such as
chronicity of trauma exposure (childhood and adulthood versus adulthood exposure
only), age of first trauma exposure, cumulative exposure to different types of trauma
(IPV, IPV and childhood attachment related abuse, and attachment related abuse and non
personal forms of trauma), and social support (general social support and trauma related
social support) affect the aforementioned cortisol measures.

To begin with, chapter one, provides a context for the study’s population of
interest by reviewing the current status of IPV as a public health concern and its
consequent mental health sequelae. Chapter two presents a theoretical framework for the
study and discusses Trauma theory (Herman, 1992) as a basis to understand longitudinal
mechanisms of psychopathology in IPV, particularly the phenomenology of chronic and

severe PTSD in IPV. Within this theoretical framework, mechanisms associated with

early trauma exposure (e. g., childhood abuse) that can constitute a diathesis for
victimization in adulthood and later psychological disorders are discussed to better
understand trauma-related mental health outcomes in adulthood. Chapter three reviews
studies examining basal and challenged cortisol outcomes and the diurnal pattern of
cortisol in adults exposed to trauma. Studies examining cortisol outcomes in early
developmental stages are briefly reviewed to provide a developmental context. Finally,
studies with adult female victims of IPV examining cortisol measures are discussed.
Problem of IPV

The US. Census estimates that the number of adult women (age 18 or older)
experiencing IPV annually is approximately 1.5 million with approximately 4.8 million
incidents of IPV perpetrated against women each year in the US. (Tjaden & Thoennes,
1998; Tjaden & Thoennes, 2000a). According to two national crime surveys,
approximately 20 to 64% of all violence against women is accounted for by IPV
(Rennison, 2003; Tjaden & Thoennes, 2000b) Lifetime prevalence estimates for IPV are
high. Rates of partner rape range between 8 to 10% (Finkelhor & Yllo, 1987; Russell,
1990; Tjaden & Thoennes, 2000b)and rates of physical assault by partners are estimated
at about 22% (Bureau of Justice Statistics, 1998; Tjaden & Thoennes, 2000b)
Community-based studies, which also include psychological abuse in their definition of
IPV, have produced higher estimates ranging between 18 to 57% (Meisel, Chandler, &
Rienzi, 2003; Smith, Thornton, DeVellis, Earp, & Coker, 2002; Waltermaurer, Ortega, &
McNutt, 2003). Abused women are at risk for a range of mental health problems

(Golding, 1999; Kemp et al., 1995), physical injury, (Rennison, 2003; Tjaden &

Thoennes, 1998; Tjaden & Thoennes, 2000a, 2000b), and even fatal injuries due to an
abusive partner (Rennison, 2003), making it a significant public health concern.
Mental health consequences of IPV

Battered women are at high risk for developing PTSD (Ceballo, Ramirez,
Castillo, Caballero, & Lozoff, 2004; Coker etal., 2002; Frasier et al., 2004; Houskamp &
Foy, 1991; Kemp et al., 1995; Kemp et al., 1991; Lipsky, Field, Caetano, & Larkin, 2005 ;
Mertin & Mohr, 2000; Nixon, Resick, & Nishith, 2004; N011, Horowitz, Bonanno,
Trickett, & Putnam, 2003; Pica-Alfonso et al., 2004; Sharhabani-Arzy et al., 2003). Rates
of PTSD among battered women vary between 45% and 81% based on sample
characteristics, the definition of IPV, and history of previous interpersonal trauma
(Houskamp & F oy, 1991; Kemp et al., 1995; Sharhabani-Arzy et al., 2003; Stein &
Kennedy, 2001). In a recent meta-analysis, Golding (1999) calculated the weighted mean
prevalence of PTSD among abused women to be 64% across 11 individual studies
examining the relationship between IPV and PTSD. Furthermore, studies suggest that
frequency and severity of IPV (Cascardi et al., 1992; Houskamp & Foy, 1991; Mertin &
Mohr, 2000; Pico-Alfonso et al., 2004) and chronicity of IPV (Bogat, Levendosky,
Theran, von Eye, & Davidson, 2003) are related to risk and severity of PTSD.

Another common consequence of IPV is depression (Cascardi et al., 1992;
Cascardi & O'Leary, 1992; Christopoulos et al., 1987; Coker et al., 2002; Doyle et al.,
1999; Frank & Dingle, 1999; Kemp et al., 1991; Mitchell & Hodson, 1983; Moore et al.,
1989; Nixon et al., 2004; Olson et al., 2003; Stein & Kennedy, 2001; Wolfe, Crooks, Lee,
McIntyre Smith, & Jaffe, 2003). In a meta-analytic study of 18 studies, Golding (1999)

calculated the mean weighted prevalence rate of 48% for MDD. Other mental health

10

sequelae of IPV include generalized anxiety (Coker et al., 2002; Kemp et al., 1991;
Moore et al., 1989; Olson et al., 2003; Wolfe et al., 2003), somatization (e.g., headaches;
dizziness; gastrointestinal disturbances, joint pain; numbness, tingling, or pain in the
extremities) (Frasier et al., 2004; Lown & Vega, 2001), and dissociation (Dorahy et al.,
2007). In addition, research also suggests that battered women are more likely to report
suicidal ideation (Coker et al., 2002), and a greater number of suicide attempts relative to
non-abused women (Doyle et al., 1999; Frank & Dingle, 1999; Kemic, Wolf, & Holt,
2000; Olson et al., 2003; Roberts, Lawrence, O'Toole, & Raphael, 1997).

It is notable that PTSD and depression are often co-morbid (Golding, 1999). For
instance, in one study of women with recent experiences of IPV recruited from IPV
agencies and medical clinics, researchers found that PTSD and MDD co-occur more
often than would be expected by chance (Stein & Kennedy, 2001) The study also found
that 43% of IPV victims with current IPV-related PTSD also suffered from MDD.
Similarly in another sample of recent IPV victims, Nixon and colleagues (2004) found
that co-morbid PTSD and MDD diagnoses (49%) were more common than a diagnosis of
PTSD alone (27%). The study also found that individuals with comorbid diagnoses had
more severe PTSD and MDD symptoms relative to individuals with a diagnosis of PTSD
alone. Similar outcomes were also reported by Lipsky (2005).,who sampled female IPV
victims fiom an urban emergency department to assess the relationship between past year
PTSD symptomatology and current depressive symptomatology. The study found that
approximately half the sample had symptoms of PTSD. In addition they also had
significantly higher mean total depression scores and higher mean scores on a majority of

the depression subscales than those without PTSD. Finally, the study found that

11

depressive symptomatology, among other factors independently predicted PTSD
symptoms.

IPV is also associated with personality disorders in the women survivors. For
instance, Stanley and Penhale (1999) conducted a pilot study of 13 mothers with severe
mental health problems whose children were involved in the child protection system. The
study found that 6 of the women had been formally diagnosed with a personality disorder
and all 13 women had experienced a history of IPV. Sansone, Reddington, Sky, and
Wiedennan (2007) also reported a relationship between borderline personality disorder
and IPV among a sample of female primary care patients. Sixty four percent of battered
women scored in the clinical range on a measure of borderline personality disorder, as
compared to only 11.1% of non-abused women. These preliminary findings implicate
IPV as an important risk factor for women’s mental health problems, particularly PTSD
and MDD.

In addition to the role of victimization in mental health outcomes adulthood, it is
also important to examine the effects of trauma exposure in preceding developmental
periods to better understand the evolution of mental health outcomes observed in
adulthood. There is evidence to suggest that trauma exposure in childhood likely
constitutes a diathesis for later victimization and hence, the role of early vulnerability

factors is also important to consider

12

CHAPTER 2
Trauma Theory
Development of PTSD fiom IPV

Trauma theory posits mechanisms for the physiological and psychological
sequelae of exposure to traumatic events such as IPV and childhood abuse (Herman,
1992). It explicates the processes underlying early, chronic and severe forms of trauma,
and the role of childhood abuse in dysfunctional and violent relationships in adulthood.

The Diagnostic and Statistical Manual of Mental Disorders Text Revision (DSM-
IV-TR) operationalizes a traumatic event as a situation in which a person perceives a
threat to their life or physical integrity of the self or others. To receive a diagnosis of
PTSD, the person must experience intense fear, helplessness, or horror as a result of such
a perception (American Psychological Association, 2000). Characteristic responses to
trauma exposure involve a complex integration of mental and physical responses. After a
traumatic event the system of self-preservation goes into sustained alert, as though the
danger might return at any moment. Adaptive changes in arousal, attention, perception,
and emotion occur to mobilize the person to fight or to take flight.

Physiological arousal continues unabated and symptoms such as the startle
response and irritability to small provocations are typical. Trauma victims have an
intense reaction to specific stimuli associated with the traumatic event. They respond to
repetitive stimuli associated with, or reminiscent of, the threat as though they are novel
and pose a renewed danger. This hyperarousal also affects sleeping patterns. As noted

earlier, a victim may also suffer from an array of other anxiety symptoms. Following the

13

traumatic exposure they do not Show a return to normal states of arousal but a state of
“relaxed attention” i.e., an elevated baseline of arousal (Herman, 1992, p.36).

Trauma victims also demonstrate intrusive symptoms (e.g., flashbacks).
Traumatic experiences become encoded in an abnormal form of memory which
spontaneously intrudes into consciousness both as flashbacks during the waking states
and also as traumatic nightmares during sleep. Several symptoms of constriction or
negative symptoms that suggest the absence of seemingly natural sequelae are also
characteristic of trauma victims (e.g., calmness instead of the lack of overwhelming
emotions). It has been suggested that during a traumatic event, the overwhelming
helplessness can force individuals to ‘escape’ by altering their state of consciousness,
referred to as “numbing” (Herman, 1992, p.42). This can be described as an ostensibly
paradoxical state of detached calmness, which serves to protect against extreme pain.
Similarly subjective feelings of detachment, enhanced perception of imagery, distortion
of reality, depersonalization, and derealization are also commonly seen in trauma victims
(Herman, 1992). The overwhelming and threatening nature of traumatic events seem to
“. . .recondition the human nervous system” (Herman, 1992, p.36).

Thus, both polarities between heightened perception and numbing symptoms are
frequently noted in trauma victims. Negative or constrictive processes strive to keep
traumatic memories out of consciousness allowing only a fragment of the memory to
surface as an intrusive symptom. This dialectic of opposing states is believed to be the
most characteristic feature of PTSD, and as the person vacillates between intense
flooding feelings and vacant states of no feeling, the sense of unpredictability and

helplessness is heightened, guarding against the integration of the traumatic event.

14

In addition to the physical symptoms, traumatic experiences can have a lasting
impact on the internal representations or schemas of victims. Basic human beliefs, about
relationships and the sense of self that is formed and sustained in relation to others are
shattered. The victim’s fundamental assumptions about safety of the world, positive value
of the self and meaningful order of creation are violated (Ebert & Dyck, 2004; Herman,
1992). In sum, due to the overwhelming nature of traumatic threats, there are lasting
physiological arousal, memory, emotion, attention, and cognitive changes, particularly in
the face of repeated or chronic trauma.

IPV victims are typically exposed to both psychological and physical domination,
resulting in significant distortions in the representations of the perpetrator (Herman,
1992). Perpetrators’ techniques involve organized efforts directed towards
disempowerrnent and disconnection of the victim by instilling terror and subjugation and
destroying the victim’s sense of self in relation to others. This may take on the form of
threats against others (e. g., friends, relatives, children, parents), who are important to the
victims or may harbor or protect the victim. Often loyalty towards the perpetrator
requires severing relationships or attachments with others. This typically manifests as
relentless accusations of infidelity, demonstrations of jealousy and demands of both
physical and symbolic disconnection from others. For instance, token concessions and
sacrifices (e. g., burning photographs or letters of loved ones) maybe required.

Fear is typically instilled through unpredictable amounts of violence and
enforcement of random petty rules that not only seek to instill fear but also a sense of
gratitude for being allowed to live. After experiencing several cycles of reprieve from

death, the victim eventually comes to see the perpetrator in the role of a savior. The

15

physical disconnection increases the victim’s dependence and survival on the perpetrator
because the more frightened they are the more they cling to their abuser or savior. In
doing so victims seek out the humanity in the perpetrator and may eventually come to see
the world through the perpetrator’s perspective

However, psychological control of a victim is only complete when she has been
forced to violate her own moral principles. Violation of principles may involve sexual
humiliation and coercion into practices that they find immoral, or disgusting. This might
also extend to abuse of the victims’ children. Several studies show a significant
association between partner abuse and child abuse (Duhamel & F ortin, 2004; Taj ima,
2004). This pattern of betrayal may start small but eventually progresses into outrageous
physical or sexual abuse (Herman, 1992).

Traumatic events destroy the belief that one can be oneself in relation to others.
In some cases survivors may direct their rage and hatred against themselves. The
internalization of the blame or fear possibly from the traumatic experience may lead to
the development of other psychological disturbances (Olff, Langeland, & Gersons, 2005)
and suicidality may become a form of resistance (Herman, 1992).

Chronic trauma, including IPV, can erode the personality structure of a victim.
Chronic abuse amplifies hyperarousal symptoms of PTSD, as they are continually
hypervigilant, anxious and agitated. Avoidance and constriction also become prominent
as the victim goes into sustained survival mode and psychological constriction is critical
to such survival. Staggering psychological dysfunction and loss can also result in a state
of depression. In such conditions, Hermann (1992) argues that chronic hyperarousal and

intrusive symptoms of PTSD may fuse with vegetative symptoms of depression. Thus,

16

attachment disruptions, the loss of faith and beliefs merge with the isolation and
hopelessness of depression. The debased self-irnage of chronic trauma forms the basis for
guilty ruminations in depression and in extreme cases dissociative symptoms as well.

However, there is evidence to suggest that adults exposed to IPV have also
experienced significant trauma in earlier stages. For instance, survivors of childhood
abuse and neglect are also involved in dysfirnctional and/or violent relationships in
adulthood (Drapeau & Perry, 2004; Haller & Miles, 2003; Seedat et al., 2005), being
raped or sexual harassed (Heim et al., 2002; Russell, 1986). This suggests that a)
chronicity of trauma predates victimization in adulthood, b) observed mental health
outcomes could be a result of a more longitudinal course of trauma and c) developmental
mechanisms across the lifespan need to be examined to better understand outcomes in
adulthood.
Early trauma exposure as a vulnerability factor for IPV

Trauma theory not only explicates processes associated with chronic IPV but also
posits mechanisms associated with exposure to abuse in childhood that can lead to
psychological problems and an increased risk for revictimization in adulthood. According
to the theory, abused or neglected children have to adapt to an unsafe and often
horrifyingly unpredictable environment. These experiences lead to resourceful, but also
destructive, capacities for abnormal states of consciousness, which manifest as an array
of perceptual, cognitive, somatic, psychological, and memory-related distortions or
difficulties (Herman, 1992; Pollak, Klorrnan, Thatcher, & Cicchetti, 2001; Pollak, Vardi,
Putzer Bechner, & Curtin, 2005). Children growing up in an environment of domination

and abuse develop pathological attachments to their abusers, attachments that they strive

l7

to maintain even at the expense of their own well-being (Bowlby, 1982). Adaptation to
such a climate of constant danger requires a constant state of alertness and children in an
abusive environment develop extraordinary abilities to scan for warning signs.
Consequently, Hermann (1992) posits that the development of psychological disorders is
rooted in the array of psychological defenses utilized to cope with such an unpredictable
and threatening environment. For instance, some experiences maybe blocked off from
conscious awareness and memory, and other experiences maybe minimized or
rationalized so that they are not construed as abuse, essentially creating pathways for
cognitive distortions and dissociative states (Herman, 1992)

One consequence of these seemingly adaptive defenses is that emotion regulation
is severely affected as normative feelings of anger, rage, and hurt have to be contained
and compliance has to be maintained. The development of a cohesive and well integrated
sense of sense or self-representation becomes a challenging task because certain
experiences are exaggerated and split off (Bowlby, 1982). Such processes are believed to
be the basis for self-blame i.e., a sense of inherent badness to make sense out of the
abusive environment that can be used to justify future negative experiences in adulthood
as well, and form the basis of a fragmented or dysfunctional personality, consciousness,
and memory (Herman, 1992).

The unpredictable and dictatorial parental power of an abusive parent is akin to an
adult violent partner’s demands for complete control and subjugation. Hermann (Herman,
1992) further argues that IPV in adulthood forces victims to revisit developmental
conflicts and relive her earlier struggles of autonomy, initiative, competence, identity,

and intimacy. With fundamental problems in trust, autonomy, independence and

18

intimacy, childhood abuse survivors are driven by fear of abandonment, or exploitation
and there is a continual quest for rescue through a powerful savior, who will protect and
care for them. The tendency to denigrate oneself, and engage in minimization,
rationalization, and idealize those that the victim is attached to, clouds the judgment of
the victim, and makes the victim attuned and obedient to the wishes of others, making her
vulnerable in the future. It is notable that these processes do not implicate that abuse is
actively sought out but rather that the victim’s internal representation of intimate
relationships is distorted to fear abuse as an unavoidable fate and accepted as the cost of a
relationship. Consequently adult survivors of trauma and abuse are at a greater risk for
repeating victimization in adult life.

In sum, childhood abuse and neglect has a significant negative impact on the
psychological make-up and personality of an individual. These effects can be long lasting
due to an increased risk for psychopathology and maladaptive cognitive schema that
extend into later developmental stages.

Implications for trauma characteristics

Within this theoretical framework various trauma characteristics are posited to
influence psychological outcomes, and are reviewed below.

Age of trauma exposure

One characteristic of trauma exposure that has been theoretically and empirically
posited to be an important factor is the age of trauma exposure. Studies with humans
(e.g., Swett, Surrey, & Cohen, 1990; Teicher, Glod, Surrey, & Swett, 1993) and animal
models (see Heim & Nemeroff, 2001 for a summary of findings) have consistently shown

that early exposure to traumatic events can have a lasting negative impact. The effects of

19

such trauma exposure are believed to be more magnified and/ or enduring, when they
occur during the formative years, when physical and neurobiological systems are
maturing, and attachment relationships with significant caregivers are still developing
(Schore, 2002a). The critical period for the establishment of an attachment relationship
also overlaps with rapid physiological and brain maturation (Schore, 2002b). Traumatic
experiences during such a critical period of development, in the absence of a protective
caregiving presence, or worse, if the caregiving system itself is a source of the trauma, is
likely to result in significant levels of arousal and inadequate reparative experiences.
Given the importance of this developmental period, trauma exposure in early
developmental periods can lead to a dysfunctional trajectory of physiological, emotional,
and psychological development, (Cicchetti & Curtis, 2006; Heim & Nemeroff, 2001;
Pryce et al., 2005).

The most commonly examined traumatic event is childhood sexual abuse
(Banyard & Williams, 1996; Bunce, Larsen, & Peterson, 1995; Johnson, Pike, & Chard,
2001). However, studies with other types of abuse and trauma exposure such as the
holocaust also report similar findings (Yehuda, Schmeidler, Siever, Binder-Brynes, &
Elkin, 1997). In general studies report an inverse relationship between age of childhood
sexual abuse and the severity of depression, dissociation (Johnson et al., 2001), and
anxiety symptoms (Bunce et al., 1995) and low self-esteem (Bunce et al., 1995) in
adulthood. As noted earlier, the rates of revictimization among survivors of childhood
abuse victims is high and hence, it is difficult to assess the independent impact of the age
at the time of trauma exposure is responsible for adult psychological problems,

particularly as it is based on retrospective reports. For instance, Nishith, Mechanic, and

20

Resick (2000) examined PTSD symptoms as a function of childhood sexual physical
abuse versus adult sexual and physical abuse. This study found childhood abuse and adult
victimization together, were more predictive of PTSD symptoms rather than childhood
abuse alone.

In a study by Banyard and Williams (1996), childhood sexual abuse victims were
interviewed prospectively (soon after the experience of abuse after receiving emergency
services) and age of trauma experience was found to be an important predictor of mental
health outcomes in adulthood. However, when the same participants were re—exarnined
20 years later in adulthood, and asked for retrospective reports of the same abuse
information, these age-related effects were no longer significant. It notable that many in
the sample also experienced high rates of revictimization in adulthood. Thus, differences
in findings could reflect a methodological confound of retrospective reports as
recollections of the details of the abuse maybe influenced by concurrent levels of distress
in adulthood (Henry, Moffitt, Caspi, Langley, & Silva, 1994) and/ or the findings could
reflect the confounding effects of chronicity/ cumulative experiences of trauma, such that
outcomes in adulthood could be a result of the cumulative effects of trauma across the
lifespan.

In a retrospective study of Holocaust survivors Yehuda and colleagues (1997)
examined the impact of the Holocaust 50 years after the experiences and found that age at
the time of Holocaust was inversely related to PTSD symptoms such as psychogenic
amnesia, emotional detachment, and hypervigilance. Thus, while age of trauma exposure
is an important characteristic for understanding mental health outcomes in adulthood,

chronicity of trauma is a common confounding factor due to high rates of revictimization

21

in adulthood in childhood abuse survivors. In addition, these findings are difficult to
examine retrospectively. Finally, experiences of trauma in adulthood are also likely to
independently contribute to this pre-existing vulnerability and needs firrther examination.
Cumulative Eflects of Trauma Exposure Based on Relationship to Perpetrator

One aspect of trauma related research that has received considerable evidence
with respect to theoretical development but limited empirical examination is the
relationship of the perpetrator to the abuse victim. There is limited evidence from
empirical studies suggesting that an abuse victim’s perceptions of, and reactions to, the
traumatic experience is affected by her relationship with the perpetrator (e. g., Ketring &
Feinauer, 1999; Leahy, Pretty, & Tenenbaum, 2004; Lucenko, Gold, & Cott, 2000).

According to attachment theory, the relationship between a child and her primary
caregiver has important survival implications for the infant (Bowlby, 1982). The quality
of the caregiver’s responses reinforces certain patterns of behaviors that are learned and
internalized because they ensure proximity with the caregiver and consequently survival
for the infant. These internalized schemas form an information processing template by
incorporating expectations, feelings, and behaviors towards others. In this way, lived
experiences with the caregiver help the infant develop a core self of self and others, and
are considered important for psychological, affective, and behavioral regulation.
Similarly, trauma theory also posits that abuse within the family is comparable to extreme
forms of trauma exposure such as war-related torture, because of the horrific
transgression that it represents (Golding, 1999; Herman, 1992).

The effect of the relationship of the perpetrator to the victim is most commonly

examined in childhood abuse literature. A national survey of child rape found that 48% of

22

sexual crimes were perpetrated by a trusted non-relative, 41% by relatives, and 11% by
strangers (Saunders, Kilpatrick, Hanson, Resnick, & Walker, 1999). A commonly cited
reason for these findings is that family members and close non-relatives are most likely to
have the opportunity to perpetrate. In cases where family members are perpetrators, the
source of abuse is also the source of safety and basic needs, which poses a tremendous
psychological challenge for victims.

Studies that have examined the impact of perpetrator relationship to victim, on the
psychological outcomes of abuse have found some support for the fact that abuse at the
hands of a caregiver or attachment figure leads to more deleterious outcomes relative to
perpetration at the hands of a stranger. However, only a limited number of studies have
examined these outcomes using heterogeneous methodologies and varying sample
characteristics. Most importantly, studies that have failed to find a difference with respect
to perpetrator status have not examined the impact of possible protective factors, making
it difficult to interpret the lack of differential effects.

For instance, Banyard and Williams (1996) found that the relationship to the
perpetrator was a significant predictor of outcomes 20 years later such as emotional
distress, sleep problems, dissociative experiences, and overall psychological symptoms.
Similarly Leahy and colleagues (2004) reported significantly higher level of PTSD
symptoms and dissociative symptoms for survivors of childhood sexual abuse by trusted
individuals, guardians/caretakers compared to sexual abuse by other individuals.
Perpetration by a father figure has been found to be predictive of high levels of

psychological symptoms in adulthood, followed by family members and acquaintances,

23

and finally strangers (Ketring & Feinauer, 1999). Findings from these studies suggest that
the survivor’s relationship with the perpetrator influences adult psychological symptoms.

In contrast, in one study, the effects of perpetrator relationship, caregiving duties,
and residential proximity (i.e., if the perpetrator resides with the victim) in adult survivors
of childhood sexual abuse were examined in relation to PTSD symptoms (Lucenko et al.,
2000). The authors reported that PTSD symptoms were higher in survivors of childhood
sexual abuse perpetrated by persons that did not have caretaking responsibilities for the
victims. In another study Johnson and colleagues (2001) found that the relationship and
level of trust with the perpetrator was not significantly related to PTSD, depression, or
dissociation symptom severity. While these studies present contradictory results, it is
notable that both studies included samples from a population of treatment seeking
victims, which may not be representative of all survivors of childhood sexual abuse. In
comparison, studies that found significant differences in psychological symptoms based
on relationship to perpetrator were recruited from random surveys.

In addition to the differential impact of perpetrator type on mental health
sequelae, there is also evidence to suggest that cumulative trauma exposure has
deleterious effects on later psychological outcomes (Briere, Stacey, & Green, 2008;
Suliman et al., 2009). For instance, in a large college study of women, Briere and
colleagues (2009) found a linear relationship between exposure to different types of
traumatic events (cumulative trauma) in childhood and symptom complexity in
adulthood. Similar findings were reported by Suliman and colleagues (2009) in a large
adolescent sample who had experienced multiple traumatic stressors with respect to

PTSD and depressive symptoms.

24

Despite evidence for the effects of perpetrator relationship to victims and
cumulative trauma exposure on the severity of psychological outcomes, no study has
examined the impact of cumulative trauma exposure in the context of perpetrator type on
cortisol outcomes.

Social Support

An important moderator of trauma related outcomes is social support. Typically
social support networks include family members, relatives, friends, and peers (Rosenthal,
F eiring, & Taska, 2003). Trauma can erode the sense of trust in others, and Herman
(1992) argues that positive social support is a necessary aspect of recovering fiom
traumatic experiences. Furthermore, trauma theory also posits that recovery from a
traumatic event is associated with the type of support received in relation to the traumatic
experience. Thus, while it is important to examine general levels of social support which
has been shown to have a significant moderating influence on the impact of trauma on
psychological outcomes (Bal, De Bourdeauhuj, Crombez, & van Oost, 2005; Banyard &
Cantor, 2004; Gold et al., 2000; King, King, Foy, & Gudanowski, 1996; Levendosky et
al., 2004; Regehr et al., 2007) it is also critical to examine support received in the
immediate aftermath of trauma exposure (Davis & Brickman, 1991).

However, the quality of social support is also an important characteristic. For
instance, Davis and Brickman (1991) examined whether type of social support moderated
psychological adjustment in adult rape victims. This study found that while positive
social networks did not influence psychological symptoms, unsupportive social networks
had a negative impact on psychological outcome. Similarly, in a study of pregnant

Women exposed to IPV, Levendosky and colleagues (2004) examined the impact of the

25

quality of social support on psychological outcomes. This study found that having a high
ratio of supporters who had also experienced IPV to supporters who had not experienced
IPV predicted impaired quality of support among battered women. It is possible that
social support network members suffering from similar problems are unable to provide
support to others that can help them rebuild their sense of trust. Thus, findings suggest
that not all forms of social support are beneficial for positive health outcomes and it is
crucial to examine the level and quality of support received from others, in relation to the
traumatic event.

In sum, several theoretically driven moderators of trauma outcomes have been
posited to influence the longitudinal mechanisms of psychopathology in the context of
trauma. These need to be better integrated in empirical research examining outcomes of
traumatic experiences at multiple levels including neurobiological and psycho-emotional
functioning to gain a more comprehensive understanding of traumatology and as a next

step, to help tailor psychosocial and pharmacological interventions.

26

CHAPTER 3
Neurobiological model of PTSD: The HPA Axis
The HPA axis is one of the biological systems that has been the focus of trauma-
related research. Within this system, cortisol is the main hormone that has been
examined. Activation of the HPA axis begins in the locus coeruleus and results in the
release of neurotransmitters such as norepinephrine, serotonin, and dopamine. They, in
turn, activate the amygdala to stimulate the hypothalamus to release corticotrophin-
releasing factor, which stimulates adrenocorticotropic hormone (ACTH) secretion.
ACTH secretion results in elevated cortisol levels. To avoid the detrimental effects of
prolonged HPA activation and to inhibit its own release, cortisol acts on pituitary and
brain receptors a negative feedback mechanism to return these hormonal levels to a state
of equilibrium (Heim & Nemeroff, 2001; Heim et al., 2002). Thus, the axis forms a
closed loop negative feedback system, which regulates cortisol levels.

These neuroendocrine changes, or allostatic adjustments, are meant to help short-
term adaptations in the face of a stressor. Thus, chronic high levels of stress have been
associated with damaging consequence, and the cost of maintaining allostasis i.e.,
stability or homeostasis through physiological or behavioral change, is referred to as
allostatic load. This allostatic load has been shown to have negative effects on various
physiological systems such as hormonal imbalance and HPA axis dysregulation (Heim et
31-, 2000; King, Mandansky, King, Fletcher, & Brewer, 2001; Saltzman, Holden, &
Holahan, 2005), neuronal loss in the hippocampus (Bremner et al., 1995; Sapolsky,

1 996; Tupler & De Bellis, 2006), electroencephalographic abnormalities (e. g., Anda et

31-, 2002; Ito et al., 1993; Teicher et al., 1997), skin conductance responsivity, increased

27

heart rate and blood pressure (e.g., Perry, 1994; Saltzrnan et al., 2005), and changes in
immune functioning (e. g., Altemus, Cloitre, & Dhabhar, 2003). However, despite
significant evidence of neurobiological changes and dysfunction, studies examining
cortisol outcomes in the context of exposure to traumatic events present a complicated
picture.

Chronic activation of the HPA system, typical in the context of repeated exposure
to trauma, can have deleterious effects on physiological functions. However, there is
considerable variability in findings of cortisol outcomes in adults, with several studies
indicating elevated levels of basal cortisol (Lemieux & Coe, 1995; Maes et al., 1998;
Rasmusson et al., 2001), and findings fiom a recent meta-analysis which included 37
studies (PTSD N=828 ; Control N= 800) suggesting no differences in basal cortisol levels
(Meewisse et al., 2007).

The lack of uniformity in findings is confounded with methodological differences
across studies. One key issue in this regard is related to the timing, frequency, and type of
cortisol measurement. For instance, studies examining blood or salivary cortisol levels,
particularly those using a single sampling of cortisol, do not take into account individual
variation in sleep cycles. This is a crucial issue because cortisol levels have a specific
diurnal cycle such that there is steady decline in cortisol levels after it peaks
approximately 30 minutes post-awakening. Thus, the variation in cortisol outputs is
significantly increased even with a difference of several nrinutes in wake-time.

Another important issue related to diurnal differences in cortisol outcomes is the
type of cortisol measurement. While salivary and urinary cortisol levels typically reflect

“free” or an ambient fraction of the cortisol hormone, plasma samples indicate total

28

cortisol. Thus, the type of cortisol measurement and the number of cortisol measurements
are both important methodological indicators. For instance in their meta-analytic study
Meewisee and colleagues (2007) conducted subgroup analyses assessing the effects of
type of cortisol on basal cortisol levels and found that plasma or serum studies showed
significantly lower levels of cortisol in PTSD samples rather than control or non-exposed
groups (Meewisse et al., 2007). However, it is notable that this study used the “earliest”
(with respect to time of day) sample of cortisol available in each study in their analyses
thereby using only one data point from each study rather than calculating a combined
effect size for each individual study when salivary/ urinary samples were utilized. In fact
several researchers argue in favor of utilizing salivary cortisol because it allows an
assessment of free or ambient cortisol, which coupled with multiple samplings, provides
a more nuanced examination of the trajectory of diurnal cortisol as well as challenged
cortisol outcomes. Also, salivary cortisol offers significant advantages over urinary free
cortisol with respect to ease of collection, and assays and greater reliability relative to
other types of cortisol (Young & Breslau, 2004b).

In addition to the methodological issues associated with timing, frequency, and
type of cortisol, other issues such as small sample sizes, adequate control for trauma
characteristics while examining the effects of diagnostic status and vice versa are
commonly seen in the literature and are reviewed in further detail ahead. However, not all
variations are attributable to methodological differences alone and certain commonalities
have emerged in the literature. For instance, some researchers have suggested that
variations in basal cortisol alterations may represent biological subtypes of PTSD.

Repeated activation and hyperarousal typically seen in the face of chronic trauma is

29

believed to be countered by increased negative feedback to maintain homeostasis and
regulate levels of plasma cortisol. This increased negative feedback is believed to be the
basis fOr lower levels of basal cortisol outcomes (Yehuda, 2002). Low cortisol and
enhanced negative feedback are understood to represent a biological subtype of PTSD
associated with more chronic, or early exposure to, trauma (Miller et al., 2007;
Rasmusson et al., 2001; Yehuda, 2002; Yehuda, Halligan, & Grossman, 2001). Other
evidence from studies examining the effects of PTSD and MDD comorbidity suggest that
another biological subtype of PTSD, associated with higher levels of cortisol, is likely to
be comorbid with depressive disorders (Olff, de Vries, Guezelcan, Assies, & Gersons,
2007; Olff, Guezelcan, de Vries, Assies, & Gersons, 2006; Rasmusson et al., 2001;
Yehuda, 2002; Young & Breslau, 2004a, 2004b).

Characteristics of trauma such as chronicity, age of trauma exposure, role of
protective factors such as social support, and type of trauma exposure have also received
some attention in adult populations. For instance, chronicity of trauma has been examined
in multiple studies as a predictor of cortisol outcomes in adulthood. As noted earlier
researchers have hypothesized that the enhanced negative feedback inhibition likely
develops over time in response to the chronic trauma and represents a biologic subtype of
PTSD (Yehuda, 2002).

Research in child and adult samples has shown dysfunction in HPA axis. Thus
individuals’ outcomes in adulthood need to be examined as a function of early childhood
exposure to trauma as well as IPV, particularly because there is evidence to suggest that

early childhood constitutes a critical period of experience-dependent brain development

30

and consequently outcomes of early childhood trauma can extend into adulthood (e.g.,
Anderson, Teicher, Polcari, & Renshaw, 2002).
Review of basal cortisol outcomes in PTSD in children

In general, the limbic system, which plays a critical role in emotion regulation, is
most affected by adverse exposure during childhood when these systems are still
developing (McCollum, 2006). Although the developing and limited sensory and
perceptual systems of young children place limits on the amount of sensory information
processing they can occur, children’s innate tendencies to adapt, results in increased
attendance to the more salient cues in the environment at the expense of other aspects.

For instance, maltreated children’s organization of the emotional systems
themselves become based upon processing highly salient cues Of interpersonal hostility or
threat to the self. A number of studies have found support for this form of selective,
experienced based learning in maltreated children’s perception of emotion and attention
regulation (Pollak, 2005; Pollak, Cicchetti, Homung, & Reed, 2000; Pollak & Kistler,
2002; Pollak et al., 2001; Pollak & Sinha, 2002; Pollak & Tolley-Schell, 2003; Pollak et
al., 2005). For instance, maltreated preschoolers have been found to perceive angry faces
as highly salient in contrast to other facial displays of emotions (Pollak et al., 2000),
display a lower threshold to detect angry facial expressions (Pollak & Sinha, 2002), and
have altered abilities to discriminate and categorize angry facial expressions such that
they use broader perceptual boundaries for anger perception (Pollak & Kistler, 2002).
Similarly, studies also found that maltreated children engage in anticipatory monitoring
of the environment for anger related cues (Pollak, 2005). A series of event-related

potential studies also found that maltreated children demonstrate differential neural

31

processing of anger related stimuli, but not for other emotional expressions or non-
emotional content when compared to age matched peers (Pollak et al., 2001).

There is also evidence for HPA axis dysfunction in childhood and adolescence in
the context of trauma (e.g., Carrion et al., 2002; DeBellis et al., 1999; Goenjian et al.,
1996; Hart, Gunnar, & Cicchetti, 1996; Kaufman etal., 1997; King et al., 2001; Lipschitz
et al., 2003; Saltzrnan et al., 2005). For instance, Saltzrnan and colleagues (2005)
examined HPA axis functioning in children, between 5 and 13 years of age, exposed to
IPV (n=21) in comparison to a clinical group of children (n=27) who were receiving
mental health services for symptoms of anxiety, depression, and disruptive behavior, but
had no documented or self-reported history of IPV in the family. Salivary cortisol was
assessed pre- and post-interview to assess basal functioning, and the response to
interview which included an assessment of their IPV exposure and trauma symptoms.
With respect to HPA axis functioning, IPV exposure was associated with higher levels of
basal salivary cortisol. The mean basal cortisol levels were 62% higher in IPV exposed
children, and they continued to display higher levels of cortisol post-interview as well.
This study did not assess the timing or chronicity of IPV exposure, nor did it control for
the high comorbidity of child abuse (direct physical violence from a caregiver) in the
children exposed to IPV (48%). While this is likely to be representative of what children
from households with IPV generally experience, this makes it difficult to examine the
unique effects of IPV exposure and child abuse. Similarly, others studies have examined
the effects of trauma or depression, due to various types of abuse and neglect, on HPA
functioning, without assessing the contribution of specific types of traumatic events

(Carrion et al., 2002; Kaufman et al., 1997; Lipschitz et al., 2003). For instance, Carrion

32

and colleagues (2002) compared 51 trauma-exposed children (30 boys and 21 girls) to 31
age and gender matched healthy controls (age range 7-14 years) on their diurnal salivary
cortisol measured 4 times a day over the course of 3 days. Their study found significantly
elevated cortisol levels in the trauma exposed group compared to the control group.
Nearly 51% of the children in trauma-exposed sample had experienced multiple
traumatic events.

In another study Kaufman and colleagues (1997) assessed HPA axis functioning
in children with a history of abuse using a corticotropin-releasing hormone challenge
intravenously. The sample consisted of depressed abused (n=13), depressed nonabused
(n=13) and healthy control children (n=13). The depressed abused children were further
segregated as those who continued to experience ongoing adversities (e.g., emotional
abuse, poverty, IPV exposure) and those that were living in fairly stable home
environments. The authors found significantly elevated levels of cortisol levels in the
group of abused depressed children who were also experiencing concurrent adversity.
The other subgroups displayed similar levels of cortisol levels. While this finding is
consistent with Hart and colleagues (1996), who reported greater aftemoon salivary
cortisol levels in depressed maltreated children when compared to depressed
nonmaltreated children, it is in contrast to DeBellis and colleagues (1999) study with
sexually abused girls who were also administered a CRH challenge. However, in the
latter study the girls were living in fairly stable homes. In a later study DeBellis and
colleagues (1999) compared cortisol levels in children exposed to multiple form of
trauma, who were diagnosed with PTSD (n=15), with age and gender matched children

with other anxiety-disorders only (n=10) and healthy nonabused controls (n=24), and

33

found significantly increased cortisol levels in the PTSD group compared to all other
comparison groups.

In studies examining cortisol levels in adolescents (Goenjian et al., 1996;
Lipschitz et al., 2003) the findings have been mixed. Goenjian (1996) reported lower
basal cortisol levels in adolescents (n=37) in two Armenian cities, 5 years after they had
experienced an earthquake. In contrast Lipschitz and colleagues (2003) examined cortisol
levels in adolescents with current PTSD (n=20), controls with trauma-exposure and no
PTSD (n=9) and healthy controls (n=l9). In response to a chemical challenges using DST
all groups performed similarly with respect to cortisol outcomes. However, all subjects
who had PTSD and comorbid diagnoses of major depression had significantly higher
levels of basal salivary cortisol compared to the other adolescents. In a sample of children
and adolescents (ages 8-18) Delahanty and colleagues (2005) examined cortisol levels in
56 boys and 26 girls. The sample was recruited from hospital trauma centers and most of
the participants were involved in a vehicular accident. This found that higher levels of
cortisol were associated with greater PTSD symptoms.

Review of basal cortisol outcomes in PTSD in adults

While cortisol outcomes in children have implicated dysfunction in the HPA axis,
they have typically indicated higher levels of cortisol output. In contrast, findings from
adult studies, which also indicate HPA axis dysfunction, have typically shown lower
levels of basal cortisol relative to healthy controls. Thus, researchers have posited that in
the face of chronic exposure, unlike exposure limited to childhood, the HPA axis
develops an enhanced negative feedback inhibition (Yehuda, 2002).Typically studies

with adults that have examined recently traumatized subjects have reported elevated

34

cortisol levels, (Lemieux & Coe, 1995; Maes et al., 1998; Rasmusson et al., 2001).
Relatedly, studies taking into account the effects of prior victimization provide further
support for this hypothesis. For instance, in a study of female victims of rape, Resnick
and colleagues (1995) reported lower levels of cortisol in women who also had a prior
history of assault. Only women without a prior history of traumatization had higher levels
of cortisol. Women with lower cortisol levels and prior history of assault also had a
higher probability of developing PTSD, implicating the role of early vulnerability factors
and/or the impact of cumulative trauma exposure.

Evidence that prior history of trauma and lower protective factors affects cortisol
outcomes also comes from a study of police recruits enrolled in basic constable training
program by Regehr and colleagues (2007). Study participants (n = 84; 71.4% male) were
exposed to a stressful simulation of a policing procedure. Cortisol outcomes were related
to subjective reports of psychological stress which in turn was predicted by prior history
of trauma and reduced social support. The study found no direct relationship between
cortisol levels and prior history of trauma or trauma symptoms, suggesting a mediated
model of alterations for cortisol outcomes such that a vulnerability to psychological
stress, induced through a history of traumatization, is heightened or reactivated in later
situations of acute stress resulting in altered cortisol outcomes. This is the only study
examining the impact of social support on cortisol outcomes.

The development of an enhanced negative feedback inhibition in response to
chronic trauma also suggests that other characteristics of trauma such as severity and
potentially the age of trauma exposure could also have an impact on cortisol outcomes.

With respect to severity of symptoms, findings suggest an inverse relationship between

35

cortisol levels and severity of trauma consistent with the enhanced negative feedback
inhibition mechanism (Boscarino, 1996; Yehuda, Boisoneau, Lowy, & Giller, 1995). For
instance Boscarino (1996) found lower basal cortisol in a large epidemiologic sample of
over 2000 Vietnam veterans with PTSD compared to those without PTSD. Cortisol levels
were significantly lower in combat veterans with very high exposure compared with
those with low or no exposure. Similar findings were also reported in a smaller sample of
Vietnam veterans with respect to combat severity and morning cortisol outcomes
(Yehuda et al., 1995). In sum, victims exposed to chronic forms of trauma, particularly a
combination of childhood and adult victimization are more likely to evidence lower
levels of basal cortisol while those experiencing relatively recent traumatic events only
are more likely to demonstrate elevated levels of basal cortisol.

Relatedly, studies also suggest that severity of PTSD symptoms, which are likely
to be positively correlated with severity of trauma exposure, is also inversely related to
cortisol levels. For instance, Olff and colleagues (2006) reported evidence of this inverse
relationship in a sample of chronic PTSD patients exposed to civilian trauma (e.g., abuse,
loss of a loved one, vehicular accident). Similarly studies examining whether cortisol
dysfunction is related to trauma exposure or the presence of diagnostic levels of PTSD,
also indicative of symptom severity, one study suggests that diagnostic levels of PTSD,
indicating severity of symptoms, is important. Wessa and colleagues (2006) examined
diurnal cortisol patterns in three groups, trauma exposed with PTSD (n = 29), without
PTSD (n = 19) and non exposed controls (n = 15). While the three groups did not differ
with respect to the waking response, PTSD subjects showed significantly lower levels of

cortisol for the peak response compared to trauma exposed and healthy subjects. This

36

pattern remained stable throughout the day. Although the two trauma-exposed groups did
not differ with respect to the type of trauma they experienced or the time span since
trauma onset, it is unclear whether the groups were similar with respect to duration of
trauma exposure, suggesting a confounding effect of chronicity as well as a possible
lifetime diagnosis of PTSD.

With respect to chronicity and age of traumatic events researchers have reported
that lower cortisol levels are associated with an early traumatic history (Carpenter et al.,
2007; Rasmusson et al., 2001; Santa Ana et al., 2006; Yehuda, Halligan, & Grossman,
2001). For instance Yehuda and colleagues (2001) reported an inverse relationship
between childhood emotional abuse and cortisol levels among adult children of holocaust
survivors. Also, Santa Ana and colleagues (2006) assessed differences in cortisol
functioning in individuals with childhood (n = 25) versus adult exposure to trauma (n=
33). This study found that participants with a history of childhood trauma (conceptualized
as prior to age 18) had lower levels of cortisol at baseline compared to individuals with a
history of victimization in adulthood (age of trauma exposure after 18). In a sample of
adults without current psychopathology Carpenter and colleagues (2007) compared
subjects with a history of moderate to severe childhood maltreatment (n = 23) to those
without such a history (n = 27) and found lower levels of baseline cortisol in the group
with a childhood history of abuse. However, neither of the studies examined whether the
age of trauma exposure coincided with a critical period of biological maturation of the
limbic system or dyadic emotion regulation as suggested by empirical evidence
(McCollum, 2006) and theoretical implications (Schore, 2002b). While retrospective

report poses a tremendous methodological challenge particularly given the pathoplastic

37

effects of concurrent stressors (Henry et al., 1994), this issue needs further examination to
expand theoretical definitions of critical stages of development.

Relatedly, some researchers have reported a lack of significant differences across
trauma type (Young et al., 2004) however, others have noted that the type of trauma
exposure (e. g., interpersonal/ attachment-related versus combat related) could be an
important issue (Meewisse et al., 2007). This issue relates to perpetrator relationship
discussed before, which has been shown to have a differential impact on psychological
outcomes. In their meta-analysis Meewisse and colleagues (2007) conducted subgroup
analyses to examine the effects of type of trauma on basal cortisol. Four types of
traumatic events were coded - war veterans, victims of sexual or physical abuse, refugees,
and various trauma. Findings indicated lower cortisol levels in victims with victims of
sexual or physical abuse but no differences were found for other types of trauma when
compared with healthy controls. However, as the authors note, their findings could be
confounded with gender effects because the lack of adequate information regarding the
break up between gender and each trauma type from each study did not allow the authors
to control for the effects of gender. Similarly, the authors also note that these findings
could also reflect the effects of chronicity or age of onset of trauma as sexual or physical
abuse typically begin early in the developmental lifespan and tend to be chronic relative
to other types of trauma such as combat war, but the lack of adequate information did not
allow for statistical control of these issues (Meewisse et al., 2007).

Finally, with respect to the issue of comorbidity between PTSD and depressive
disorders and biological subtype of PTSD, only a handful of studies have examined the

effects of such diagnostic comorbidity on cortisol outcomes (Olff et al., 2006; Yehuda,

38

Golier et al., 2004; Yehuda, Halligan et al., 2004; Yehuda et al., 1990; Yehuda, Teicher,
Trestrnan, Levengood, & Siever, 1996; Young & Breslau, 2004b; Young et al., 2004).
Among them, two studies, which included samples exposed to civilian trauma (e.g.,
abuse, loss of a loved one, vehicular accident) (Olff et al., 2006) and a sample of Vietnam
combat veterans (Yehuda et al., 1990) reported no significant effect of depression on
cortisol outcomes with comorbid PTSD. In contrast, some other studies reported elevated
basal cortisol as a result of an interaction effect between PTSD comorbid depression
(e.g., Yehuda, Halligan, & Bierer, 2002; Young & Breslau, 2004b; Young et al., 2004).
For instance, in a large community epidemiologic study of 516 individuals Young and
Breslau (2004b) found that individuals with a lifetime PTSD diagnosis, exhibited
elevated salivary cortisol, but only when they had a comorbid diagnosis of lifetime MDD.
None of the other conditions i.e., exposure to trauma, lifetime diagnosis of PTSD or
MDD alone were associated with alterations in basal cortisol. Similar findings were also
reported by Yehuda, Halligan, and Bierer, (2001) in a sample of Holocaust survivors. The
preponderance of evidence suggests that the PTSD and MDD comorbid condition may
represent a specific subtype with a neuroendocrine profile distinct from a diagnosis of
PTSD alone.

In addition to findings about basal cortisol levels in PTSD, an examination of the
diurnal pattern of cortisol also provides information about specific aspects of HPA axis
dysfunction in PTSD and their relationship to diagnostic classification and trauma
characteristics.

Diurnal Rhythm of Cortisol

39

Cortisol facilitates the alert state upon awakening in animals and humans. It has a
natural circadian rhythm in humans, with high levels in the morning followed by a steady
decline to low levels at night. In general studies have found that individuals with PTSD
tend to have significantly lower cortisol levels at several points during the circadian
rhythm particularly in the early mornings and late evening (de Kloet et al., 2007 ;
Rohleder, Joksimovic, Wolf, & Kirschbaum, 2004; Wessa et al., 2006; Yehuda, 2002).
However, studies have provided mixed evidence about whether the blunted cortisol is
seen in the awakening response (de Kloet et al., 2007; Rohleder et al., 2004; Yehuda et
al., 1996) or in the hour after awakening (Wessa et al., 2006). Findings have been
replicated across different types of trauma including war veterans (de Kloet et al., 2007;
Yehuda et al., 1996) and refugees (Rohleder et al., 2004) In addition, at least one study
reported similar findings for individuals diagnosed with PTSD as well as trauma exposed
veterans without PTSD (de Kloet et al., 2007).

There is limited evidence to suggest that these outcomes are likely related to
trauma characteristics such as latency of exposure and chronicity of the trauma. For
instance, it is notable that the trauma exposures in each of the aforementioned studies
represent multiple incidents of trauma exposure with a considerable latency period
between exposure and cortisol assessment. However, in a study of a shelter population of
IPV victims Johnson and colleagues (Johnson et al., 2008) examined the impact of PTSD
severity and abuse chronicity on the cortisol awakening response in a sample of 52
battered women. Findings suggested that IPV-related PTSD and abuse chronicity have
different, opposite, effects on waking salivary cortisol in battered women. While PTSD

severity was associated with significantly greater cortisol output in the first hour after

40

awakening, chronic abuse was associated with lower total cortisol output in the first hour
after awakening. While the association between chronic abuse and lower cortisol output
after awakening is consistent with other studies and the enhanced negative feedback
mechanism, the association between IPV related PTSD severity and cortisol in the first
hour after awakening could be understood as reactivity of the HPA axis in response to
more recent IPV experiences i.e., since this was a shelter population for whom the
latency of IPV exposure was relatively short and the experience of being in the shelter
itself implied safety concerns that the association with cortisol could reflect reactivity to
more recent and/ or current stressors, which is consistent with findings from studies
examining more recent forms of trauma exposure (Lemieux & Coe, 1995; Maes et al.,
1998; Rasmusson et al., 2001; Resnick et al., 1995) and also with findings suggesting
greater cortisol reactivity to day to day stressors in PTSD (Yehuda, 2002).

Research examining the diurnal pattern of cortisol also suggests that one key
feature of PTSD is a pattern of greater cortisol reactivity. For instance, Yehuda and
colleagues (1996) conducted a comprehensive circadian rhythm analysis through plasma
cortisol sampling every 30 minutes over a 24 hour period under controlled laboratory
conditions, with three groups of patients, combat veterans with PTSD, veterans and
civilians with MDD, and non psychiatric control subjects. Individuals with PTSD
displayed a more dynamic range of cortisol concentrations such that the lower the trough
(lowest point in the circadian rhythm) among PTSD individuals the greater the time spent
at the zenith (peak response), the lower the mean levels of basal cortisol, even though
there was no significant difference in mean levels of peak responses between the PTSD

and comparison control group. This pattern was found to be distinct from MDD

41

individuals who had higher levels of basal cortisol and an elevated trough. Similar
findings have also been reported by Thaller et al. (1999) and Hoffman et a1. (1989). who
compared peak and trough responses, which also indicated great variability between these
points relative to control comparisons.

Researchers suggest that these findings of an increased range of cortisol in PTSD
indicate that the HPA axis may be hyperresponsive to stress related cues, including day to
day environmental challenges. Relatedly studies assessing challenged cortisol to
investigate HPA reactivity also yield mixed evidence, but a preponderance of evidence
indicates support for cortisol hypersuppression in individuals with PTSD.

Challenged Cortisol

Several studies have examined HPA axis reactivity by examining challenged
cortisol either in the face of a psychosocial stressor (e. g., Bremner et al., 2003; Carpenter
et al., 2007; Elzinga et al., 2008; Heim et al., 2000; Santa Ana et al., 2006; Simeon,
Knutelska, Yehuda et al., 2007) or more commonly through a chemical challenge such as
the DST (e.g., Atrnaca, Kuloglu, Tezcan, Onal, & Ustundag, 2002; Griffin et al., 2005;
Newport, Heim, Bonsall, Miller, & Nemeroff, 2004; Stein et al., 1997; Yehuda, Golier et
al., 2004; Yehuda, Halligan et al., 2004; Yehuda, Halligan, Grossman, Golier, & Wong,
2002). However, only a handful of studies have used psychosocial or cognitive stressors
to assess challenged cortisol in adults with trauma exposure. Three of these studies
examined challenged cortisol across various diagnostic groups in the context of
childhood trauma (Bremner et al., 2003; Heim et al., 2000; Santa Ana et al., 2006) and
two studies have examined such outcomes in preclinical samples of individuals without

current psychiatric diagnosis (Carpenter et al., 2007; Elzinga et al., 2007. One other study

42

has examined different diagnostic groups using a combination of a psychosocial stressor
and DST primarily focusing on the effects of dissociative disorders/ symptoms (Simeon,
Knutelska, Yehuda et al., 2007)

Methodological limitations discussed in the context of basal cortisol studies also
extend to studies with challenged cortisol with a lack of controls for comorbid symptoms,
small sample sizes, and the lack of appropriate comparison groups. It should also be
noted that most studies examined populations with early and/or chronic forms of trauma.
Taken together these findings generally indicate a blunted response to stressors.

For instance, Heim and colleagues (2000) examined cortisol outcomes in women
after sexual and physical abuse in childhood (defined as prior to their first menses).
Forty-nine women were recruited into 4 groups: no history of childhood abuse or
psychiatric disorder (n=12), those diagnosed with MDD with a childhood history of
abuse (n=13), those without a diagnosis of MDD with a childhood history of abuse
(n=14), and those with a current diagnosis of MDD without a childhood history of abuse
(n=10). Using the Trier Social Situations Test (TSST) as a psychosocial stressor, the
study reported significant group differences such that women with a history of childhood
abuse and depression exhibited higher cortisol responses than all other groups. The four
groups also differed with respect to cortisol concentrations such that abused women with
current depression had increased levels of cortisol compared to all other groups. This
study did not control for symptoms of anxiety and PTSD, and women with a history of
childhood abuse had current comorbid symptoms, thus these findings should be
interpreted with caution, as they do not reflect the unique or independent effects of

depressive symptoms alone. In another study, which examined the effect of PTSD, in a

43

mixed sample of men and women, as a result of trauma in childhood (defined as prior to
age 18) (n=25) were compared with individuals with PTSD, as a result of trauma in
adulthood (defined as after age 18) (n=33), and healthy controls (n=31), on a cold-water
immersion task (Santa Ana et al., 2006). Subjects with childhood trauma had lower
cortisol at baseline and all post-task measurements. They also did not show decline in
cortisol over a 2-hour post stress period as seen in individuals with trauma exposure in
adulthood and controls.

In another study by Carpenter and colleagues (2007) also used the TSST as a
psychosocial stressor, to assess the effects of significant childhood maltreatment in a
nonclirrical sample of healthy adults (defined as individuals without a current psychiatric
diagnosis). Two groups of participants included a group with moderated to severe
childhood maltreatment (n=23) and another with subjects without such a history (n=27).
The study found that compared with the group without the childhood history of
maltreatment, the maltreated group showed significantly lower baseline to peak change
responses, and no differences were found with respect to baseline cortisol concentrations.
These findings suggest blunted HPA axis responsivity to a psychosocial stressor, even
though subjective ratings of anxiety induction in both groups were equivalent. Since
participants in this study did not meet criteria for PTSD or MDD or other psychiatric
diagnoses, it is possible that the findings represent enduring outcomes in the face of
childhood maltreatment. Altemately, the findings may represent functioning in a
population of maltreated individuals with subthreshold but not diagnostic levels of
psychopathology. In the third study which examined cortisol outcomes in the context of

childhood abuse and PTSD, Bremner and colleagues (2003) reported no differences

44

between the PTSD (n = 23) and healthy control groups (n = 18), in a mixed sample of
men and women. Although the PTSD had several comorbid diagnoses of mood- and
anxiety-related disorders the study did not control for the effects of concurrent diagnoses
or possible effects of daily stressors. Also subjects were included if they had experienced
child abuse, defined as abuse before the age of 18 such as rape, molestation physical
assault etc., thereby including a wide time line of exposure to traumatic events.

Finally, Elzinga and colleagues (2008) assessed cortisol in a college population of
healthy women and men (i.e., without current psychopathology) but with a history of
high (n=33) to low (n=47) childhood abuse using the TSST. Consistent with prior studies,
results indicated a blunted cortisol response among individuals with a history of abuse
compared to those with low or no such history. The groups did not differ with respect to
subjective ratings of anxiety of the task and baseline cortisol. However, it is notable that
these findings were primarily driven by the men in the sample, and women did not
demonstrate the blunted responses. As the authors note these findings in women could be
confounded by the effects of contraceptives or menstrual cycle, which was not controlled
for in this study.

Several studies have examined HPA reactivity and challenged cortisol using a
chemical challenge (e.g., Atrnaca et al., 2002; Griffin et al., 2005; Lindley et al., 2004;
Newport et al., 2004; Stein et al., 1997; Yehuda, Golier et al., 2004; Yehuda, Halligan et
al., 2004; Yehuda, Halligan, Grossman et al., 2002). Despite some inconsistencies in
findings, a majority of these studies are consistent with findings from studies employing
psychosocial stressors suggesting cortisol hypersuppression. For instance, Stein and

colleagues (1997) examined plasma cortisol in 19 women with severe childhood sexual

45

abuse (which included various diagnoses and comorbid conditions that are common
sequelae of childhood trauma such as MDD, dissociation disorders, and PTSD) and 21
control women, in a low dose DST and reported that the abused group had significantly
enhanced suppression of plasma cortisol. Similar findings were also reported by other
researchers (Kellner, Yehuda, Arlt, & Wiedemann, 2002; Yehuda, Golier et al., 2004) in
samples of combat war veterans and Holocaust survivors. These findings of challenged
cortisol in PTSD populations are significantly different from evidence for cortisol non
suppression in populations with MDD, suggesting different neuroendocrinological
profiles across diagnoses.

Finally, one study examined the effects of TSST and DST in a mixed sample of
men and women with dissociative disorders, PTSD, and healthy controls (Simeon,
Knutelska, Yehuda et al., 2007). Although findings from this study suggested no
differences between the three groups, with respect to cortisol reactivity to the TSST, the
group underwent the TSST while the HPA axis was still under the influence of the DST,
making it difficult to interpret the findings.

In sum, findings from studies examining HPA axis sensitivity have produced
somewhat mixed evidence, as a result of multiple methodological issues, and the role of
frequently co-occurring mental health conditions in trauma exposed populations, which
are still being explored. However, a majority of the findings thus far, indicate evidence
for cortisol hyper suppression in trauma exposed populations.

Studies examining IPVand cortisol outcomes
With respect to cortisol outcomes in adult IPV victims, only six studies have

examined cortisol outcomes in IPV victims (Griffin et al., 2005; Inslicht et al., 2006;

46

Johnson et al., 2008; Pico-Alfonso et al., 2004; Seedat et al., 2003; Young et al., 2004).
Seedat and colleagues (2003) examined the basal cortisol levels in female IPV victims.
The sample included 10 subjects with a current diagnosis of PTSD, 12 subjects without a
current or lifetime diagnosis of PTSD, and 16 control subjects. The study found IPV to be
the primary distinguishing factor across groups, such that individuals exposed to IPV
demonstrated significantly lower levels of basal cortisol compared to controls, regardless
of a PTSD diagnosis. However, it is notable that the IPV exposed group also differed
significantly with respect to a childhood history of abuse/ trauma from the control group
and the analyses did not control for the effects of childhood trauma suggesting that the
observed outcomes could be a result of more chronic exposure to trauma, starting early in
the developmental lifespan.

In contrast, in a later study Pico-Alfonso and colleagues (2004) reported elevated
cortisol outcomes after controlling for age, smoking, pharmacologic treatment, and
lifetime history of victimization. The study compared salivary cortisol outcomes between
women exposed to physical (n =70) or psychological (n = 46) violence and nonabused
control women (n = 46). Findings suggested that IPV victims had more severe symptoms
of depression, anxiety, incidence of PTSD and higher levels of evening cortisol compared
with control women, regardless of the type of abuse. IPV was found to be the main
predictor of changes in hormonal levels and diagnostic status did not have a mediating
effect on the impact of IPV on hormonal levels. However, this study did not examine the
effects of PTSD comorbid with MDD, and it is unclear how many individuals had
comorbid diagnoses, which has been associated with elevated level of cortisol (e. g.,

Young & Breslau, 2004a; Young & Breslau, 2004b). In addition, this sample included

47

women who were currently in abusive relationships unlike the sample in Seedat et al.’s
(2003) study, and hence these findings could reflect the effects of concurrent stressors.

In a different study, Griffin and colleagues (2005) compared plasma cortisol of
female IPV survivors with PTSD (n = 15), with PTSD and depression (n=27), those
without PTSD or depression diagnoses (n=8), and a matched group of nontraumatized
participants (n=14). IPV survivors with PTSD, regardless of comorbid depression, had
significantly lower baseline morning cortisol compared to healthy controls and trauma
survivors without diagnoses. Additionally, this is the only study to date that has examined
challenged cortisol outcomes in IPV victims. The study found that IPV survivors with
only a PTSD diagnosis showed significantly greater cortisol suppression to a low-dose
DST compared to the healthy controls and the comorbid group, consistent with the
enhanced negative feedback inhibition in PTSD.

In another study, Inslicht and colleagues (2006) examined salivary cortisol
outcomes in female IPV victims with lifetime (current or remitted) PTSD (n=29) and in
women who were exposed to IPV but never developed PTSD (n=20). This study found
that women with lifetime PTSD had significantly higher cortisol levels across the day
compared to abuse-exposed participants without PTSD, after controlling for age,
depression, severity, and latency of abuse. However, the study did not control for
concurrent stressors nor did it include a control comparison group of non abused women.

In a study of low income women Young and colleagues (2004) found no
differences between women who were recently assaulted versus those that IPV. They also
reported no effects on cortisol secretion for IPV if the last exposure occurred more than 1

year prior to cortisol assessment. However the sample of women who had experienced

48

IPV was very small subset (n=17) of a larger study. Thus, it is possible that the small
sample size restricted detection of any significant group differences. Finally, Johnson and
colleagues (2008) examined the waking response in IPV victims and found that PTSD
severity and abuse chronicity have different, opposite, effects on waking salivary cortisol
in battered women. While chronicity was associated with low awakening cortisol ,
severity of trauma was associated with increased cortisol concentrations.

In sum, only a handful of studies have examined cortisol outcomes in battered
women. Taken together the findings are relatively mixed and present various
methodological differences and shortcomings. Notably most of the studies have not
examined the role of any theoretically informed trauma characteristics on cortisol
outcomes except for the role of trauma chronicity, which has typically been limited to the
experiences of IPV alone, despite evidence for the presence of other types of abuse

exposure in early developmental stages in such a population.

49

CHAPTER 4
Rationale and Hypotheses
This study proposes to examine basal (defined as the average of the four salivary
cortisol samples across the diurnal cycle), diurnal rhythm (i.e., trajectory of cortisol
concentrations as assessed at four time points through the day) and challenged (defined as
changes in cortisol concentrations in the context of a cognitive stress task) cortisol
measures in a sample of pre-menopausal non pregnant adult women. The goal of the
study is to examine these cortisol measures as a function of diagnostic classifications
(PTSD only, PTSD and MDD comorbid, and subthreshold symptoms) and trauma
characteristics (e. g., chronicity, earliest age of trauma exposure, cumulative trauma
experiences based on types of trauma exposure, and social support). Thus, hypotheses are
based on two organizing frameworks — (1) diagnostic classifications and (2) trauma
related characteristics.
Specific Hypotheses

A. Basal Cortisol
Hypotheses based on diagnostic clagsflication:

Women were grouped into (1) PTSD only, (2) PTSD and MDD, (3) Subthreshold

symptoms, and (4) Control
1. Women with a lifetime PTSD diagnosis, without comorbid MDD, will have lower

levels of basal cortisol compared to women in the control group.
2. Women with a lifetime PTSD diagnosis, without comorbid MDD will have lower

levels of basal cortisol compared to the trauma exposed women with subthreshold

symptoms.

50

3. Women with comorbid diagnoses of lifetime PTSD and lifetime MDD will have
higher levels of basal cortisol compared to women in the control group.

4. Women with diagnoses of lifetime PTSD and comorbid lifetime MDD will have
higher levels of basal cortisol compared to the trauma exposed women with
subthreshold symptoms.

Hypotheses based on trauma characteristics:

 

Groupings for trauma characteristics are proposed to be based on naturally occurring

variation found in the sample and did not form the basis for recruitment into the study.

The following group difilerences are hypothesized based on chronicity:

Women were grouped to distinguish 1) women with childhood abuse and IPV, 2) women

with IPV only but no history of childhood abuse, and 3) control comparison group.

5. Women with a childhood history of trauma and IPV will have lower levels of basal
cortisol compared to women in the control group.

6. Women without a childhood history of trauma and only a history of IPV in adulthood
will have higher levels of basal cortisol compared to women in the control group.

The following is hypothesized based on age of trauma exposure:

Only for women with childhood abuse and IPV.

7. Age of trauma exposure will be positively related to basal cortisol such that earlier
trauma exposure will be related to lower levels of basal cortisol.

The following is hypothesized based on cumulative trauma exposure and relationship to

perpetrator:

Only for women with childhood abuse and IPV.

51

8. Childhood trauma perpetrated by primary caregivers and unrelated but close
individuals will result in more significant dysfunction as seen in lower levels of basal
cortisol compared to unrelated perpetrators.

The following is hypothesized based on social support:

9. Social support will moderate the impact of trauma on cortisol outcomes such that
women exposed to lifetime trauma without social support will have lower cortisol
outcomes relative to women with social support form their network.

B. Diurnal Rhythm of Cortisol

Hypotheses based on diagnostic classification:

Women were grouped into (1) PTSD only, (2) PTSD and MDD, (3) Subthreshold
symptoms, and (4) Control

1. Women with a lifetime diagnosis of PTSD will have significantly lower levels of
cortisol at all four time points through day compared to women in the control group.

2. Women with comorbid diagnoses of lifetime PTSD and MDD will have higher levels
of cortisol at all time points through day compared to women in the control group.

3. Women with comorbid diagnoses of lifetime PTSD and MDD will have significantly
higher levels of cortisol at all time points through day compared to women in the
PTSD only group.

4. Women with a lifetime diagnosis of PTSD will show a greater range of cortisol
responses as assessed through the difference between the peak to trough cortisol

assessments.

52

5. NO Specific hypotheses are made with respect to the women with subthreshold
symptoms. Exploratory analyses will examine trajectories of diurnal cortisol
outcomes in this group.

Hypotheses based on trauma characteristics:

The following group differences are hypothesized based on chronicity:

Women were grouped to distinguish 1) women with childhood abuse and IPV, 2) women
with IPV only but no history of childhood abuse, and 3) control comparison group.

6. Women with a childhood history of tramna and IPV will have significantly lower
levels of cortisol at all four time points through the day compared to women in the
control group.

7. Women without a childhood history of trauma and only a history of IPV in adulthood
will have higher levels of cortisol at all four time points through the day compared to
women in the control group.

T he following is hypothesized based on age of trauma exposure:

Only for women with childhood abuse and IPV.

8. Early trauma exposure will be positively related to the awakening cortisol response as
well as cortisol at later points in the day.

The following is hypothesized based on cumulative trauma exposure and relationship to

perpetrator:

Only for women with childhood abuse and IPV

9. Childhood trauma perpetrated by primary caregivers and unrelated but close
individuals will result in more significant dysfunction as seen in lower levels of basal

cortisol compared to unrelated perpetrators.

53

The following is hypothesized based on social support:

10. Social support will moderate the impact of trauma on cortisol outcomes such that
women exposed to lifetime trauma without social support will have lower cortisol
outcomes at each time point relative to women with social support form their
network.

C. Challenged cortisol

Hypotheses based on diagnostic classification:

Women will be grouped into (1) PTSD only, (2) PTSD and MDD, (3) Subthreshold
symptoms, and (4) Control

1. Women with a lifetime diagnosis of PTSD will have lower levels of cortisol in
response to a stress manipulation relative to the control group.

2. Exploratory analyses will examine challenged cortisol outcomes in women with
comorbid lifetime diagnoses of PTSD and MDD relative to the control group.

3. Exploratory analyses will examine challenged cortisol outcomes in women with
subthreshold symptoms.

Hypotheses based on trauma characteristics:

The following group differences are hypothesized based on chronicity:

Women will be grouped to distinguish 1) women with childhood abuse and IPV, 2)

women with IPV only but no history of childhood abuse, and 3) control comparison

group.

4. Exploratory analyses will examine how trauma chronicity is related to challenged
cortisol outcomes.

The following is hypothesized based on age of trauma exposure:

54

Only for women with childhood abuse and IPV.

5. Exploratory analyses will examine if and how age of trauma exposure is related to
challenged cortisol outcomes.

The following is hypothesized based on cumulative trauma exposure and relationship to

perpetrator:

Only for women with childhood abuse and IPV

6. Exploratory analyses will examine if and how perpetrator relationship is related to
challenged cortisol outcomes.

The following is hypothesized based on social support:

7. Exploratory analyses will examine if and how social support moderates challenged

cortisol outcomes.

55

CHAPTER 5
Msthsfi

Participants

The sample consists of 92 women including 12 women for a control comparison
group, who had no lifetime exposure to IPV or other interpersonal forms of trauma or
lifetime diagnosis of mood disorders or PTSD. Additionally, 14 participants meet lifetime
criteria for PTSD only, 43 participants meet lifetime criteria for PTSD and MDD, and 19
women were classified having subthreshold PTSD or PTSD and MDD symptoms, based
on the DSM-IV-TR criteria (American Psychological Association, 2000). Four women
met full criteria for MDD only and were removed from analyses. See Table 1.
Procedures

Participants from diverse ethnic/cultural and socioeconomic backgrounds were
recruited from the greater Lansing area. Specifically, 52% of the sample identified
themselves as being Caucasian, 25% Afiican American, 8% Hispanic, 7%Asian, 6%
Multiracial and 2% Biracial. Additionally, 25% of the sample identified as having a High
School or GED degree, 51% reported completing “some college”/ trade school/
Associates degree, 13% reported completing a bachelor’s degree, and 11% reported
completing “some graduate school”/ a graduate degree. The mean age of the sample was
27 years (range: 18.7 years — 41.9 years) and the mean monthly income was $2332.31
(range: $00.00 - $12,500). See Tables 2, 3, and 4 for demographic information about the
sample organized by diagnostic group status.

Participants were recruited by informing key community stakeholders (e.g.,

Personal Protection Order Office, Work First, Salvation Army, Ballentine’s Stepping

56

Stones, Cristo Rey, Faith Based agencies and churches) via letters, flyers, and formal
appointments with directors of programs. Flyers were also posted in various community
locations such as grocery stores, laundromats, hospital emergency rooms (e. g., Sparrow
and Ingham Hospital Emergency Rooms), and other community health facilities (e. g.,
Women's Center of Greater Lansing, Women's Personal Growth and Therapy Center,
Clinton Eaton Ingham Community Mental Health Counseling Center, Insight Recovery
Center). To over sample for IPV victims, particularly women with more severe IPV
exposure, recruitment efforts were focused on a local domestic violence shelter - End
Violent Encounters Inc. (EVE). In addition to posting flyers at EVE, recruitment
announcements were also made at their support group meetings. Approximately 28 % of
the sample reported living in a domestic violence shelter at some point in their life (n =
25), including 11% (n=10) who reported living in the shelter during the study. Only 7%
(n = 6) of the sample reported being in an abusive relationship during the study.
Interested participants who contacted the MSU project office underwent a 15
minute phone screen to assess for multiple inclusion and exclusion criteria. To be
included all women had to be (1) English-speaking, (2) between 18 to 41 years old, (3)
not pregnant, (4) not lactating or breast feeding, (5) no diagnosis of neuroendocrine
disorders (e. g., Dai, Buijs, & Swaab, 2004) or endocrine disorders (Cushings, Addisons
Diseases), cancer, or those currently receiving cancer therapy (see Findling & Raff, 2006;
Golden et al., 2007), (6) free of any lifetime diagnoses of a psychotic disorder or
cognitive impairments, (7) could not meet criteria for substance use dependence or abuse
in the past three months, (8) been involved in a heterosexual romantic relationship for at

least 6 weeks in the past 2 years, and (9) have a minimum grade 6 education to ensure

57

that informed consent could be obtained. Additional criteria for IPV exposed women
included (1) the last IPV experience should have occurred within the past two years and
(2) the women had to endorse minimum two symptoms of PTSD or PTSD and MDD
criteria on the phone screen. The study was designed to recruit groups based on
diagnostic groups. Hypotheses and analyses based on trauma characteristics were based
on naturally occurring variation found in this population, thus recruitment did not screen
for trauma characteristics.

Trained undergraduate assistants conducted the initial intake over phone, which
began with a standardized introduction to the study, followed by a screen for the
aforementioned inclusion and exclusion criteria. See Appendix C for the screening
procedure. Additionally, the Alcohol Use Disorders Identification Test (AUDIT) (Babor,
de la Fuente, Saunders, Grant, & World Health Organization, 1992) measure was used to
screen for alcohol use and dependence. A score of 8 or higher indicates the presence of
alcohol dependence. Thus, to meet criteria for participation in the study the women
would have to score 7 or lower on the AUDIT. Women who reported drug use for non
medical reasons more than 1-2 times and / or indicated impairment in daily functioning
more than 1-2 times in the past 3 months were deemed ineligible for the study.

Eligible participants were scheduled for an interview at the MSU research office.
However, residents of EVE were offered the option of completing the interview at EVE
itself. This was done to facilitate recruitment and participation of a Shelter population
who represent a high risk population of interest with limited resources and differ from

community populations experiencing IPV (e.g., Levendosky et al., 2004). All participants

58

were scheduled at 05.30 pm in the evening to standardize time of cortisol sampling
during the interview process.

Trained graduate and undergraduate research assistants conducted interviews. All
graduate students were advanced graduate students who had completed their Masters
degree in clinical psychology and were trained in the adnrinistration of Structured
Clinical Interview for DSM-IV Axis I & II Disorders (SCID) (First, Spitzer, Gibbon, &
Williams, 1996a) through a workshop in the department of psychology at Michigan State
University. Additionally, all graduate assistants were observed during two mock
administrations of the SCID to assess for reliability. Graduate research assistants also
served as evaluative observers for the psychosocial stress task with participants and were
trained on the requisite protocol and observed during two mock interviews.

Undergraduate assistants were trained in administering all remaining measures by
having them observe a mock interview, followed by an administration of the interview to
the principal investigator, and finally the principal investigator observing the assistant
administer the interview to a mock participant. To ensure fidelity to the interview
protocol, undergraduate assistants were observed twice in vivo during administration of
interviews with participants — the first time within the first three interviews and on a
second occasion, after approximately six interviews.

All participants began by completing a consent form approved by the Institutional
Review Board (IRB), informing them of their rights as participants, and the steps taken
by the project to ensure their confidentiality (e. g., identifying information will not be
stored with their data and will be kept in a secure location in accordance with IRB rules).

Participants were informed about the payment they would receive for their time spent in

59

the interview. A total of $30 was paid to the first 55 participants; $20 upon completion of
the interview and $10 upon obtaining the three saliva samples from the take home kit.
Subsequently, $40 was paid to the remaining participants; $25 upon completion of the
interview and $15 upon obtaining the three saliva samples from the take home kit.
Payment was increased to facilitate recruitment of the required sample size within the
available time line, following IRB approval.

Following the requisite consent forms participants completed a brief screener
about any foods and drinks they consumed, and how many cigarettes they had smoked in
the past few hours and a demographic questionnaire. See Appendix C. Next, participants
were given a five minute rest period following which they gave their first saliva sample
(i.e., baseline saliva sample). Next, the cognitive stress protocol [i.e., an adapted version
of the Trier Social Stress Test (TSST) (Kirschbaum, Pirke, & Hellhammer, 1993)] was
administered to induce moderate psychosocial stress under laboratory conditions (see
Appendix C for cognitive stress task protocol details), to provide estimates of HPA
reactivity. The TSST has been used in a number of studies assessing the effects of
psychosocial stress and has been found to effective in eliciting a stress response (e.g.,
Elzinga et al., 2008; Simeon, Knutelska, Yehuda et al., 2007).

Upon completion of the cognitive stress challenge task, three saliva samples were
collected — immediately after the stress task, and 10- and 25-minutes post completion of
the stress task. The interviewer noted the exact time of each saliva sampling. Saliva was
collected from participants following procedures developed by Granger and colleagues
(2007). See Appendix C for protocol for saliva collection. During the post task period

participants were asked to rate their perceived stressfulness of the cognitive challenge

60

task and were debriefed about the cognitive challenge. See Appendix C for the cognitive
challenge and debriefing protocol.

Next, the graduate assistant conducted a structured clinical interview to assess for
current and lifetime PTSD and MDD (SCID-I) and borderline personality disorder
(SCID-II). After this, the undergraduate assistants helped participants complete
questionnaires related to domestic violence, childhood history of trauma, daily stressors,
PTSD, anxiety, depression, dissociative symptoms, and social support. In addition
participants completed two brief checklists 1) to assess for the presence of any
autoimmune disorders and to get information about related treatments/ medication use
(see Appendix C) and 2) to assess their smoking habits and substance use in the last 48
hours (see Appendix C). Finally, interviewers provided participants with take home kit
and explained the protocol of obtaining saliva samples for the following 48 hours (one
sample at 9 pm the following night, a second sample immediately after awakening, and a
third sample within 45 minutes of awakening sample). Assistants also made plans to
collect samples from the participants, which could be any location of the participant’s
choosing.

Cortisol enzyme-immunoassay (EIA)

Cortisol were assayed using a commercially available enzyme immunometric
assay specifically designed for use with saliva without modification to the manufacturer’s
recommended protocol (Salirnetrics, 2008). The assay (25 pl test volume) is 510K
cleared (US FDA) as a diagnostic measure of adrenal function: range of detection is from
0.003 to 3.0 ug/dl. The assay is highly specific to cortisol, with less than 0.5% cross-

reactivity for other steroids. All assays were performed in duplicate by the principal

61

investigator, with assistance from two undergraduate assistants, all of whom were trained
and supervised by Dr. Lonstein. All assay plates had standard curve correlations of 0.90
or higher. The mean inter assay variation was 12.8 per cent and intra assay variability
was 7.75 per cent.

Measures

Demographics. Participants completed a demographic questionnaire to identify
information about their age, race/ethnicity, education level, and family income. See
Appendix C for a copy of the measure.

Alcohol Use Disorder Identification Test (A UDIT, Babor & Grant, 1989). This
measure was developed as a brief multi-cultural screening tool for the early identification
of at-risk problem drinkers (Babor et al., 1992). It was created by a working group of the
World Health Organization by choosing questions that discriminated high risk drinkers in
a six nation study. It contains a series of ten questions that include three questions on use,
four dependence questions, and three items about problems. The 10 questions are
designed to be administered as an interview or as pencil and paper questionnaire. A cut-
off score of 11 or more generally indicates dependence while a score of 8 or higher
indicates high risk for abuse.

Severity of Violence Against Women Scales (S VA WS, Marshall, 1992). The
SVAWS is a 46-item instrument designed to assess IPV, defined as adult male violence
and threats of violence against female romantic partners. The questionnaire is composed
of nine subscales: symbolic violence; mild, moderate, and serious threats of physical
violence; minor, mild, moderate, and serious actual physical violence; and sexual

violence. Example items include, “Hit or kicked a wall, door, or furniture,” “Threatened

62

to hurt you,” “Pushed or shoved you,” “Beat you up,” and “Physically forced you to have
sex.” Ratings are on a 4-point scale with response choices ranging from “Never” to
“Many times.” The SVAWS has good psychometric properties. Marshall (1992) reported
coefficient alphas for the nine subscales ranging from .89 for symbolic violence to .96 for
both mild and serious physical violence. In the current study the reliability coefficient
was 0.98. In order to exclude mild violence (e. g., “Shook a finger at you”), and examine
the effects of physical and sexual violence, only item numbers 14 and higher were used to
create a sum score as an indicator of the severity of IPV. A dichotomous score was
created based on the sum score to indicate the presence (i.e., any score greater than 0) or
absence (i.e., sum score equal to 0) of IPV.

Childhood Trauma Questionnaire -— Short Form (CTQ, Bernstein et al., 2003) The
CTQ is a 28-item, self-report measure for retrospectively assessing multiple types of
abuse and neglect experienced during childhood and adolescence. The questionnaire has
five clinical scales each consisting of five items: physical, sexual, and emotional abuse,
and physical and emotional neglect. The instrument also includes a 3-item
minimization/denial scale to detect under-reporting of maltreatment. Example questions
include, “People in my family hit me so hard it left me with bruises or marks,” “Someone
tried to touch me in a sexual way,” and “People in my family called me things like
‘stupid,’ ‘lazy,’ or ‘ugly.’” Items are rated on a 5-point Likert scale with response
options ranging from “Never” to “Very Often True.” The CTQ is a reliable and valid
measure of childhood trauma across a variety of individuals who differ in terms of age,
sex, ethnicity, socioeconomic status, psychopathology, and life experiences. Test-retest

reliabilities range from .79 for the physical neglect scale to .86 for the entire measure in a

63

sample of adult substance abusers (Bernstein & Fink, 1998) Bernstein and Fink (1998)
reported internal consistency reliability coefficients ranging from a median of .66 for
physical neglect to a median of .92 for sexual abuse across a variety of clinical and non-
clinical samples. In the current study the reliability coefficient was 0.86 for the physical
abuse scale and 0.93 for the sexual abuse scale. A sum score was calculated using
endorsements of physical and sexual abuse items. Also, a dichotomous score was created
to indicate the presence (i.e., any score greater than 0) or absence (i.e., sum score equal to
0) of childhood abuse or neglect.

Posttraumatic Diagnostic Scale (PDS, F 0a, 1995). This 38-item self-report scale
assesses all symptoms from all 6 criteria sets of PTSD based on the DSM-IV. The PDS
begins with a list of l3-items that screen for the experience of a traumatic event including
sexual victimization during childhood or adulthood, accident/fire, torture, and life
threatening illness. If more than one event is endorsed participants are asked to identify
the traumatic event bothered her the most. Participants who did not endorse any items in
this section do not complete the subsequent sections of the PDS.

To assess for feeling of danger for DSM-IV-TR criterion A, participants were
asked to answer 6-items related to each traumatic event (e.g., thinking that her life or
someone else’s life was in danger and feeling helpless or terrified) using a yes-no format.

Characteristics of Traumatic Events: To assess for severity of the traumatic event,
participants were also asked to report severity of injuries, how traumatic the event was at
the time for each event endorsed. Each item was measured on a 4-point Likert scale
ranging fiom “Not at all” to “A lot.” Items were be summed for the worst traumatic event

to produce a traumatic event severity score. Participants were asked to report the age at

64

which each endorsed traumatic event occurred. The youngest age at the time of the
traumatic event that the participant identifies at being the most distressing was utilized to
assess earliest age of trauma exposure.

In the case of interpersonal traumatic events, participants were asked to report
their relationship to the perpetrator, which included 3 options - family member (e. g.
father, brother, step-father), family fiiend or neighbor, stranger, except item 3 in which
participants could also endorse spouse/ partner as a perpetrator. In addition, due to high
rates of revictimization participants were asked how often she has experienced each
event. Two categorical variables were created to indicate the amount of cumulative
trauma exposure based on relationship to perpetrator. First, a categorical variable was
created using two different categories of attachment related trauma —— 1) intimate partner
violence and 2) familial childhood abuse and intimate partner violence and 3) multiple
types of trauma exposure including attachment related trauma (intimate partner violence
or intimate partner violence and familial childhood abuse) and non attachment related
forms of trauma exposure (e.g., house fire, accident, tornado). A second categorical
variable was created as follows - 1) attachment related (intimate partner violence or
intimate partner violence and familial childhood abuse) and 2) non attachment related
forms of trauma exposure.

The PDS is reported to have high test-rest reliability for total symptom severity
(alpha=.82) and for each of the symptoms clusters (alpha range= .77-.85). It was also
found to have high convergent validity with the PTSD portion of the SCID, kappa=.65

(F 0a, 1995). In the current study the reliability coefficient was 0.98.

65

Dissociative Experiences Scale (DES, Carlson & Putnam, 1993). The DES is a
28-item self-report measure that helps identify dissociative psychopathology. It inquires
about dissociative experiences in the daily lives of subjects. Example items include,
“Some people have the experience of finding themselves in a place and having no idea
how they got there”, “Some people find that they have no memory for some important
events in their lives (for example, a wedding or graduation)”, and “Some people find that
they become so involved in a fantasy or daydream that it feels as though it were really
happening to them”. The scale has been used in clinical and non clinical adult
populations including samples of individuals diagnosed with PTSD. The measure has
been reported to have high reliability and validity coefficients. For instance Rosenthal
and Rosnow (1991) reported test retest reliability coefficient of .84 and F rischolz and
colleagues (1990) reported a coefficient of .96. The scale has also been shown to have
good construct and criterion validity (Carlson & Putnam, 1993). In the current study the
reliability coefficient was 0.94. The measure uses a scale from 0 to 100 and a total score
is calculated by averaging scores across all 28 items. The total score will be utilized as a
measure of the extent of dissociation.

Structured Clinical Interview for DSM-I V Axis I Disorders (SCID-I, First et al.,
1996a). The SCID-I is a semi-structured interview for diagnosing most major DSM-IV
Axis I psychiatric diagnoses. It is one the most widely measures in research studies of
psychopathology. This measure is well suited for both inpatient psychiatric patients as
well as non-clinical populations, including female IPV victims (e. g., Griffin et al., 2005;
Inslicht et al., 2006). The SCID-I contains specific modules corresponding to specific

DSM-IV diagnoses that can be used independently of one another, depending on the

66

purpose of the study. For the current study the anxiety and mood-disorder modules were
used to assess for DSM-IV diagnoses and symptoms. High test-retest and inter rater
reliability and validity coefficients have been reported for both anxiety and mood-
disorder modules (e. g., Shea, Zlotnick, & Weisberg, 1999; Zanarini et al., 2000). In the
current study the reliability coefficient was 0.96 for current MDD, 0.95 for past MDD,
and 0.96 for PTSD. A total symptom count for PTSD and MDD as well as a dichotomous
score indicating the presence or absence of both PTSD and MDD were calculated. Next a
categorical variable was created to identify the presence Of PTSD, PTSD and comorbid
MDD, individuals with subthreshold symptoms, and a control comparison group with no
symptoms. It is notable that four individuals were classified as meeting criteria for MDD
only. Due to the small sample size of the group, these individuals were removed fi'om
further analyses.

Structured Clinical Interview for DSM-IVAxis II Disorders (SCID-II, First,
Spitzer, Gibbon, & Williams, I996b) The SCID-II is a widely used semi-structured
interview for making DSM—IV Axis II (Personality Disorder) diagnoses. Akin to the
SCID-l, the SCID-II also contains specific modules corresponding to specific DSM-IV
Axis II diagnoses that can be used independently of one another. For the current study the
borderline personality disorder module will be used. High inter rater reliability (k = 0.91)
and validity coefficients have been reported for the borderline personality disorder
module (e.g., Maffei et al., 1997). In the current study the reliability coefficient was 0.94.
A dichotomous score indicating the presence or absence of borderline personality
disorder was calculated.

Daily Hassles and Uplifts Scale (DH US, DeLongis, F olkman, & Lazarus, I 988).

67

The DHUS is a 53-item self measure that assesses the impact of events and relationships
that affect individuals on a daily basis. Participants are asked to rate each item (e. g.,
friends, relatives, work load, church or community organizations, cooking, health) with
respect to how much of a hassle or irritant each of them and to what extent they were an
uplift in their life. This measure has been widely used and shown to have high reliability
(alpha =0.94) (e. g., Day, Therrien, & Carroll, 2005). In the current study the reliability
coefficient was 0.94. For this study item 4 “Your spouse” will be changed to “Your
partner”. A sum score was calculated for the hassles to assess daily stressors.

Crisis Support Scale (CSS, Joseph, Andrews, Williams, & Yule, 1992). This 7-
item measure assesses perceptions of received social support. Respondents are asked to
rate their perceptions of 1) general current social support in past 4-6 weeks and 2) social
support immediately following the traumatic event that bothered them the most. A 7-
point Likert scale ranging fi'om “Never” to “Always” is utilized to assess the reception of
social support after the experience of a traumatic event. Examples of the items in the CSS
are “Someone willing to listen,” “Sympathy and support from others,” and “Feeling let
down.” In a review of 11 studies that used the CSS, Elklit and colleagues (2001) reported
good internal consistency, discriminant validity, and a mean alpha of .74. In the current
study the reliability coefficient was 0.91 for current social support scale and 0.81 for the
trauma related social support scale. Items were summed to create two social support

scores: social support at the time of the traumatic event and current social support.

68

CHAPTER 6
Be_sult_s
Missing Data
Data were checked for missing values, expected range, and the presence of outlier
values. With respect to cortisol data, missing data (i.e. nine participants who did not
return the take home kit which equals 27 samples, i.e. 4% of total cortisol samples) and
undetectable levels of cortisol values were substituted on a case by case basis, using
mean values for the diagnostic group under which the participant was classified and the
specific time of sampling that was missing (41 samples across 14 cases,‘i.e. 6.7% of total
cortisol samples were mean substituted). Regarding outlier values above the mean
(defined as three standard deviations above the mean of each diagnostic group) or
salivary cortisol values beyond the normative human range, only one saliva sample was
found to be an outlier. This data point was not substituted using mean substitution and
was removed from pertinent analyses using listwise deletion. See Table 5 for descriptive
statistics for cortisol values pre and post mean substitution.
Data transformation
Cortisol data were checked to determine whether the distribution of variables
meets the assumptions of statistical tests. As is typical for cortisol data, cortisol
distributions were found to be positively skewed. Hence, log transformed cortisol values
using logarithmic transformations (to the base 10) were used for all analyses.
ijotheses Testing
Prior to specific hypothesis testing, the shelter population was compared with IPV

exposed women who completed the interview at MSU with respect to demographics (i.e.,

69

age, ethnicity, income, and education). The groups did not differ significantly with
respect to these factors and were combined for all analyses. In the next step, diagnostic
groups were compared using univariate Analysis of Variance (AN OVA) or chi-square
tests to assess for differences in demographics (i.e., age, ethnicity, income, and
education) and other factors known to affect cortisol concentrations that could confound
findings (i.e., use of medication and contraception, dissociative symptoms, daily
stressors, borderline personality diagnosis, time of saliva sampling, food and alcohol
consumption, or cigarette smoking immediately prior to saliva sampling). Dissociative
symptoms were found to significantly differ across diagnostic groups (F334 = 5.40, p <
.01). See Table 6. Post-hoe analyses were conducted using the Games-Howell test to
account for differences in sample size and variance of the groups, which indicated that
the control group endorsed significantly fewer dissociative symptoms relative to all other
trauma-exposed diagnostic groups (i.e. PTSD, PTSD and MDD, subthreshold groups).
Also, the subthreshold groups endorsed significantly fewer dissociative symptoms than
the PTSD and MDD comorbid group. Thus, dissociative symptoms were included as a
covariate in all analyses that examined differences across all four diagnostic groups but
was not included in analyses which only examined differences between trauma-exposed
diagnostic groups.

Finally, due to the relatively high inter assay variation, which appeared to be driven
by three assay plates, all analyses were also conducted using a subset of the data (n=74),
after removing data from those three plates. Findings were consistent with data from the
complete data set, and hence, findings from the complete data are presented.

Hypothesis for basal cortisol based on diagnostic classification

70

The first hypothesis examined differences across diagnostic groups with respect to
basal cortisol concentrations. Analysis of Covariance (ANCOVA) indicated that there
were no significant differences across diagnostic groups (F333 = .379, n.s.). However,
dissociative symptoms were a significant predictor of basal cortisol values (F133 = 4.683,
p<.05). See Table 8 and Figure l for mean levels of basal cortisol concentrations across
groups. To further examine whether posttraumatic symptoms and depressive symptoms
account for variation in basal cortisol concentrations, post hoc analyses using continuous
data (i.e., sum scores of post traumatic stress symptoms and depressive symptoms) were
entered in a step wise regression model to predict basal cortisol concentrations. In the
final step dissociative symptoms was included in the model. The final model which
included dissociative symptoms, indicated a trend towards significance (p=.07) and
consistent with prior categorical analyses, only dissociative symptoms was a significant
predictor of basal cortisol concentrations (p<.05).

Hypothesis for basal cortisol based on trauma characteristics: chronicity

The next hypothesis sought to examine whether differences in chronicity of
trauma exposure accounted for variations in basal cortisol concentrations. A categorical
chronicity variable was created to indicate whether individuals had not experienced
trauma (n=12), versus trauma in adulthood only (i.e., intimate partner violence) (n=21),
versus trauma in childhood and adulthood (childhood physical and/or sexual abuse and
intimate partner violence) (n=55). Univariate F test indicated that there were no
significant differences across chronicity groups (F235 = .295, n.s.). Based on prior
findings related to the effects of dissociative symptoms on basal cortisol concentrations

post hoc analyses were conducted to examine differences in dissociative symptoms

71

across chronicity groups. Univariate F test indicated that the three chronicity groups
differed significantly. Games Howell post hoc test indicated that the group with no
trauma exposure had significantly lower dissociation symptoms. However, groups with
trauma exposure regardless of whether they experienced trauma in adulthood or more
chronic trauma (i.e., both childhood and adulthood) did not differ from each other. Thus,
as a next step, AN COVA with chronicity groups as a predictor, and dissociative
symptoms and age of participants as covariates [age was included as a covariate because
it could be a confounding factor for abuse chronicity and is significantly correlated to
chronicity (p<.05)]. Chronicity (F233 = .532, n.s.) and age were not significant predictors
for basal cortisol. However, disSociative symptoms (F133 = 4.648, p<.05) predicted basal
cortisol concentrations beyond chronicity and participant age.
Hypothesis for basal cortisol based on trauma characteristics: earliest age of trauma
exposure

To assess whether the earliest age of trauma exposure affects basal cortisol
concentrations, age of earliest trauma exposure was entered into a regression model with
dissociative symptoms, which was found to be significantly correlated with earliest age
of trauma exposure (r = -0.213, p=.05). Dissociative symptoms (t = -2.173, B = -.246, p
<.05), but not earliest age of trauma exposure, was a significant predictor of basal cortisol
concentrations.
ijothesis for basal cortisol based on trauma characteristics: cumulative trauma
exposure based on relationship to perpetrator

To examine whether relationship to perpetrator affects basal cortisol

concentrations, two types of categorical variables used. First, a categorical variable

72

examining whether two different categories of attachment related trauma — 1) intimate
partner violence (n= 11) and 2) familial childhood abuse and intimate partner violence
(n= 7), and 3) multiple types of trauma exposure including attachment related trauma
(intimate partner violence or intimate partner violence and familial childhood abuse) and
non attachment related forms of trauma exposure (e.g., house fire, accident, tornado) (n=
58) was created. A second categorical variable which examined 1) attachment related
(intimate partner violence or intimate partner violence and familial childhood abuse) (n=
18) and 2) non attachment related forms of trauma exposure (n= 58) was created.
Univariate F tests did not indicate significant findings for either type of classifications for
basal cortisol concentrations.
Hypothesis for basal cortisol based on trauma characteristics: social support

The effects of two types of social support on basal cortisol concentrations were
assessed — 1) general levels of perceived social support and 2) perceived social support at
the time of the event identified by the participant as being the most traumatic. Bivariate
correlations indicated that neither type of social support is significantly correlated with
basal cortisol levels. Univariate F tests indicated that neither type of social support is a
significant predictor of basal cortisol.
Hypothesis for diurnal rhythm of cortisol based on diagnostic groups

Repeated measures ANCOVA were used to examine the effect of diagnostic
groups, with dissociation as a covariate, on the diurnal rhythm of cortisol. The model
indicated a significant effect for dissociative symptoms only (F 132 = 3.878, p=.05) with a
significant linear trend (p <.01). However, as noted earlier, this finding appears to be

driven by the association between dissociation and awakening cortisol as dissociative

73

symptoms are not associated with cortisol concentrations at any other time in the day. See
Table 9 for the between subjects effects across diagnostic groups and Figure two.
Additionally, there was a significant quadratic trend for time of day (p <.001). Graphical
analyses indicates that all four groups showed a linear increase in cortisol concentrations
from night to wake up to the 45 minutes post awakening sample and a decline in cortisol
concentrations towards the evening as assessed through the pre cognitive stress task
baseline sample.

Additional post hoc analyses were also conducted to examine whether diagnostic
groups may predict cortisol variations at circumscribed times during the day. For instance
there is evidence to suggest that trauma exposed groups, particularly those that have
experienced chronic trauma exposure, may not Show the typical increase in cortisol
concentrations within the first hour of the day, relative to healthy control comparison
groups (Johnson et al., 2008). To further assess this issue, difference scores were
calculated by subtracting the 45-minutes post wake up cortisol concentration values from
the wake up cortisol concentration values. Next, these difference scores were used as
outcome variables in univariate F tests with diagnostic groups as predictors. This method
has been used to assess change in cortisol concentrations in the literature (Simeon,
Knutelska, Smith, Baker, & Hollander, 2007). Similar to prior findings the results did not
indicate significant differences in changes in cortisol concentrations in the first hour of
awakening between diagnostic groups. However, dissociative symptoms were a
significant predictor of changes in cortisol concentrations within the first hour of waking
up (p =.05). The relationship between dissociative symptoms and changes in cortisol

concentrations is likely due to its significant correlation with the waking up sample (r = -

74

0.257, p<.05), as dissociative symptoms are not correlated with the 45 minutes post wake
up sample or the difference scores.
Hypothesis for diurnal rhythm of cortisol based on trauma characteristics: chronicity

Repeated measures ANCOVA were used to examine the effect of chronicity, with
dissociation as a covariate, on the diurnal rhythm of cortisol. The model indicated a trend
towards a significant effect for dissociative symptoms (F133 = 3.334, p=.07) with a
significant linear trend (p <.01), and no significant effects for chronicity. Post hoc
analyses using difference scores were consistent with these findings, indicating
significant effects for dissociative symptoms (F133 = 3.849, p=.05) but not chronicity
(F233 = .717, n.s.).
Hypothesis for diurnal rhythm of cortisol based on trauma characteristics: earliest age of
trauma exposure

Repeated measures F test was used to examine the effect of earliest age of trauma
exposure. Consistent with analyses for basal cortisol, dissociation was included in the
model. Analyses indicated a significant effect for dissociative symptoms (F132 = 3.914,
p=.05) with a significant linear trend (p <.01), but no significant effects for earliest age of
trauma exposure. Post hoc regression analyses using difference scores as the outcome
variables suggested consistent findings, with a significant effect for dissociative
symptoms (p<.05) but not earliest age of trauma exposure.
Hypothesis for diurnal rhythm of cortisol based on trauma characteristics: cumulative
trauma exposure based on relationship to perpetrator

Repeated measures ANOVA, with previously described categorical variables was

used to assess the effects of attachment- and non—attachment related trauma experiences

75

on the diurnal rhythm of cortisol. However, F tests were not significant for either
predictor. Univariate analyses using difference scores as outcomes also did not indicate
significant effects for perpetrator type on changes in cortisol concentrations in the first of
hour of waking up.
Hypothesis for diurnal rhythm of cortisol based on trauma characteristics: social support

Bivariate correlations indicated that neither 1) general levels of perceived social
support nor 2) perceived social support at the time of the most traumatic event is
significantly correlated with cortisol concentrations at any point in the day. Thus, F tests
indicated that neither type of social support is a significant predictor of the diurnal
rhythm of cortisol. These findings were consistent with regression analyses using
difference scores as outcome variables and social support as predictor variables.
Hypothesis for challenged cortisol based on diagnostic classification

Repeated measures ANCOVA was used to examine the effect of diagnostic
groups, with dissociation as a covariate, on challenged cortisol. The model indicated a
trend towards mean differences across diagnostic groups (p=.07). However, no other
trends were found to be significant over time. See Table 10 for the between subjects
effects across diagnostic groups and Figure three. To further assess changes in cortisol
concentrations as a result of the cognitive stress task two difference scores were
calculated — 1) difference between baseline cortisol concentrations and the saliva
sampling immediately post task and 2) difference between the saliva sampling
immediately post task and the final post task cortisol sampling (i.e., 25 minutes post
task). These times were chosen based on the rationale that individuals would show the

largest increase in cortisol concentrations between baseline and immediately post task.

76

Subsequent to the cortisol sampling post task individuals were debriefed about the stress
task, and typically control subjects would show a decline in cortisol concentrations
thereafter, demonstrating the greatest changes in cortisol concentrations from peak
response post task to the final sampling 25 minutes post task (Simeon, Knutelska, Smith
et al., 2007). These two difference scores were used as outcome variables in univariate F
tests with diagnostic groups as predictors. Similar to prior findings the results did not
indicate significant differences in changes in cortisol concentrations related to different
diagnostic groups. Dissociative symptoms were included as a covariate and were also non
significant.
Hypothesis for challenged cortisol based on trauma characteristics: chronicity

Repeated measures ANCOVA was used to examine the effect of chronicity
groups, with dissociation as a covariate, on challenged cortisol. However, neither
chronicity nor dissociative symptoms were significant predictors of mean differences or
trends in cortisol concentrations over time. These findings were consistent with results
from univariate F tests using the two difference scores as outcome variables, chronicity
groups as predictors, and dissociative symptoms as a covariate.
Hypothesis for challenged cortisol based on trauma characteristics: earliest age of
trauma exposure

Repeated measures analyses using earliest age of trauma exposure and
dissociative symptoms as predictors, indicated that neither factor was a significant
predictor of mean differences or trends in cortisol concentrations over time. These
findings were consistent with results from regression analyses using both difference

scores as outcome variables.

77

Hypothesis for challenged cortisol cortisol based on trauma characteristics: cumulative
trauma exposure based on relationship to perpetrator

Repeated measures ANOVA was used to examine the effect of relationship to
perpetrator on challenged cortisol. However, F tests were not significant for either
predictor. Univariate analyses using difference scores as outcomes also did not indicate
significant effects for perpetrator type on changes in cortisol concentrations related to the
cognitive stress task.
Hypothesis for challenged cortisol based on trauma characteristics: social support

Repeated measures analyses using general levels of social support and
dissociative symptoms as predictors, indicated that neither factor significantly predicted
mean differences in cortisol concentrations, or trends in changes in cortisol
concentrations over time. These findings were consistent with results fi'om regression
analyses using both difference scores as outcome variables. Similar results were found
for perceived social support at the time of most traumatic event identified by the

participant.

78

CHAPTER 7
Discussion
The goal of the current study was to examine whether and how typical mental
health disorders seen in the context of IPV and chronic trauma exposure, and various
trauma related characteristics, are associated with salivary cortisol measures, as an
indicator of HPA axis dysfunction. Controlling for multiple methodological confounds
typically seen in the literature, the study found that diagnostic groups were not
differentially related to any cortisol measures. An examination of other common trauma
sequelae including dissociative symptoms and borderline personality diagnosis,
suggested that dissociative symptoms were the only significant predictor of cortisol
concentrations. Specifically low levels of awakening cortisol concentrations were
associated with high levels of dissociative symptoms, suggesting that psychological
factors other than the commonly explored PTSD and mood disorders are important for
future examination.
Basal and diurnal cortisol findings
Findings from the current study did not support the primary hypotheses of
differences in basal cortisol concentrations across various diagnostic groups PTSD,
PTSD and MDD, subthreshold trauma/ trauma and depressive symptoms relative to the
control comparison group. These findings are inconsistent with the majority of the extant
literature, though partially consistent with a meta-analytic study, which did not find
differences between PTSD and control subjects with respect to basal cortisol
concentrations (Meewisse et al., 2007). As noted earlier, this meta-analytic study used

only one data point, i.e. the earliest available cortisol measure (with respect to time of

79

day), from each study rather than calculating a combined effect size for each study. This
methodology could have influenced study findings. Altemately, the lack of significant
differences between PTSD and control comparison groups, could suggest that differences
in basal cortisol concentrations typically noted in the literature are accounted for by other
frequently co-occuring trauma related factors (e. g., dissociation).

Findings in the current study also did not support hypotheses regarding
differences in basal cortisol concentrations related to differences in trauma related
characteristics such as chronicity of trauma exposure (i.e., adulthood versus childhood
and adhulthood trauma), differences in the types of cumulative trauma experienced (i.e.,
interpersonal versus interpersonal and non-personal forms of trauma), age of earliest
trauma exposure, and the amount of general social support and/ or trauma-related social
support available to women.

Although the study’s primary hypotheses were not supported, dissociative
symptoms were consistently found to predict basal cortisol concentrations. This
association was specific to the relationship between awakening cortisol and dissociative
symptoms. Women with trauma exposure differed from their control counterparts and
reported significantly higher levels of dissociative symptoms, which was significantly
associated with lower levels of awakening cortisol. These findings are partially consistent
with the limited literature examining the relationship between dissociative symptoms and
cortisol levels in adults with a history of trauma exposure (Neylan et al., 2005; Simeon,
Knutelska, Smith et al., 2007; Simeon et al., 2008). For instance, Neylan and colleagues
(2005) examined the relationship between PTSD and dissociative symptoms and salivary

cortisol concentrations, in 30 active duty police officers and found that dissociative

80

symptoms at the time of trauma exposure were inversely related to cortisol at awakening.
However, after accounting for the effects of age, PTSD symptoms and peritraumatic
distress (panic and related negative reactions) only PTSD symptoms were found to
significantly predict cortisol at awakening.

In a different study, Simeon and colleagues (2008) examined dissociation and
posttraumatic stress and cortisol in adults approximately nine months after being exposed
to the World Trade Center attack on 9/11. Twenty one highly exposed adults (1/3 rd of
whom met full PTSD criteria) were compared with 10 healthy controls without major
trauma exposure. The two groups did not differ on cortisol measures however
dissociative symptoms were significantly associated with lower levels of morning plasma
cortisol concentrations. The study findings also suggested that dissociation and
posttraumatic stress may differ with respect to both phenomenological and biological
correlates. Specifically the study reported that dissociation at the time of assessment was
associated with childhood trauma while posttraumatic stress was not. Similarly other
factors such as exposure magnitude, peritraumatic distress, and early posttraumatic stress,
were also associated with posttraumatic stress but not with dissociation at the time of
assessment. The authors suggest that this may reflect two different processes i.e. while
factors associated with posttraumatic stress tap into arousal dissociation represents
“..Shut-down processes...” (Simeon et al., 2008, p.327).

The conceptualization posited by Simeon and colleagues (2008) is consistent with
the phenomenological understanding of dissociative features. As per trauma theory,
Hermann (1992) suggested that the development of psychological disorders is rooted in

the psychological defenses used to cope with an unpredictable and threatening

81

 

 

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environment. Thus, experiences that are not integrated into conscious awareness and
memory lay the cornerstone for cognitive distortions and dissociative states. As a result,
dissociative symptoms are commonly seen in the face of trauma exposure (Herman,
1992; van der Hart, Nijenhuis, & Steele, 2006). Though ostensibly adaptive in the Short
term, this results in a disruption of functions of consciousness, memory, identity or
perception, and also appears to be associated with specific neuroendocrinological
dysfunction, which maybe different from other co-occurring trauma related conditions
such as PTSD and MDD.

There is evidence to suggest that dissociative symptoms predict autonomic
hyporesponsivity as assessed through diminished heart rate and galvanic skin responses
(Griffin, Resick, & Mechanic, 1997; Sierra et al., 2002). In behavioral terms dissociative
symptoms, which present as mind-blanking, lapses in memory and attention, symptoms
of depersonalization and derealization etc., are viewed as coping mechanisms to mentally
and emotionally disconnect one self from traumatic stressors (Carlson & Putnam, 1993;
van der Hart et al., 2006). Thus it is likely that major stress systems such as the HPA axis
and the noradrenergic axes may function differently in the presence of dissociation. As
these systems play a key role in attention and arousal, the presence of posttraumatic stress
symptoms in the absence of dissociation maybe associated with hyperarousal and
intrusive symptomatology, but in the presence of dissociative symptoms, maybe
indicative of autonomic blunting and reflected through low cortisol levels. This may in
turn explain dissociative symptoms as being characterized by ‘shutting down’ behaviors,
as a means for women to turn their attention away from very overwhelming traumatic

experiences.

82

The current study’s findings are also reminiscent of studies showing low basal
(Yehuda, 2002) and awakening cortisol in populations with chronic trauma (Delahanty et
al., 2005). However, it has been suggested that low cortisol may not be associated with
the diagnosis of PTSD per se but may predate and be a risk factor for the development of
PTSD, marking greater HPA axis vulnerability to traumatic events in relation to early life
trauma (King et al., 2001; Young & Breslau, 2004b). Thus it is possible that the current
study’s findings reflect that low awakening cortisol is a risk factor associated specifically
with dissociative symptoms which in turn could mediate the effects of trauma exposure
on PTSD.

Findings in the literature also suggest that factors such as peritraumatic
dissociation (i.e. dissociation at the time of trauma exposure) may be relevant to examine.
While peritraumatic dissociation has been associated with PTSD (e. g., Nishi et al., 2010)
and dissociation at later stages (Bremner & Brett, 1997; Simeon, Greenberg, Nelson,
Schmeidler, & Hollander, 2005), a growing body of literature shows that the contribution
of peritraumatic dissociation to later PTSD declines alter accounting for baseline PTSD
severity (Marshall & Schell, 2002) or accounting for other factors such as peritraumatic
distress (i.e., fear of death, loss control, etc.) (Gershuny, Cloitre, & Otto, 2003). In the
current study, the trauma-exposed groups had significantly higher dissociative symptoms
than the control group and diagnostic groups were not predictive of basal cortisol. Thus,
it is possible that other factors such as peritraumatic dissociation and peritraumatic
distress which were not evaluated in the current study, may better account for the
findings and observed relationships. For instance, the presence of peritraumatic

dissociation at the time of a traumatic event may be a more important factor rather than

83

the development of PTSD at a later stage, and its effects may be mediated by later
dissociative symptoms.

Another factor that may have influenced the lack of findings in the current study
is the assessment of specific psychological constructs. For instance, the measure of
dissociative symptoms asks participants to report how often they engage in specific
behaviors or experience certain events that represent dissociative symptoms. While
reports on the measure of dissociation is more likely to assess current or recent behaviors/
experiences, diagnoses and posttraumatic stress symptoms in the current study were
assessed based on the event identified by the participant as being most traumatic, which
could have occurred at any time in their life. It is possible that a current or more proximal
diagnosis of PTSD i.e. related to more recent events only (e. g., IPV specific PTSD) may
be better predictive of cortisol concentrations. Some support for this idea comes from
findings from Simeon and colleagues’ (2005) study, which found that the effects of
dissociation following a recent traumatic event on cortisol was distinguishable from
posttraumatic stress related to childhood trauma history. However, this issue needs
further examination due to the limited number of studies examining the effects of
dissociative symptoms, and the significant differences in sample characteristics and types
of trauma examined, between the current study and the aforementioned studies examining
the role of dissociation on cortisol concentrations.

Finally, another possibility for assessing whether there are different subtypes of
neuroendocrine profiles in trauma exposed women which is associated with unique
psychological factors as predictors could beto examine whether there are distinct clusters

of cortisol profiles and examine which psychological factors or trauma related

84

characteristics are associated with these cortisol profiles. Although this methodology has
not been used in the literature examining cortisol measures in trauma exposed women,
studies examining behavioral measures have found it effective in identifying unique
predictors for differing behavioral clusters (Tremblay et al., 2004).

It is notable that the current study improves on a number of methodological issues
in the literature by accounting for diagnostic and symptomatic comorbidity, use of
medication and contraception, substance abuse/ dependence, and physical health
problems that have been shown to influence cortisol measures. After accounting for these
factors, this study did not find support for the impact of factors typically noted in the
literature (e. g., diagnostic classification, chronicity). Dissociation was the only robust
predictor of awakening cortisol, which is consistent with the limited number of studies
examining the association between dissociation and cortisol measures. As dissociation
and other trauma sequelae (e. g., PTSD, MDD) are frequently comorbid and most studies
have not examined the effects of dissociation on cortisol concentrations, findings from
the current study suggest a need for further examination of the differential correlates of
typical trauma sequelae.

Challenged cortisol

With respect to challenged cortisol measures, the study did not find evidence of
group differences in changes in cortisol concentrations across diagnostic groups or
related to differences in trauma related characteristics such as chronicity of trauma
exposure (i.e., adulthood versus childhood and adulthood trauma), differences in the

types of cumulative trauma experienced (i.e., interpersonal versus interpersonal and non—

85

personal forms of trauma), age of earliest trauma exposure, and the amount of general
social support and/ or trauma-related social support available to women.

These findings are inconsistent with extant literature which has demonstrated
differences in the stress response system in adults exposed to traumatic events relative to
control comparison groups (e. g., Bremner et al., 2003; Carpenter et al., 2007 ; Elzinga et
al., 2008; Heim et al., 2000; Santa Ana et al., 2006; Simeon, Knutelska, Yehuda et al.,
2007). There were no significant differences in mean levels of cortisol concentrations
across diagnostic groups or differences in changes in cortisol concentrations pre- and
post-paradigm. However, due to a trend in these findings, it is possible that unequal and
small sample sizes across diagnostic groups may have influenced the lack of significant
findings. This is also supported by the fact that the mean ratings of perceived stress due
to the cognitive stress task was in the moderate to high range across all groups. See Table
7. Altemately, it is possible that despite the participants self perceived stress ratings, the
stress paradigm was not effective in mobilizing the stress response system. The current
study used an adapted version of the TSST paradigm. While the original paradigm has
been shown to be effective in mobilizing the stress response system and has shown
differences in rates of changes in cortisol concentrations relative to diagnostic status
(Carpenter et al., 2007; Elzinga et al., 2008; Heim et al., 2000; Simeon, Knutelska,
Yehuda et al., 2007), this is the only study to use the adapted protocol. Differences in the
current study’s paradigm, particularly the mock recording using an audiotape rather than
a videotape, as in the original paradigm, may have affected these findings. It is possible
that the stress perceived as a result of having to give a speech, and be interviewed, while

being videotaped is likely to be more anxiety provoking than being audio recorded only.

86

Limitations

The use of retrospective reporting within a cross sectional design precludes the
possibility of a comprehensive and accurate assessment of lifetime exposure to traumatic
events. Also, sample sizes varied across diagnostic groups, with very small cell sizes in
some groups, which may have made it difficult to detect group differences, particularly
with respect to challenged cortisol measures.

Findings in the current study are partially consistent with the limited literature
examining the association between dissociative symptoms and cortisol measures.
Findings from one of these studies suggests that other factors such as peritraumatic
dissociation and peritraumatic distress may be important mediators in predicting cortisol
concentrations. These factors were not assessed in the current study and suggest an
important area for future examination. Another, methodological issue that needs further
examination is whether diagnoses and assessment of posttraumatic stress symptoms
based on the event identified by the participant as being most traumatic or more proximal
diagnosis of PTSD i.e. related to more recent events only (e. g., IPV specific PTSD) is a
better predictor of cortisol concentrations.

The lack of significant findings related to challenged cortisol measures maybe
attributable to the use of an adapted version of the original TSST. It is likely that using
the original TSST, which has consistently been shown to be effective in mobilizing the
stress response system, may have yielded different results. Additionally, the use of
chemical stressor such as dexamethasone test may also provide a more effective measure

of the stress response system.

87

Finally, factors related to cortisol sampling could also have affected the lack of
findings. For instance, the study relied on self report of participants regarding time of
cortisol collection. The use of MEMS cap provides a more accurate and objective means
of measuring participants’ compliance to the protocol of collecting saliva samples at
specific times. Additionally, the study had no way of ensuring participants’ fidelity to
instructions of storing saliva samples in their freezer at home prior to pick up. Another
limitation of the current study was the use of only one sampling for each time of day.
Repeated sampling of salivary cortisol at the same time of day, across multiple days,
would have provided a more accurate measure of cortisol levels.

Conclusion

The goal of the current study was to examine differences in basal, diurnal, and
challenged cortisol measures in a sample of premenopausal non pregnant adult women,
who differed with respect to diagnostic status (PTSD, PTSD and MDD, subthreshold
symptoms) and trauma characteristics (chronicity of trauma, differences in cumulative
trauma types, age of first trauma exposure, and social support) relative to control
comparison counterparts.

The study did not find evidence in support of the major hypotheses for the
differential effects of diagnostic groups and trauma characteristics, after controlling for
typical methodological limitations. Results indicated a relationship between dissociative
symptoms and awakening cortisol such that trauma exposed women, regardless of their
diagnostic status had higher levels of dissociative symptoms relative to women in the
control group, which was inversely related to cortisol levels at awakening. Findings

suggest that HPA axis functioning may be different in the presence of dissociative

88

 

 

symptoms and may differ from HPA axis functioning in the presence of PTSD when
dissociative symptoms are not present. Studies examining the relationship between
dissociation and its biological correlates are very limited but have Shown similar results.
These findings are consistent with the phenomenological presentation of dissociative
symptoms as ‘shutting down’ mechanisms, which likely serve to protect trauma survivors
fiom the overwhelming stress associated with traumatic experiences. Future studies
should further examine whether and how stress systems such as the HPA axis function
differently in the presence of PTSD when other comorbid symptomatology such as

depression and dissociation are present.

89

APPENDICES

90

APPENDIX A

91

Table 1.

Classification of sample based on diagnostic groups

 

Diagnosis n
Control 12
PTSD only 14
PTSD and MDD 43
Subthreshold symptoms 19
MDD only 4
Total 92

 

92

Table 2.

Age and Monthly Income Across Diagnostic Groups

 

 

 

 

Diagnosis Age Monthly Income
Mean SD (Range) Mean SD (Range)
PTSD only 28.50 7.21 (18.70 - 41.00) 1338.43 907.48 (300.00 - 3000.00)

PTSD and MDD 28.19 6.44 (18.76 - 41.50) 1984.91 2219.32 (160.00 - 12000.00)
Subthreshold 25.84 7.78 (19.55 - 40.44) 3115.12 3819.81 (00.00 - 12000.00)

Control 22.78 2.13 (18.99 - 26.28) 3510.00 3501.55 (400.00 - 12500.00)

 

No significant dyferences in age or monthly income across diagnostic groups

93

Table 3.

Education information across diagnostic groups percentage of total)

 

 

Education PTSD PTSD + MDD Subthreshold
Control
(n) % (n) % (n) % (n) %

High school/ GED (4) 4.50 (15) 17.00 (2) 2.30 (1) 1.1
Some college/

Trade School/

Associates Degree (5) 5.70 (22) 25.00 (13) 14.80 (5) 5.70
College (2) 2.30 (3) 3.40 (3) 3.40 (3) 3.40
Graduate (3) 3.40 (3) 3.40 (1) 1.10 (3) 3.40

 

No significant diflerences in education levels across diagnostic groups

94

Table 4.

Ethnicity information across diagnostic groups percentage of total)

 

 

Ethnicity PTSD PTSD + MDD Subthreshold
Control
(n) % (n) % (n) % (n) %
African American (7) 8.00 (8) 9.10 (5) 5.70 (1) 1.10
Caucasian (6) 6.80 (20) 22.70 (12) 13.60 (8) 9.10
Hispanic (0) 0.00 (6) 6.80 (1) 1.10 (1) 1.10
Other (1)1.10 (9) 10.20 (1)1.10 (2) 2.30

 

No significant difiizrences in ethnicity across diagnostic groups

95

Table 5.

Descriptives for Cortisol Values Pre and Post Mean Substitution by Diagnostic Group

 

Pre mean substitution Post mean substitution

 

 

 

Mean (SD) Mean (SD)
PTSD

Baseline .35 (.11) .35 (.09)
Immediately post task .34 (.10) .34 (.01)
10 minutes post task .33 (.12) .33 (.11)
25 minutes post task .31 (.10) .31 (.09)
Night .30 (.13) .30 (.13)
Awakening .32 (.12) .32 (.12)
45 minutes post awakening .41 (.12) .41 (.12)

 

96

Table 5 continued.

Descriptives for Cortisol Values Pre and Post Mean Substitution by Diagnostic Group

 

Pre mean substitution Post mean substitution

 

 

 

Mean (SD) Mean (SD)
PTSD + MDD

Baseline .27 (.13) .27 (.11)
Immediately post task .28 (.10) .28 (.09)
10 minutes post task .28 (.11) .28(.10)
25 nrinutes post task .28 (.12) .28 (.11)
Night .27 (.13) .27 (.11)
Awakening .37 (.20) .37 (.17)
45 minutes post awakening .46 (.32) .46 (.27)

 

97

Table 5 continued.

Descriptives for Cortisol Values Pre and Post Mean Substitution by Diagnostic Group

 

Pre mean substitution Post mean substitution

 

 

 

Mean (SD) Mean (SD)
Subthreshold

Baseline .27 (.11) .27 (.11)
Immediately post task .26 (.11) .26 (.11)
10 minutes post task .26 (.11) .26(.12)
25 minutes post task .26 (.12) .25 (.12)
Night .26 (.13) .25 (.16)
Awakening .39 (.17) .39 (.16)
45 minutes post awakening .46 (.32) .48 (.27)

 

98

Table 5 continued.

Descriptives for Cortisol Values Pre and Post Mean Substitution by Diagnostic Group

 

Pre mean substitution Post mean substitution

 

 

 

Mean (SD) Mean (SD)
Control

Baseline .23 (.19) .23 (.19)
Immediately post task .20 (.13) .20 (.13)
10 minutes post task .21 (.13) .21(.13)
25 minutes post task .21 (.14) .21 (.14)
Night .33 (.42) .33 (.38)
Awakening .37 (.22) .37 (.21)
45 minutes post awakening .47 (.25) .47 (.23)

 

99

Table 6

Dissociative Symptoms and Daily Hassles Diagnostic Groups

 

 

 

 

Diagnosis Dissociative Symptoms Daily Hassles
Mean SD Mean S.D .
PTSD only 583.57 (452.41) 56.29 (23.89)
PTSD and MDD 531.21 (443.13) 56.46 (22.62)
Subthreshold 317.79 (173.67) 49.00 (18.59)
Control 112.50 (59.72) 40.50 (9.98)

 

No significant diflkrences across groups with respect to daily hassles. All trauma exposed

groups significantly differ from control group with respect to dissociative symptoms.

100

Table 7

Self Perceived Stress Ratings for Cognitive Stress Task across Diagnostic Groups

 

 

 

Diagnosis Stress Ratings
Mean SD
PTSD only 58.46 25.44
PTSD and MDD 74.05 17.26
Subthreshold 70.53 17.79

Control 58.33 16.42

 

101

Table 8.

Between Subjects Effects for Basal Cortisol Concentrations Across Diagnostic Groups

 

 

(ANCOVA)

Source df F p 112 Power
Diagnosis 3 .38 .77 .01 .12
Dissociation l 4.68 .03 .05 .57

 

102

Table 9.
Repeated Measures AN C 0 VA for Diurnal Cortisol Concentrations Across Diagnostic

 

 

 

Groups
Source df F p 112 Power
Between subjects
Diagnosis 3 1.39 .25 .05 .36
Dissociation 1 3.88 .05 .05 .50
Within subjects
Diurnal
Linear 1 .54 .47 .01 .1 1
Quadratic l 19.38 .00 .19 .99
Cubic 1 1.68 .20 .02 .25
Diurnal * Diagnosis
Linear 3 1.12 .35 .04 .29
Quadratic 3 1.26 .30 .04 .33
Cubic 3 .45 .72 .02 .14
Diurnal * Dissociation
Linear 1 7.68 .01 .09 .78
Quadratic 1 .27 .60 .00 .08
Cubic 1 1.36 .25 .02 .21

103

Table 10.

Repeated Measures ANCO VA for Challenged Cortisol Concentrations Across Diagnostic

 

 

 

Groups
Source df F p 112 Power
Between subjects
Diagnosis 3 2.36 .07 .07 .57
Dissociation 1 .01 .93 .00 .05
Within subjects
Challenged
Linear 1 .02 .88 .00 .05
Quadratic 1 .02 .88 .00 .05
Cubic l .50 .48 .01 .11
Challenged * Diagnosis
Linear 3 1.01 .36 .04 .28
Quadratic 3 .13 .95 .01 .07
Cubic 3 .88 .46 .03 .23
Challenged * Dissociation
Linear 1 .47 .50 .01 .10
Quadratic 1 .03 .85 .00 .05
Cubic 1 1.20 .28 .01 .19

104

APPENDIX B

105

Figure 1.
Basal Cortisol Concentrations Across Diagnostic Groups

 

0.50"

0.40" __

 

0.30‘ __

 

 

Mean Basal Cortisol Concentrations

0.20“

 

 

 

 

I l I
PTSD PTSD + MDD Subthreshold Control

* Error bars represent +/- 1 Standard deviation ** PT SD= Posttraumatic Stress
Disorder, MDD = Major Depressive Disorder, Subthreshold = Subthreshold symptoms
of PTSD or PT SD and MDD, Control = Control comparison group with no lifetime
exposure to intimate partner violence/ interpersonal forms of trauma, or PT SD/ mood
disorder diagnoses.

106

Figure 2.
Diurnal Cortisol Concentrations Across Diagnoses

 

 

 

 

 

 

 

 

 

0.6
0.5 —
0.4 .
-o-P'rso 1
0 3 +PTSD + MDD {
' +Subthresholdl
—o—Conuol l
0.2
0.1 -
o A Y r
Night Awakening 45 mins post Evening (baseline)
awakening

 

 

PTSD = Posttraumatic Stress Disorder, MDD = Major Depressive Disorder,
Subthreshold = Subthreshold symptoms of PTSD or PTSD and MDD, Control = Control
comparison group with no lifetime exposure to intimate partner violence/ interpersonal
forms of trauma, or PTSD/ mood disorder diagnoses.

107

 

Figure 3.
Challenged Cortisol Concentrations Across Diagnoses

 

 

 

 

 

 

 

I
I
I fi\.

0.3 I
0.25 I

I I-o-PTSO I

. I +SubthresholdI

i —O—Control I
0.15 I
|
I
0.1 j
I.
0.05 I
I

 

0 +,_’.____ '— T“ Tar—— T—— ’—'T#_ T— T "-fi

Baseline PostTask 10 minutes post 25 minutes post
task task

 

 

 

PTSD = Posttraumatic Stress Disorder, MDD = Major Depressive Disorder,
Subthreshold = Subthreshold symptoms of PT SD or PT SD and MDD, Control = Control

comparison group with no lifetime exposure to intimate partner violence/ interpersonal
forms of trauma, or PT SD/ mood disorder diagnoses.

108

APPENDIX C

109

Phone Screen
Standardized protocol to introduce study: “Thank you for your interest in the
Women’s Health Study. Let me tell you a little bit about our study so you know what the
study is about. I also need to ask you some background questions and some health-related
questions to make sure that you are eligible for our study. This will take about 10
minutes, is this a good time for you to talk?”
Following the standardized protocol to introduce the study, the following questions

will be asked to screen participants for the study:

1. What is your date of birth <MM/ DD/ YYY>? / /

 

2. What is the highest level of education you have completed?

I. Gradezl 2 3 4 5 6 7 8 9 10 11 12 13=GED

11. Some college
111. College (B.A/ B Sc)

IV. Trade School (Cosmetology, Nursing, TechnicalNocational)

V. Associates degree
V1. Some graduate school

VII. Graduate School

 

 

VIII. Other (if less than grade 6 > Not Eligible)
3. Are you currently pregnant? Y ——> Not Eligible
4. Are you currently breast feeding? Y N

I. If yes ——’ Not Eligible

If No —* Continue with screen

110

5. Are you currently married or living with a male partner?

I.

II.

6. Has your partner ever been violent towards you? _, If No skip to

I.

Y N

If yes -- when did you get married/ start living together <MM/ YYYY>

/

If no -- in e past two years have you been involved in a romantic
relationship with a man, for 6 weeks or longer (i.e. 1.5 months)?

Y N A, Not Eligible

 

 

Q. no. 8

 

 

 

If yes, has your partner been violent towards you in the past 2 years?

 

 

 

If No Not eligible

 

 

 

 

 

 

Screener for PTSD/ MDD Symptoms

7. In the past month have you experienced any of the following:

I.

II.

III.

Have experienced thoughts/ memories/ images in your mind about those
difficult experiences? Y N
Have you had dreams/ nightmares about those difficult experiences?
Y N
Have you had the feeling that some of those events might be happening

again? Y N

111

IV. Do you have a strong reaction when you are faced with reminders of some
Of those incidents? Y N

Note examples

 

V. Do you try to avoid thinking/ feeling/ talking about those experiences?
Y N
VI. Do you try to avoid activities/ places/ people that remind you about those
experiences? Y N
VII. Are there large parts of those experiences that you cannot remember?
Y N
VIII. Do you feel that you have lost interest in activities that you used to enjoy
before these incidents with your partner?
Y N
IX. Do you feel detached/ disconnected! removed from others since these
incidents? Y N
X. Do you feel unable to experience certain emotions since theses experiences
(e.g., loving feelings/ angry feelings/ sadness/ crying)
Y N
XI. Do you feel like you may not do certain things in life, like have a career or
some other goal you may have previously wanted to do?
Y N
XII. Do you have difficulty falling asleep, or difficulty staying asleep?
Y N

XIII. DO you feel irritable or have outbursts of anger?

112

XIV.

XV.

XVI.

XVII.

XVIII.

XIX.

XXII.

XXIII.

Y N
DO you experience difficulty concentrating?
Y N
DO you feel like you are on edge / vigilant/ worrying about things?
Y N
Do you have a strong reaction to small firings? That you get easily scared or
upset? Y N
Do you feel depressed or sad most of the day nearly everyday?
Y N
Has there been significant changes in your weight since these incidents
(weight loss or weight gain)?
Y N
Do you find that you sleep too little or too much?
Y N
Do you feel fatigue and loss of energy a lot of the time?

Y N

. Do you find it physically difficult to do daily chores and errands (like your

body or arms/ legs heavy and you have to drag yourself to do anything)?
Y N

Do you find it hard to relax and find yourself physically restless a lot?
Y N

Do you have negative feelings about your self like feelings of

worthlessness? Y N

113

XXIV. Do you feel guilty or blame yourself a lot?

 

 

Y N
It
If “yes” to at least If “no” to
2 all the
Go to AUDIT questions

 

 

 

 

 

I

 

 

Not eligible

 

 

 

ll4

8. Have you ever had any psychological problems (e. g., depression, anxiety problems
etc)? If yes, note following details

i. Describe exact nature of the problem

 

 

 

ii. When did you first notice these problems?

 

 

 

iii. Were you ever formally diagnosed with any disorder? If yes, by whom

(psychologist! psychiatrist/primary care provider/ counselor etc.)?

 

 

 

iv. Are you Sill having similar difficulties?

 

 

 

9. Have you ever been exposed to a major traumatic event (e. g., been in danger of being

hurt or killed or witnessed a loved in danger of being hurt or killed)?

 

 

 

115

Questions to screen for other drug use related difficulties

1. Have you §v_er used any drugs for non medical purposes? (Use the following as
prompts/ rule outs)
1a. Cannabis (marijuana, pot, grass, hash, etc.)
lb. Cocaine (coke, crack, etc.)
1c. Amphetamine type stimulants (speed, diet pills, ecstasy, etc.)
1d. Inhalants (nitrous, glue, petrol, paint thinner, etc.)
1e. Sedatives or Sleeping Pills (Valium, Serepax, Rohypnol, etc.)

If. Hallucinogens (LSD, acid, mushrooms, PCP, Special K, etc.)

'-< < < -< ~< -< '<

lg. Opioids (heroin, morphine, methadone, codeine, etc.)

ZZZZZZZZ

1h. Any other drugs for non medication purposes? Y
2. In the past 3 monthshow often have you used (for each endorsement from

above)?

 

Never 1 -3 times Monthly Weekly Daily/ Almost
daily

per year 1 — 2 timed 1-3
month times/week 4 - 7 times!
week

 

Cannabis

 

Cocaine

 

Stimulants

 

Inhalants

 

Sedatives

 

Hallucinogens

 

Opioids

 

Other

 

 

 

 

 

 

 

 

116

3. During the past 3 months, how Often has your use of (fill fronflbove) led to
social, legal or financial problems or problems in daily functioning or work (e.g.
running errands, attending school, taking care of children, and reaching work on time?)

a. Never
b. l -2 times in the past 3 months
c. At least once a month
d. Weekly basis
e. Daily
4. In the past 3 months, have you received counseling/ rehabilitation services, or any

other help/ treatment for using (fill from above)? Note details of multiple treatments, if

 

 

applicable.
4a. When did you start treatment ?
4b. For how long did you receive treatment ?
4c. What kind of treatment did you receive ?

 

Questions to screen for psychotic disorders

1. Have you ever seen things that other people could not see?

a. If yes, describe

 

b. How Often does it happen?
2. Have you ever hear voices, noises or sounds that others could not?

a. If yes, describe

 

b. How often does it happen?
3. Have you smelled or tasted something strange that you could not explain and
others could not smell/ taste?

a. If yes, describe

 

117

b. How often does it happen?
Questions to screen for neurolog’cal/ endocrine/ medical disorders
1. Have you ever been diagnosed with any of the following disorders?
1a. Alzheimer’s Disease Y N
1b. Aphasia
1c. Bell’s Palsy
1d. Stroke
1e. Encephalitis
1f. Epilepsy
1 g. Huntington’s Disease
1h. Parkinson’s Disease
1i. Muscular Dystrophy or Sclerosis
l j. Cushing’s Disease
1k. Addisons Disease

11. Cancer

~<~<~<~<~<~<~<~<~<~<~<~<
zzzzzzzzzzzz

lm. Any cognitive impairments
Have you ever been diagnosed with any other major medical problem

If yes, note the name, and if undergoing any treatment

 

118

Questions to screen for medication usage

1. What medications (prescription or over the counter), including hormonal birth
control, are you currently taking?
a. If none, have you taken any medications (prescription or over the counter)
or birth control, in the past 3 months?

Name Dosage Since when (note duration)?

 

 

 

 

 

 

Questions for to establish menstrual gycle
1. Do you have a regular menstrual cycle? Y N

la. If no, please describe your typical menstrual cycle in the past 3 months (how

often did they occur and for how long each time did your periods last)?

 

 

 

2. Have you skipped any periods in the past 3 months? Y N
3. Have you skipped period in the past month? Y N

4. What is the first date of your last periods? <MM/DD/YYY> / /

 

119

5. How many days did your periods last in the past month?
6. How many days do your periods typically last?

“Our study is interested in understanding how women’s experiences with their
partners affect their psychological and physical health, and how they cope with these
experiences. Our study involves one face to face interview at the MSU campus, which
typically takes between 1.5 — 2 hours. During the interview we will ask you about your
experiences with your partner, and some questions about your moods and behaviors. We
are also interested in your daily life experiences such as taking care of the kids, going to
work etc. and any help or support you get from other people such as your friends/ family
or anyone else. Some of these questions will be in interview form and for some of them
you can fill up the questionnaires on your own. A part of the interview also involves
performing some tasks like writing a paragraph on a topic. Finally, during the interview
we will collect some saliva samples and also give you a kit to take home and collect your
saliva at specific times in the day. Will you be able to take saliva samples at home safely?
[For women who indicate currently living with their partner add: “Do you have any
concerns about having problems with your partner if you take saliva samples at home?”]

You will be paid a total of $40 for participating in our study. You will receive $25
at the completion of the interview and $15 when we receive the saliva that you collect at
home. We can collect the take home kit from you, from any location of your choice or

you can return it to our MSU project office. Do you have any questions so far?”

120

Comitive Stress Challenge

After initial rapport formation, participants will complete the demographic
questionnaire with the interviewer to allow them time to acclimatize to the research
setting. Next, participants will be given a 5 minute resting period after which they will
give their first, baseline, saliva sample. The resting period prior to the stress task is
necessary to avoid potential activation of the HPA axis, which could confound with later
activation during the cognitive stress challenge {Kirschbaum, 1993 #291 }.

Next, the interviewer (referred to as the experimenter from hereon) will inform
the participants about the task they are required to work on and introduce it as follows “I
will now ask you to perform a task. You have to deliver a speech for a job application, for
which you will have five minutes to prepare. A person trained in behavioral observation
will be joining us and she will take notes about the way you give your speech and the
things you say. You should imagine that you applied for a job position and you are being
invited by that company or place to interview. Your speech should be five minutes long.
This speech will be voice recorded and we will time you. You can make notes while you
are preparing but you cannot use the notes once you start speaking. Make sure that your
speech is believable because the observer will ask you additional questions. After this
task I will ask you to do one more task and I will tell you about that after you deliver your
speech”. The experimenter then asks whether the participant if she has any questions
regarding the protocol and will answer any such questions.

Once the participant is ready to give the speech, an advanced graduate student
(referred to as the observer from hereon) will enter the room set up a mock audio taping

device (the performance will not be recorded) and “switch on” the recording. The

121

experimenter will use a stop watch to time the participant. The observer will begin by
asking the participant their name and then ask them, “What qualifies you in particular for
this position?”

After five minutes, the experimenter will introduce the next task as follows,
“Let’s move on to the next task. Now we want you to solve a calculation task. Please
count aloud backwards from 2083 to zero in 13-step sequences. Please calculate as
quickly and correctly as possible. If you miscalculate, we will point out your mistake and
you have to start all over again fiom 2083. Do you have any questions? Please start."

Prime numbers will be used as subtractors for this task, because these make it
more difficult {Kirschbaum, 1993 #291}. Protocol sheets with all intermediate munbers
will be available to the experimenter and the observer so that they will not have to
calculate it themselves. If the participant miscalculates, the observer will respond with the
standard phrase "Error. 2083." until the participants reaches 0 or makes 4 mistakes
having started over each time. The experimenter will note the number of errors and the
number that the subject eventually reached as a performance measure.

Debriefing

Next, a detailed debriefing will be conducted with the participants, which will
include an explanation why the stress protocol had to be included for the current research
question. In addition, participants will be asked to rate the stressfulness of the paradigm
on a scale of 0 — 100. Participants will be told that the wording of the instructions and
tasks were chosen to assess how different people respond to anxiety-provoking tasks and
the task themselves were not meant to be evaluative of the participants in any way. They

will also be informed that the task had not been tape recorded. The debriefing text will be

122

as follows, “The reason we asked you to perform these tasks is because they are anxiety
provoking for most individuals and one of the things we are trying to study is how people
respond in anxiety provoking situations. The entire set up of having an observer and the
way the instructions were given was designed to make it realistic and believable for you,
so as to create the anxiety and see how people usually react in such situations. We did not
tape record this interview nor were you being evaluated or tested on your performance of
either of those tasks. Your performance on any of those tasks has no bearing for this

interview. We really appreciate your giving us your best effort.”

123

Protocol for collecting saliva samples

Participants were asked to imagine chewing their favorite food, moving their jaws
as if chewing while letting saliva collect under their tongue. Then, the participants were
asked to gently pass the saliva through a short plastic straw into a cryogenic vial. The
samples were frozen and later centrifuged for assays in Dr. Lonstein’s lab. At the end of
the interview each participant was given a kit with written instructions, 3 color coded and
labeled tubes and straws, and checklists for bedtime, awakening and 45 minutes post-
awakening. The pre-cognitive stress sampling was used to establish baseline for the stress
task and also used as the evening sample for basal cortisol. The specimen collection
procedure was shown to each participant and instruction about completing the
accompanying form was discussed (time of sample, what she ate, drank, when she
brushed her teeth or smoked in the 30 minutes prior to sampling). Participants were
contacted via telephone for reminders for the awakening and post-awakening sample (45
minutes later), if the participants provided their consent to do so. Participants were asked
to refiigerate the samples until they returned it to the research office or a research

assistant collected them at a time determined in conjunction with the participant.

124

table-3N

7.

Demographic Questionnaire

First Name

 

Last Name

 

How many biological children do you currently have?
What is your Date of Birth <MM/DD/YYYY> / /
What is your race/ ethnicity (choose only one)?

5.a. European American/ Caucasian

5.b. African American

5.c. Hispanic (not white)
5.d. Asian

5.e. Native American

5.f. Biracial

5.g. Multiracial

5.h. Other (please describe)

Choose one that best describes your current relthionship sta;u_s (choose only one):

 

6.a. single

6.b. never married but in a relationship

 

 

 

 

6.b.i. are you living with yourpartner? YES NO
I if YES, when did you start living together <MM/YYYY>
/

6.c. married

6.c.i. when did you get married <MM/YYYY> /
6.d. separated

.6.d.i. when did you separate <MM/YYYY> /
6.c. divorced

6.c.i. when did you divorce <MM/YYYY> /
6.f. widowed

6.f.i. when were you widowed <MM/YYYY> /

 

What is your religious affiliation (if any)?

 

8. Are you currently employed/ have you been employed in the past 3 months? YES NO

125

10.

ll.

12.

8.3. If yes, what is/was your occupation? (Please be specific. For example, bookeeper,

cashier, computer programmer)
8.b. Are/ were you working

8.b.i. full time

8.b.ii. part time

What is the highest level of education you have completed (choose only one)?

9.a.Grade:l 2 3 4 5 6 7 8 9 10 ll 12 13=GED

9.b. Some college
9.c. Trade School (Cosmetology, Nursing, TechnicaWocational)
9.d. AA degree
9.c. BA/BS
9.f. Some grad school
9.g. Graduate degree
9.g.i. Masters
9.g.ii. PhD.
9.g.iii. Law
9.g.iv. Medical Degree
Have you been in school during the last year? YES NO

If YES, please describe what you are currently doing in school.

 

 

What is your total family income Er month (please include financial aid/ loans/ disability/

unemployment etc. and give your best estimate)?

 

Do you currently receive services from any of the following:

12.a. Women, Infants and Children (WIC)

12.b. Temporary Assistance for Needy Families (TANF)

l2.c. Protective Services

12.d. Food Stamps

12 .e. Medicaid

12.f. Social Security Disability (SSI)

12.g. Family Independence Agency (FIA)

12.h. Any child related programs (e.g., 0-3; Mother-infant Program; Head Start)
12.i. Any other sources of support! services?

 

126

NO
N O
NO
N O
NO
N O
NO
NO
N 0

Brief Screen prior to baseline sampling

. Please note the time you finished your last meal: AM/ PM

If you have eaten anything since then, please note what it was and when you ate it

 

Did you drink anything other than water in the past 2 hours? Y N
a. If YES, please tell us what you drank (including alcoholic and non

alcoholic)

 

b. How many glasses/ cans did you drink

 

c. What time did you have the last drink

 

. Have you smoked in the past 1 hour Y N

a. How many cigarettes have you smoked

 

127

Aautoimmune diseases

Have you ever been diagnosed with any of the following?
__ Lupus
Graves' Disease
_ Hyperthyroidism
Celiac Disease
Gluten Intolerance
__ Irritable Bowel Syndrome
__ Hashimoto's Hypothyroidism
_ Polycystic Ovary Syndrome (PCOS)
Addison's Disease
__ Scleroderma (Skin thickening/ Skin ulcers on the fingers)
_ Sjogren's Syndrome
__ Multiple Sclerosis
__ Insulin-Dependent Type 1 Diabetes
__ Fibromyalgia
____Chronic Fatigue Syndrome
__ Rheumatoid Arthritis
If yesgo any of thejabove note the following individually for each disease:
Diagnosis
When were you diagnosed? <MM/ YYYY> / /
Did you undergo any treatment? Y N

 

If yes, what medications are/ were you taking?

Name

 

Dosage/ Frequency

 

When did you start the medication? <MM/YYYY> /

 

128

Substance use

1. Do you smoke? Y N
a. If yes, how often do you smoke?
i. Very occasionally 1-2 times per month
ii. 2-3 times a week
iii. 1-3 cigarettes per day
iv. 4-10 cigarettes per day
v. 1 pack per day
vi. More than 1 pack per day
vii. Other (please explain)

 

b. Have you smoked in the past 48 hours? Y N
i. If yes, please answer the following:

1. how many cigarettes did you smoke

 

2. when was the last cigarette you smoked:
Date:
Time:
c. Are you currently in the process of trying to quit smoking? Y N
i. If yes, are you using any nicotine patches/ gum/ medication?
Y N
ii. Please describe what nicotine patches/ gum/ medication you are

using

 

2. Did you consume any drinks containing alcohol in the past 48 hours? Y N
3. If yes, please answer the following:

a. how many drinks have you had in the past 48 hours?

b. when was the last drink you had
Date:

Time:

129

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130

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