Gender Differences in Posttraumatic Stress Disorder: Miranda Olff Willie Langeland

Psychological Bulletin Copyright 2007 by the American Psychological Association
2007, Vol. 133, No. 2, 183–204 0033-2909/07/$12.00 DOI: 10.1037/0033-2909.133.2.183
Gender Differences in Posttraumatic Stress Disorder
Miranda Olff Willie Langeland

University of Amsterdam University of Amsterdam and Vrije University
Nel Draijer Berthold P. R. Gersons

Vrije University University of Amsterdam
One of the most consistent findings in the epidemiology of posttraumatic stress disorder (PTSD) is the
higher risk of this disorder in women. Explanations reviewed within a psychobiological model of PTSD
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
suggest that women’s higher PTSD risk may be due to the type of trauma they experience, their younger
This document is copyrighted by the American Psychological Association or one of its allied publishers.
age at the time of trauma exposure, their stronger perceptions of threat and loss of control, higher levels
of peritraumatic dissociation, insufficient social support resources, and greater use of alcohol to manage
trauma-related symptoms like intrusive memories and dissociation, as well as gender-specific acute
psychobiological reactions to trauma. This review demonstrates the need for additional research of the
gender differences in posttraumatic stress. Recommendations are made for clinical practice.
Keywords: posttraumatic stress, gender differences, neuroendocrine stress response, cognitive appraisal,
coping
Most studies on posttraumatic stress disorder (PTSD) in the In this article, we review the empirical evidence for a range of
general population have found higher rates of PTSD in women explanations, including gender differences in trauma exposure, in
than in men (e.g., Breslau, Davis, Andreski, Peterson, & Schultz, acute stress reactions (peritraumatic dissociation in particular) and
1997; Frans, Rimmö, Åberg, & Fredrikson, 2005; Kessler, Son- in psychological and biological stress response mechanisms. Con-
nega, Bromet, Hughes, & Nelson, 1995; Olff & de Vries, 2004; sistent with the literature, we hypothesized that sex differences in
Stein, Walker, & Forde, 2000). Given that women are twice as physiological stress reactivity, under both acute and chronic con-
likely as men to develop PTSD during their lifetimes (10.4% ditions, may be one of the mechanisms underlying gender differ-
versus 5.0%; Kessler et al., 1995), it is of great clinical interest to ences in PTSD (Carter-Snell & Hegadoren, 2003; Rasmusson &
evaluate gender differences in posttrauma reactions. It is still not Friedman, 2002). We concentrated in particular depth on the
known, for example, whether women’s higher risk of PTSD is question of whether gender-specific patterns in cognitive appraisal
more strongly associated with psychosocial factors (such as the and coping processes influence neuroendocrine responses in ways
various environmental experiences of being female) or with bio- that heighten women’s risk of PTSD. Alterations in neuroendo-
logical factors (like hormonal differences; Yehuda, 1999). The crine stress response have been frequently shown in patients with
higher PTSD rates in women reported by epidemiological studies PTSD. Because gender differences in how appraisal and coping
are comparable with gender differences observed for other anxiety processes may relate to neuroendocrine response have not been
disorders as well as for major depression. Several possible expla- systematically documented in any recent enumerative review, we
nations have been advanced for women’s higher susceptibility to analyzed that research in more detail. We begin by outlining
PTSD. These include gender-specific exposure to particular types human neuroendocrine response to stressors and by setting out the
of experiences that carry higher relative risks of developing PTSD conceptual framework that underlies our approach. We then re-
and sex-specific psychological and biological reactions to trauma. view the empirical evidence pertaining to the various parts of the
model. Publications potentially relevant to the review were re-
trieved in literature searches of the PsychLit, EMBASE, and
MEDLINE databases. Keywords included trauma, posttraumatic
Miranda Olff and Berthold P. R. Gersons, Centre for Psychological
stress, gender differences, neuroendocrine stress response, cogni-
Trauma, Department of Psychiatry, Academic Medical Centre/De Meren,
University of Amsterdam, The Netherlands; Willie Langeland, Centre for
tive appraisal, and coping. Additional references were identified in
Psychological Trauma, Department of Psychiatry, Academic Medical Cen- bibliographies in the articles obtained from the search and in
tre/De Meren, University of Amsterdam and Department of Psychiatry, textbooks on trauma and PTSD.
Vrije University, Amsterdam, The Netherlands; Nel J. Draijer, Department
of Psychiatry, Vrije University.
We thank Michael Dallas for his helpful comments on an earlier draft of The Neuroendocrine Response to Stressors
this article.
Correspondence concerning this article should be addressed to Miranda PTSD has been linked to dysregulations in several neurobiolog-
Olff, Centre for Psychological Trauma, Academic Medical Centre/De ical stress-coping systems, as reflected in alterations in brain
Meren, Department of Psychiatry, University of Amsterdam, Tafelbergweg structures and functions, psychophysiological abnormalities, and
25, Amsterdam, The Netherlands 1105. E-mail: m.olff@amc.uva.nl disturbances in the neuroendocrine system (Bremner et al., 2000;
183
184 OLFF, LANGELAND, DRAIJER, AND GERSONS
Carrion et al., 2001; Metzger, Orr, Lasko, Berry, & Pitman, 1997; Stratakis & Chrousos, 1995). Not all studies have confirmed lower
Southwick et al., 1999; see also Vasterling & Brewin, 2005). For cortisol levels in PTSD, however (see e.g., Lindley, Carlson, &
reasons explained above, our review focuses mainly on the neu- Benoit, 2004; Rasmusson et al., 2001), nor is low cortisol neces-
roendocrine system. sarily a specific marker of PTSD, as indicated by reports of
The two best documented neuroendocrine response systems hypocortisolism in other stress-related disorders like chronic fa-
involved in specific stress-coping patterns are the sympathetic– tigue syndrome and fibromyalgia (see E. Fries, Hesse, Hellham-
adrenal–medullary (SAM) system and the hypothalamic– mer, & Hellhammer, 2005). Several factors may have contributed
pituitary–adrenocortical (HPA) axis. Different patterns of activa- to inconsistent findings across studies, among them genetic influ-
tion in these two hormonal axes have been linked to different ences; fluctuations in cortisol levels over time; and insufficient
styles in coping in animals (see e.g., Koolhaas et al., 1999) and in control for the use of nicotine, alcohol, and psychotropic medica-
humans (e.g., Frankenhaeuser, 1980; Henry & Stephens, 1977). tion by PTSD subjects (for a review, see Rasmusson, Vythiling-
The sympathetic component of stress response, known more com- ham, & Morgan, 2003).
monly as the fight-or-flight response or defense reaction, is a
general arousal response that coincides with threat or danger. If a
Conceptual Model
person has to “fight or flee” or has to exert effort to control a

situation, the sympathetic nervous system activates within seconds The research data we have compiled on the different pathways
in an attempt to restore homeostasis. The body releases cat- through which gender might be associated with PTSD will be
echolamines (norepinephrine and epinephrine), and blood pressure structured in this review according to our theoretical model of
and heart rate increase. However, because human stress response traumatic stress, as depicted in Figure 1. It differentiates various
has evolved for coping, adaptation, and preservation of the species, components of human response to traumatic stressors (Olff,
the effectiveness of a coping reaction to acute stress depends not Langeland, & Gersons, 2005a). As the literature shows, both acute
just on the efficiency with which physiological mechanisms are and chronic severe stress can precipitate stress-related disorders,
mobilized but also on the speed at which they are shut down again possibly through the effects of stress on neuroendocrine stress
to achieve normal recovery. In fact, recovery to baseline state is systems. Whether a particular response to extreme threats is adap-
just as important in the stress-coping pattern as the capacity to tive or maladaptive is a function of numerous factors, including the
mount an adequate stress response (McEwen, 1998). The HPA environment of the individual. Normal adaptive responses to ex-
axis plays a crucial role in this whole process. treme stress can become maladaptive under certain psychosocio-
The two major stress hormones, epinephrine and cortisol (the cultural conditions and culminate in a pathological stress response
latter released by the HPA axis), have complementary roles in the (see McEwen, 2002).
acute stress response. Sympathetic (SAM) activation sustains the The conceptual model integrates findings from both stress lit-
alarm response, whereas activation of the HPA system, which erature and trauma literature that analyze cognitive appraisal and
boosts the levels of circulating cortisol, first subserves this re- coping in relation to neuroendocrine stress responses and health
sponse and subsequently terminates the initial response by exerting outcomes. The literature clearly identifies appraisal and coping
negative feedback (Eriksen, Olff, Murison, & Ursin, 1999). Hence, processes as important codeterminants of the psychological and
when recovery cannot be achieved—that is, when effective coping biological stress responses and, hence, of the subsequent mental
is hampered, as in cases of severe prolonged stress and negative health outcomes (for comprehensive reviews, see Olff et al.,
affect—the HPA system is implicated in part (Henry & Stephens, 2005a, 2005b). It has been demonstrated that the development of
1977). In this response, known as the conservation-withdrawal or PTSD is associated with specific appraisals of the traumatic event
defeat reaction, a dysregulation of cortisol release damages the (Ehlers, Mayou, & Bryant, 1998; McNally, 2003) and with spe-
integrity of the HPA system (Frankenhaeuser, 1980; Henry & cific coping styles (e.g., Birmes, Hazane, Calahan, Sztulman, &
Stephens, 1977). Subjects feel helpless and unable to cope with or Schmitt, 1999; Bryant & Harvey, 1995; Chang et al., 2003; Gin-
control events. In PTSD, there is evidence for abnormal function- zburg, Solomon, & Bleich, 2002; Marmar, Weiss, Metzler, &
ing of both the HPA and the SAM systems (see e.g., Bryant, 2003). Delucchi, 1996). Threat appraisals and defensive coping are
We shall return to the latter below. thought to play crucial roles in determining the body’s neuroen-
Chronic activation of the HPA axis may result in dysregulation docrine response to trauma and potential mental health conse-
of the entire stress response system (Ursin & Eriksen, 2004; Ursin quences such as PTSD (e.g., Epel, McEwen, & Ickovics, 1998;
& Olff, 1993) and the maladaptive neuroendocrine responses. The Mason et al., 2001).
process can even bring about pathophysiological changes, which in Figure 1 integrates empirical findings revealing the pathways
turn induce the symptoms seen in psychiatric illness or create a that can lead from a traumatic event to cognitive appraisal, to
vulnerability to mental disorders (Rothschild, 2003). HPA-axis stress-coping processes, to neuroendocrine responses, and to
dysregulation may take the form of either chronic hypersecretion PTSD and other stress-related illnesses. The theoretical model
or chronic hyposecretion of corticotropin-releasing factor. Ele- itself and the supporting evidence have been described in more
vated HPA activity has been observed in panic disorder, detail elsewhere: “The model proposes that cognitive appraisal, the
obsessive– compulsive disorder, mood disorders (major depres- subjective interpretation of the trauma, is crucial in starting the
sion, especially the melancholic type, and psychotic depression), cascade of psychobiological responses to trauma. Virtually by
addictions, schizophrenia, and anorexia nervosa. Reduced activity definition a traumatic event is evaluated as a threat” (Olff et al.,
has been found in PTSD, chronic fatigue syndrome, hypothyroid- 2005a, p. 463). Stress research has identified individual differences
ism, postpartum depression, atypical or seasonal depression, and in cognitive appraisal—in terms of perceived threat, perceived
fibromyalgia (Ehlert, Gaab, & Heinrichs, 2001; Rothschild, 2003; controllability, and perceived coping ability—as key factors af-
GENDER DIFFERENCES IN PTSD 185
Personal, social & cultural factors

(e.g.prior history of trauma, genetically increased
stress reactivity)
coping social support

type, effectiveness,
flexibility seeking/perceiving
defense
e.g.avoidance,
disengagement
ing/ ery h ig
c op st h
high emotion-focused coping pall
a ctive tal ma iat
n o um e n iv e
r
inst cop
ing
high cognitive defense
Emotional/behavioral response
Negative appraisals e.g. peritraumatic distress PTSD
Trauma
(threat, danger, Depression
exposure harm, Addiction
uncontrollability) Neuroendocrine response Etc.
HPA-axis dysregulation,
SNS hyperactivity
Figure 1. Traumatic-stress-coping model. HPA ⫽ hypothalamic–pituitary–adrenocortical; SNS ⫽ sympathetic

nervous system; PTSD ⫽ posttraumatic stress disorder.
fecting the magnitude and the profile of neuroendocrine response denial or on emotion-inhibiting strategies (Mason et al., 2001),
(see reviews by Biondi & Picardi, 1999; Dickerson & Kemeny, probably because of reduced experience of negative affect.
2004; Levine, 2000). Negative or alarming appraisals are associ- Whether particular coping strategies or defenses will be adap-
ated with demands that exceed perceived coping abilities, high tive or maladaptive can ultimately only be assessed by considering
negative emotion, poorer coping, and alterations in reactive levels the context and time frame in which they are used. That is, the
of cortisol. Appraisals that include greater threat or loss of control effective use of defenses to ward off negative emotions may
perceptions may contribute to PTSD and other psychopathology temporarily dampen the endocrine stress response and be adaptive
because they direct coping toward excessive emotional regulation in the short term, but reduced cortisol response in defensive
and divert it from problem solving. By contrast, reduced threat subjects has been linked to sustained higher sympathetic activation
perceptions, as may occur in people who were intoxicated at the (e.g., in terms of heart rate and blood pressure; Olff et al., 1995).
time of the trauma or were unconscious in its direct aftermath, may Hence, prolonged defensive coping may eventually result in more
result in a dampened physiological stress response, thereby de- health problems (Ursin & Olff, 1993).
creasing the risk of PTSD (e.g., Maes, Delmeir, Mylle, & Alta- As further depicted in the model, a variety of personal, social,
mura, 2001; O’Brien & Nutt, 1998). Positive appraisals or reap- and cultural factors like age, gender, genetics, disturbance in early
praisals of a traumatic event have been linked to faster cortisol attachment relations, and previous trauma may also influence
habituation to subsequent stressors, indicating greater flexibility in stress-coping pathways (e.g., Barr et al., 2004; Kessler et al., 1995;
the HPA axis. Positive reappraisal of trauma may therefore serve Teicher, Andersen, Polcari, Anderson, & Navalta, 2002; True et
as a protection against developing PTSD (Epel et al., 1998). al., 1993; and see review by Bremner & Vermetten, 2001). That a
After the appraisal phase, the subject’s specific coping and sexual dichotomy of an interaction between early adversity and
defense strategies play critical roles in the subsequent emotional, genetic factors may play a role in the HPA-axis response to
behavioral, and biological responses, although some seemingly traumatic stress is suggested by findings of a study in rhesus
contradictory effects have not yet been fully explained. As a rule, macaques (Macaca mulatta; Barr et al., 2004). Serotonin trans-
maladaptive coping (i.e., when active, direct, problem-focused porter gene promoter polymorphism (5-HTTLPR)—associated
coping is not possible) has been associated with increased neu- with increased anxiety in the face of adversity—modulated the
roendocrine reactivity (Bonanno, Noll, Putnam, O’Neill, & Trick- effects of vulnerability for early adversity in particular in female
ett, 2003; Levine & Ursin, 1991). Active coping (instrumental monkeys with the short (“s”) allele. These female monkeys also
mastery) may help subjects to deal effectively with the traumatic exhibit lower cortisol responses to stress, a pattern that has been
stressors and avoid long-term emotional and physiological dys- linked to certain stress-related disorders. If these preclinical find-
regulation and posttraumatic symptoms (Bonanno, 2004; and see ings can be extended to humans, this interactive effect may un-
review by Charney, 2004). At the same time, however, reduced derlie the higher PTSD rates in women. Other influences of stress-
neuroendocrine reactivity has also been observed in subjects with coping pathways are the type of coping, the perceived
defensive coping styles based on high levels of avoidance and effectiveness of the coping strategy used, the subject’s flexibility
in using different coping strategies, and the opportunities to seek integrity of the self or others” (p. 467). To formulate mechanisms
and use social support (e.g., Murphy, 1987; Z. Solomon, Benbe- that can help account for gender differences in PTSD prevalence
nishty, & Mikulincer, 1991). rates, we therefore have to take trauma-exposure-related factors
Our particular focus in this article is on the influence that gender into consideration such as the rate of exposure, the type of trauma
may have on the pathways hypothesized in this conceptual model. experienced, the history of traumatization, and the age of trauma
After reviewing the empirical evidence for potential explanations exposure.
of gender differences in PTSD, we will present a focused, gender-
specific version of the model. The importance of such a theoretical
framework lies in its heuristic value in connecting multiple fields Rate of Exposure
of inquiry and in the promotion of further programmatic research.
The currently expanding knowledge base on psychobiological The observed higher risks of PTSD in women compared with
factors in stress-related disorders, particularly PTSD, and on gen- men do not appear to result from a higher overall rate of trauma
der differences in these processes provides a stimulus for the exposure among females. The pattern of association between gen-
development of improved psychosocial and pharmacological treat- der and trauma exposure most commonly seen in the literature is
that men have a broadly higher risk of being exposed to potentially

ment options, including gender-specific interventions. After syn-

thesizing the research findings into the model, we will therefore traumatic events (Breslau, Davis, Andreski, & Peterson, 1991;
also make some concrete suggestions for clinical practice. Breslau et al., 1997; Creamer, Burgess, & McFarlane, 2001; Frans
et al., 2005; Kessler et al., 1995; Norris, 1992; Perkonigg, Kessler,
Storz, & Wittchen, 2000; Stein, Walker, Hazen, & Forde, 1997). In
Gender and Trauma Exposure
the National Comorbidity Survey, for instance, 60.7% of men and
Symptoms of PTSD are linked etiologically to extremely trau- 51.2% of women reported at least one traumatic event in their lives
matic or catastrophic events (see “Trauma” at the lower left of the (Kessler et al., 1995). Yet, the same survey estimated the condi-
model in Figure 1). Traumatic stressors are defined by the current tional risk of developing PTSD after trauma exposure at 8.1% for
Criterion A1 for PTSD in Diagnostic and Statistical Manual of men and 20.4% for women. Those findings are in line with other
Mental Disorders (4th ed., text rev.; American Psychiatric Asso- studies indicating a gender difference in the conditional probability
ciation, 2000) as follows: “The person experienced, witnessed, or of PTSD, with approximately twofold greater odds in females
was confronted with an event or events that involved actual or compared with males (Breslau, Peterson, Poisson, Schultz, &
threatened death or serious injury, or a threat to the physical Lucia, 2004; see Table 1).
Table 1
Gender-Specific Epidemiological Data on the Prevalence of Trauma Exposure, Posttraumatic Stress Disorder (PTSD),
and PTSD Risk After Trauma
Lifetime Lifetime
trauma trauma
exposure, exposure, Lifetime PTSD, Lifetime PTSD,
Country and females males Lifetime PTSD (%) females (%) males (%)
Study age range N (%) (%) [conditional risk] [conditional risk] [conditional risk]
Helzer et al. (1987) USA 2,493 1.00 1.3 0.5

Breslau et al. (1991) USA 21–30 1,007 36.7 43.0 9.20 [30.7] [14.0]
[30.7] [14.0]
Norris (1992) USA 65.0 74.0
Resnick et al. (1993) USA 4,008 68.9 12.3
[17.9]
Kessler et al. (1995, USA 15–44 5,877 51.2 60.7 7.80 10.4 5.0
1999) 12-month PTSD: 3.90 [20.4] [8.1]
Stein et al. (2000, Canada 18⫹ 1,002 74.2 82.0 PTSD 1-month: 2.7 PTSD 1-month: 1.2
1997) [8.2]a [1.8]a
Breslau et al. (1998) USA 18–45 2,181 87.1 92.2 18.3 10.2
[13.0] [6.2]
Perkonigg et al. Germany 3,021 15.5 18.6 1.30 2.2 0.4
(2000) 14–24 [12.4] [1.6]
Creamer et al. Australia 10,641 49.5 64.5 12 month PTSD: 1.33
(2001)
Rosenman (2002) Australia 10,641 50.9 65.5 12-month PTSD: 1.50 12-month PTSD: 1.6 12-month PTSD: 1.3
[2.80] [3.8] [2.0]
Frans et al. (2005) Sweden 18–70 1,824 77.1 84.8 5.60 7.4 3.6
[6.90] [9.6] [4.2]
Note. PTSD ⫽ posttraumatic stress disorder.

a
1-month full or partial PTSD.
Type of Trauma (Breslau et al., 1997; Breslau et al., 1998; Kessler et al., 1995). The
impact of exposure to intense or prolonged stress in early child-
Despite their lower exposure to trauma, women may be partic- hood could be particularly pernicious to both sexes, as the trau-
ularly susceptible to PTSD as a consequence of greater exposure to matization takes place during a period of brain development (see
specific trauma types with the highest probability of PTSD Teicher et al., 2002). Clearly, neurobiological variables may be
(Breslau, Chilcoat, Kessler, Peterson, & Lucia, 1999). These in- important for explaining any effect that the age of trauma exposure
clude interpersonal assaults such as rape and sexual abuse in might have on gender differences in PTSD. Sex differences in the
childhood or adulthood. Indeed, several studies have shown that psychobiological effects of the early environment, particularly
females have higher rates of exposure to these trauma types (e.g., with regard to neuroendocrine programming, have been suggested
Breslau et al., 1997; Breslau et al., 1998; Kessler et al., 1995; in animal studies as well as in human studies (e.g., M. H. Andrews
Perkonigg & Wittchen, 1999). Plichta and Falik (2001), for in- & Matthews, 2004; Barr et al., 2004; Buske-Kirschbaum, Fisch-
stance, reported that more than one third of women have experi- bach, Rauh, Hanker, & Hellhammer, 2004; Carrion et al., 2002;
enced intimate partner violence within the previous 12 months. It Davis & Emory, 1995; Dienstbier, 1989; Flinn, Quinlan, Decker,
has also been suggested that girls may be particularly vulnerable to Turner, & England, 1996; Rosmalen et al., 2005; van Oers, de
the negative effects of childhood sexual abuse, whereas boys may

Kloet, & Levine, 1998). Those results are discussed in more detail
be more vulnerable to adverse effects from childhood neglect below when we examine gender differences in psychobiological
(Teicher et al., 2004). Results of a recent literature review indeed stress responses.
indicate higher vulnerability to PTSD in girls compared with boys
exposed to childhood sexual abuse (Walker, Carey, Mohr, Stein, &
Seedat, 2004), although links to specific trauma types have not Section Summary
been confirmed among adult women in epidemiological studies The reviewed literature suggests that trauma-exposure-related
(Breslau et al., 1997; Breslau et al., 1998; Frans et al., 2005; factors can only partially account for the marked difference be-
Kessler et al., 1995; Norris et al., 2002; Rosenman, 2002; Stein, tween female and male PTSD risks. Findings indicating that
Walker, & Forde, 2000). The latter studies do indicate that women women may be particularly susceptible to PTSD as a consequence
are 2.30 to 2.49 times more likely than men to develop lifetime of their greater exposure to high impact events (particularly sexual
PTSD after exposure to similar traumas. Hence, the higher female abuse) or because of preexisting major depression have not been
risk of exposure to potentially more traumatizing types of events convincing in explaining gender differences in PTSD rates.
cannot sufficiently explain gender differences in PTSD. Trauma exposure at a young age could indeed prove a more
significant risk factor for women than for men. It is clear that
History of Traumatization additional explanations are needed. We shall now turn to psycho-
logical and biological stress response mechanisms as an alternative
Also relevant to an individual’s response to traumatic events theory. In particular, it is suggested that gender-specific cognitive
may be her or his history of aversive events. Generally, individuals and biological mechanisms might be explanatory factors in the
who have experienced previous traumas are more prone to exac- observed differences in PTSD (see Bryant, 2003; Peirce, Newton,
erbated reactions to current traumas. However, several studies Buckley, & Keane, 2002; Rasmusson & Friedman, 2002).
have indicated that prior traumatization does not contribute to the
gender difference in PTSD rates (e.g., Breslau, Chilcoat, Kessler,
Gender and Cognitive Appraisal
& Davis, 1999; Bromet, Sonnega, & Kessler, 1998). In addition,
epidemiological data suggest that women’s higher rates of PTSD In our conceptual model, cognitive appraisal—the ability to
are unlikely to result from a higher number of traumatic events evaluate events and experiences—is the key to the body’s response
experienced either during childhood (Breslau et al., 1997) or to threat (see “Negative Appraisals” at the lower left of the model
during their lifetime (Breslau et al., 1997; Stein et al., 2000). in Figure 1). The appraisal process, reflecting a person’s subjective
Two epidemiological studies have also evaluated influences perception, interpretation, and evaluation of the traumatic event, is
from other preexisting psychological variables, such as anxiety the crucial first step in the cascade of psychobiological responses
disorders and major depression, as possible explanations for the that can eventually lead to pathological symptoms. A still unan-
different apparent PTSD risks in women and men. No findings swered question is whether gender-specific effects of appraisal
have yet implicated prior anxiety disorders (Breslau et al., 1997; processes—and, in particular, the effects on the body’s neuroen-
Bromet et al., 1998), whereas conflicting findings have been docrine response— can contribute to the higher rates of PTSD
reported for prior depression. Preexisting major depression was among women. We first review findings on how the appraisal of
found unrelated to the PTSD gender differences in one study the traumatic event can affect the development of PTSD and then
(Breslau et al., 1997), whereas in another study, prior depression turn the focus to possible gender differences in cognitive appraisal.
was part of the explanation (Bromet et al., 1998).
Cognitive Appraisal of the Traumatic Event
Age of Exposure
Several trauma theorists have proposed that cognitive factors
The age of trauma exposure is another possible explanatory have a critical impact on trauma response (Ehlers & Steil, 1995;
factor for gender differences in PTSD prevalence. Females have Foa, Steketee, & Rothbaum, 1989). Central to cognitive models of
been found to have higher PTSD rates than males after childhood PTSD is the assumption that perceiving a stressful event as a threat
trauma exposure in comparison with exposure after age 15 is at least as important in the development and maintenance of
PTSD as trauma severity or individual variations in pretrauma ing others and a lower risk of developing PTSD (e.g., Mak,
experience (Ehlers & Clark, 2000; Foa et al., 1989; Horowitz, Blewitt, & Heaven, 2004; Timmer et al., 1985). In an issue related
1986; Janoff-Bulman, 1985). Empirical evidence has accumulated to controllability, findings in research on motor vehicle accidents
that shows the impact of specific stress appraisals on the develop- indicate that people who attribute responsibility for the accident to
ment of posttrauma psychopathology and in PTSD in particular another person are more likely to develop PTSD. One such study
(e.g., Ehlers et al., 1998; McNally, 2003). The available meta- suggested a gender-specific pattern of control appraisal, whereby
analyses of PTSD risk factors indeed indicate that the subjective perceived loss of control was much more prevalent in females
characteristics of events are far better predictors of PTSD than the (Delahanty et al., 1997). Findings like this could be rather specific
objective facts (Brewin, Andrews, & Valentine, 2000; Ozer, Best, to motor-vehicle accident victims, however, because a greater
Lipsey, & Weiss, 2003). Subjective appraisals—which can include proportion of females might have been passengers and, hence,
individual perceptions of loss, threat, harm, or uncontrollability— literally not in control.
have been found to explain a variety of different results pertaining
to PTSD risks, such as why one person develops PTSD after Gender, Cognitive Appraisal, and Brain Functioning
stressful but seemingly noncatastrophic events like divorce,
It has been suggested that gender differences in brain engage-

whereas others do not develop it even after horrific traumas like

ment during evaluation of threat cues—that is, that females pick up
kidnapping or torture (McNally, 2003). On the basis of these
on threat signals more readily than males—may underlie reported
findings, we would suggest that gender differences in the cognitive
female–male differences in subjective stress appraisal (Kemp,
appraisal of traumatic stressors are an important issue in explain-
Silberstein, Armstrong, & Nathan, 2004; McClure et al. 2004;
ing female–male differences in PTSD prevalence rates.
Stroud, Salovey, & Epel, 2002). Another suggestion is that women
and men may react differently to traumatizing events because of
Gender Differences in Cognitive Appraisal the differential development, specialization, and functionality of
their cerebral hemispheres. Gender differences have been reported
Empirical findings in the general stress literature indicate that
in the processing of strong emotional memories (e.g., Cahill,
gender differences in primary appraisal indeed exist, with females
Uncapher, Kilpatrick, Alkire, & Turner, 2004; Canli, Desmond,
more likely to report threat and loss appraisals than males (Cole &
Zhao, & Gabriel, 2002; van Stegeren et al., 2005) and of traumatic
Sapp, 1988; Mak, Blewitt, & Heaven, 2004; Ptacek, Smith, &
memories (Spitzer et al., 2003). Sex- or gender-related differences
Zanas, 1992; van Nieuwenhuizen & de Ridder, 1994). These types
in brain structures and/or cognitive processes may hence be im-
of appraisals have been linked to greater psychopathology in
plicated in the mechanisms underlying women’s and men’s differ-
women, including higher rates of affective disorders (van Nieu-
ential sensitivity to stress and psychopathology. Research into
wenhuizen & de Ridder, 1994). Accordingly, it has been suggested
these differences could enhance our understanding of disorders
that gender differences in threat appraisal might well contribute to
that show gender-related susceptibility, such as depression and
differences between men’s and women’s HPA-axis responses to
PTSD, thereby opening the way to gender-specific treatments for
psychosocial stressors (Rasmusson & Friedman, 2002) and conse-
such disorders (see Cahill, 2005).
quently to their different PTSD risks. Women are also reported to
be significantly more likely to appraise events as stressful and to
Section Summary
report higher perceived distress in terms of a loss of personal
control and a lack of available alternative coping strategies (Eisler The reviewed findings suggest that higher perceptions of threat
& Skidmore, 1987; Timmer, Veroff, & Colten, 1985). All these or control loss in women compared with men may contribute to
gender-related factors may modulate stress responsitivity (see their higher prevalence rate of PTSD. More research is needed to
Kiecolt-Glaser et al., 1996, and Stoney, Matthews, McDonald, & confirm such indications and to further unravel the mechanisms
Johnson, 1988). In agreement with our conceptual model, studies underlying the reported gender differences in subjective traumatic
have also found that personality traits may influence whether a stress appraisals.
stressful event or situation will be appraised as a threat or as a
challenge and what the ensuing physiological reaction will be Gender in Relation to Psychological and Biological
(Roberti, 2003). This raises the possibility that gender differences Reactions to Trauma
in the prevalence of PTSD could at least in part be explained by
Psychological reactions to trauma, which include intense fear,
gender differences in personality traits because of their link with
helplessness, or horror, constitute Criterion A2 for PTSD. As
sex differences in physiological stress reactivity.
depicted in our proposed model (see “Emotional/Behavioral Re-
In the trauma literature, it has likewise been suggested that the
sponse” at the lower center of the model in Figure 1), the imme-
higher risk for stress-related disorders in females begins at the
diate emotional, behavioral, and biological reactions to trauma
stage of appraisal, or subjective interpretation of events, rather
appear shortly after the appraisal phase. The nature of these reac-
than at the objective exposure to trauma stage (Norris et al., 2002).
tions is influenced in the model both by the subject’s appraisal of
There is empirical support for this notion (Anderson & Manuel,
the traumatic event and by the specific coping and defense strat-
1994; Delahanty et al., 1997; Goenjian et al., 2001; Kario, Mc-
egies that the subject uses.
Ewen, & Pickering, 2003; Lerner, Gonzalez, Small, & Fischhoff,
2003). Data indicate that women and men show different “control
Acute Reactions to Trauma
appraisals,” a type of appraisal that is a strong predictor of PTSD
(Dickerson & Kemeny, 2004); men show higher levels of per- The initial reaction to a traumatic event is called the acute stress
ceived control, which is associated with a lower reliance on blam- response. It includes the psychological and biological response
during and shortly after the event. Females could be hypothesized body of data on possible gender-specific effects of peritraumatic
to have gender-specific acute stress responses that make them dissociation, both on PTSD risk and on the underlying biological
more prone than males to develop PTSD after trauma exposure. mechanisms, we review that literature separately in the sections
In terms of acute biological reactions in a general sense, there is below.
evidence suggesting an association between these and subsequent A further potentially harmful psychological phenomenon in the
PTSD. Some studies have reported that subjects who were later to early response to trauma involves maladaptive interpretations of
develop PTSD showed higher sympathetic nervous system activa- acute trauma symptoms like racing thoughts, anxious feelings, or
tion (e.g., higher resting heart rates) in the acute posttrauma phase physiological arousal. Negative cognitive appraisals of common
(e.g., Bryant, Marosszeky, Crooks, Baguley, & Gurka, 2000; Sha- symptoms like these have been linked to PTSD (see Ehlers & Steil,
lev et al., 1998). Alterations in the acute cortisol response to 1995) chiefly because the appraisals prolong a sense of serious
trauma have been found in similar individuals (e.g., Delahanty, impending danger (Ehlers & Clark, 2000). In other words, trauma
Raimonde, & Spoonster, 2000; McFarlane, Atchison, & Yehuda, victims’ appraisals of the acute symptoms, rather than the symp-
1997; Resnick, Yehuda, Pitman, & Foy, 1995). It remains unclear toms themselves, could be critical in determining the influence
how sex differences in acute physiological responses might con- those symptoms will have on subsequent adaptation (McNally,
tribute to the development of PTSD, as almost no studies have 2003). Several cross-sectional and prospective studies, carried out
compared these acute responses across gender. Consistent with the in the aftermath of various traumatic events, appear to confirm the
proposed conceptual model are findings showing that elevated critical role that individuals’ ominous appraisals of acute symp-
cortisol levels are more common in men than among women MVA toms play in the maintenance of PTSD (Clohessy & Ehlers, 1999;
survivors at 1-month posttrauma (Hawk, Dougall, Ursano, & Dunmore, Clark, & Ehlers, 1999, 2001; Ehlers, Mayou, & Bryant,
Baum, 2000). However, available data do also show a greater 1998; Engelhard, Macklin, McNally, van den Hout, & Arntz,
likelihood of acute physiological symptoms, especially arousal, in 2001; Engelhard, van den Hout, Arntz, & McNally, 2002; Fedor-
women than in men after exposure to a disaster stressor (Norris, off, Taylor, Asmundson, & Koch, 2000; Halligan, Michael, Clark,
Perilla, Ibanez, & Murphy, 2001). Beyond that, the lack of studies & Ehlers, 2003; Steil & Ehlers, 2000). Such factors may indirectly
designed explicitly to examine gender differences in the relation- contribute to both the development of PTSD and its persistence.
ship between acute physiological reactions and later PTSD pre- They fuel coping processes in which the chosen cognitive and
cludes any further conclusions at present on gender-specific acute behavioral strategies tend to hinder recovery, such as cognitive
physiological reactions. avoidance and attempts to suppress thoughts about the trauma. In
With regard to acute psychological responses to trauma, numer- terms of gender, empirical data are still lacking on possible dif-
ous retrospective and prospective studies have demonstrated the ferences in how women and men interpret acute trauma symptoms.
predictive value of acute emotional reactions and acute dissocia- Future research should assess whether women’s higher risk of
tive reactions for the later onset of PTSD. A particularly large PTSD could be related to gender-specific maladaptive interpreta-
number of studies concern peritraumatic dissociation, a state of tions of acute symptoms.
limited or distorted awareness during and immediately after the On the basis of the findings reviewed so far, it can be hypoth-
trauma. Results of a meta-analysis of PTSD predictors have sug- esized that gender differences in acute reactions to trauma may go
gested that peritraumatic psychological processes, and not pre- a long way toward explaining the elevated PTSD risk in women.
trauma personal characteristics, are the strongest predictors (Ozer To deepen our understanding of that role, it would be helpful to
et al., 2003). Peritraumatic dissociation, and to a lesser extent analyze the relationships between acute physiological, emotional,
peritraumatic emotional responses, appear most prominent of all. and dissociative trauma reactions and the later onset of PTSD
Several studies have indeed shown that victims with immediate explicitly in terms of gender. To date, the available information
dissociative responses to diverse types of trauma exposure may be mostly concerns the links between peritraumatic dissociation and
at greater risk for PTSD (Birmes et al., 2001; Fullerton et al., 2001; subsequent PTSD. The empirical evidence for gender differences
Koopman, Classen, & Spiegel, 1994). in peritraumatic dissociation, as well as for possible gender-
Gender differences have been reported in both emotional and specific biological mechanisms related to immediate dissociative
dissociative acute reactions. Women appear more likely than men reactions to trauma, warrants separate attention in the sections to
to report acute emotional responses (Brunet et al., 2001) including follow.
intense fear, helplessness, horror, intrusive thoughts, avoidance,
panic, and anxiety (Bryant & Harvey, 2003; Freedman et al., 2002; Gender and Peritraumatic Dissociation
Holbrook & Hoyt, 2004; Livanou, Başoğlu, Şalcioğlu, &
Kalender, 2002). Although reactions like fear are normally adap- Peritraumatic dissociation is a state of limited or distorted
tive responses that initiate defensive behavior to protect people awareness at the time of a traumatic event or in its immediate
from danger, anxiety disorders such as PTSD can develop if fear aftermath. As noted above, women are shown to have higher rates
is inappropriately regulated. A unique aspect of PTSD is that the of peritraumatic dissociation than men (e.g., Bryant & Harvey,
stress response system seems not to switch off but instead contin- 2003; Grieger, Fullerton, & Ursano, 2003). Moreover, findings
ues to operate as if the fear-provoking danger were still present. In suggest that peritraumatic dissociative symptoms increase the risks
addition to fear, women appear more likely than men to report for PTSD (Bryant & Harvey, 2003; Fullerton et al., 2001) and for
acute dissociative responses (e.g., Bryant & Harvey, 2003; Fuller- concurrent PTSD and increased alcohol use significantly more in
ton et al., 2001). These findings suggest that gender-specific acute women (Grieger, Fullerton, & Ursano, 2003) than in men with
emotional and dissociative reactions in women might make them similar symptoms. Dissociation at the time of a motor vehicle
more prone than men to develop PTSD. Given the relatively large accident has been reported to explain gender differences in sub-
sequent PTSD, whereas passenger injury, previous traumatiza- chiatric symptoms and in stress resilience. Perhaps other individual
tions, PTSD, major depression, and/or other anxiety disorders have factors could help explain the variability in the processes of stress
not (Fullerton et al., 2001). In this study, women reporting peri- adaptation or maladaptation. Moreover, animal research has sug-
traumatic dissociation were over seven times more likely to de- gested it is not the absolute amount of hormone released, but rather
velop PTSD than men reporting peritraumatic dissociation. These the pattern and the occupation of receptors that mediates the adaptive
findings suggest that prompt assessment of peritraumatic dissoci- or maladaptive function of the HPA axis (de Kloet & Derijk, 2004).
ation may be particularly indicated for traumatized women. The This work indicates that stress can bias the receptor signaling path-
same authors suggest that the greater PTSD risk among females ways in the brain that are involved in the predisposition to and
may be partly due to fundamental sex differences in neurobiolog- pathogenesis of stress-related disease, changing “good” corticosteroid
ical factors that contribute to peritraumatic dissociation. A better actions into “bad.” Corticosteroids act via mineralocorticoid and glu-
understanding of sex differences in such biological processes cocorticoid receptors (MRs and GRs, respectively) in the brain. The
could result in more specific psychosocial and/or pharmacological different receptor affinities permit low amounts of corticosterone to
interventions. occupy predominantly MRs, whereas higher hormone levels induced
by stress progressively occupy GRs. Through occupation of GR sites,
Biological Mechanisms Related to Peritraumatic the MRs determine the threshold or sensitivity of the stress response.
Dissociation These data also emphasize the role of personal characteristics in
heterogeneous stress responses in the form of genetic factors that may
Peritraumatic dissociation has recently been linked to low cor- significantly contribute to the interindividual variations in MR–GR
tisol in police officers, although higher peritraumatic responses did balance and HPA regulation. Gender differences have yet to be
not predict lower cortisol levels independently of PTSD symptoms investigated in this area of research.
(Neylan et al., 2005). One might argue that peritraumatic dissoci-
ation is linked to reduced HPA-axis activity. That would be con- Two Distinct Acute Response Patterns to Threat:
sistent with findings in the stress literature on the relationship Dissociation and Hyperarousal
between acute stress, cortisol, and passive and defensive respond-
ing (Henry, 1993). Laboratory experiments have found psycholog- We turn now to a promising theoretical framework, based on
ical defenses to be associated with an attenuated neuroendocrine research findings in traumatic stress in children, which points to
response to an acute stressor, probably because of subjects’ re- gender differences in trauma response patterns. It describes two
duced experience of negative affect (e.g., Olff et al., 1995). Some distinct acute response patterns to threat, one characterized by
observers have suggested that disengagement (such as the psycho- dissociative symptoms and the other characterized by hyperarousal
logical defenses of denial, emotional numbing, avoidance, and symptoms. It should be of particular interest in future analyses of
withdrawal that are used to cope with psychosocial stress) may biological mechanisms involved in immediate responses to trauma,
shield individuals psychologically from threat and result in de- as it suggests that two gender-specific pathways may exist that
creased HPA-axis activation and lower cortisol (e.g., Henry, 1993; have different underlying neurobiological mechanisms and lead to
Mason et al., 2001). According to our proposed model, such a different PTSD subgroups.
response might indeed be adaptive in the short term. However, as The framework, proposed by Perry and colleagues for under-
outlined above, whether particular defenses are adaptive or mal- standing traumatic stress in children, describes gender differences
adaptive depends on the context and time frame in which they are in trauma response patterns (Perry & Pollard, 1998; Perry, Pollard,
used. Blakley, Baker, & Vigilante, 1995). It identifies two major neu-
Clinical studies have shown a relationship between peritrau- ronal patterns— dissociation and hyperarousal—that occur in chil-
matic dissociation and the stress-induced release of glucocorti- dren in acute response to threat. Most individuals will use various
coids (Morgan et al., 2001) or, more specifically, between reduced combinations of the two response patterns during any given trau-
levels of dissociation during extreme stress and increased dehy- matic event. However, age and gender are thought to play a part in
droepiandrosterone sulfate (DHEA-S) to cortisol ratios (Morgan et individual variations in the use of one response pattern or the other.
al., 2004). The authors hypothesized that nonsulfated metabolite The younger an individual is, the more likely she or he is to use
DHEA can inhibit glucocorticoid action, which may contribute to dissociative adaptations over hyperarousal responses.
an upregulation of the HPA axis in PTSD. DHEA-S, in turn, does Females also appear to use dissociative adaptations more than
not exert antiglucocorticoid properties. Gender differences in lev- males. The authors reason that males are more likely to have
els of DHEA-S and DHEA have also been reported, with higher sensitized physiological hyperarousal systems (resembling the
DHEA-S levels in men than in women— both among healthy classical fight-or-flight paradigm) with related symptoms such as
adults (Orentreich, Brind, Rizer, & Vogelman, 1984) and among poor impulse control, aggression, and hypervigilance; they exhibit
adult refugees with PTSD (Söndergaard, Hansson, & Theorell, conditions such as conduct disorder, attention-deficit hyperactivity
2002)—and higher DHEA levels in healthy women than in healthy disorder, and adult antisocial personality disorder. Women are said
men (Sulcaova, Hill, Hampl, & Straka, 1997). to more often have sensitized dissociative systems (resembling
Notably, several findings suggest that higher levels of DHEA-S— more passive defense mechanisms) and to be more likely to exhibit
as more often seen in traumatized and healthy men— could protect corresponding symptoms like anxiety, physical complaints, and
against comorbid depression in PTSD (see Rasmusson et al., 2003). withdrawal and disorders like anxiety disorders, major depression,
However, the same authors point out that findings on the relationship and dissociative disorders. Preliminary studies by Perry et al.
between DHEA, DHEA-S, and PTSD remain inconclusive, with (1995) indicated lower heart rates in traumatized children with
evidence implicating DHEA and DHEA-S both in stress-related psy- dissociative symptoms than in those with hyperarousal symptoms;
in children with persistent hyperarousal symptoms, cue-specific dissociation-related subtypes, each with different neuropsycholog-
increases in heart rate were observed. ical profiles and attendant symptoms.
In a similar vein, Bremner (1999) has suggested that dissociative
symptoms constitute one of two subtypes of the acute stress Gender Differences in Coping
response, differing both physiologically and subjectively from
responses with predominantly hyperarousal or intrusive symp- Our model shown in Figure 1 proposes that a subject’s specific
toms. There is evidence that high levels of peritraumatic or per- coping and defense strategies influence the nature of the reactions
sisting dissociative symptoms may be related to a suppression of to trauma. We therefore need to investigate possible gender dif-
autonomic physiological responses in adults (Delahanty, Royer, ferences in coping, as these could mediate differences between
Raimonde, & Spoonster, 2003; Griffin, Resnick, & Mechanic, females and males in the incidence of various stress-related phys-
1997; Koopman et al., 2004; Williams, Haines, & Sale, 2003). ical and psychological disorders. Different stress-regulating coping
This implies a possible downregulation of both sympathetic and strategies might therefore be effective in men and in women to
HPA responses to stress. reduce both acute symptoms and posttraumatic symptoms. More
specifically, there may be gender differences with regard to which
Lower basal cortisol levels have been reported in patients with

depersonalization disorder—a condition in the Diagnostic and coping methods are used and how they are used, as well as in the
Statistical Manual of Mental Disorders (4th ed., text rev.; Amer- psychological and psychiatric outcomes thereafter.
ican Psychiatric Association, 2000) dissociative disorders category Rather consistent gender differences have been reported in the
(Stanton et al., 2001). There is some evidence supporting corti- types of strategies of coping and defense that females and males
colimbic disconnection in depersonalized states, with medial pre- use (e.g., Bullitt & Farber, 2002; Gavranidou & Rosner, 2003;
frontal activation accompanied by reciprocal inhibition of the Mahalik, Cournoyer, DeFranc, Cherry, & Napolitano, 1998;
amygdala resulting in diminished arousal and blunted emotionality Matud, 2004; Ptacek, Smith, & Dodge, 1994; Ptacek et al., 1992;
(Lanius et al., 2002). Patients with depersonalization disorder Siegler & George, 1983; Watson & Sinha, 1998). The stress
have also been found to show marked declines in norepineph- literature also points to gender differences in aspects of coping and
rine levels, accompanied by increasing symptoms of deperson- physiological responding (see Peirce et al., 2002). Findings in the
alization (Simeon, Guralnik, Knutelska, Yehuda, & Schmeidler, general literature suggest that women may use less effective com-
2003). Gender differences in these associations have yet been binations of coping strategies than men (Ptacek et al., 1994;
investigated. Tamres, Janicki, & Helgeson, 2002).
A recent study has pointed to the prominent role of hyperarousal For both genders, findings in the trauma literature most consis-
in the natural course of posttraumatic psychological distress in tently show that coping responses such as disengagement, social
males, whereby subjects with high hyperarousal profiles were most isolation, self-destructive behaviors, denial, rumination, and blam-
at risk for chronic disturbances (Schell, Marshall, & Jaycox, 2004). ing oneself or others are likely to be maladaptive in contexts of
As already noted, baseline cortisol and sympathetic arousal levels uncontrollable extreme stress (see e.g., reviews by Norris et al.,
have been linked to differential response styles (coping or defense) 2002, and Spaccarelli, 1994). As a rule, women’s coping styles
in humans, but information on possible gender differences in these have been found to be more emotion- and avoidance-focused than
processes is lacking. Additional research is clearly needed on this men’s (Matud, 2004). Women may be more prone to traumatic
topic, too. stress responses like problematic alcohol use and to trauma-related
symptoms like psychological dissociation (e.g., Lipschitz, Grilo,
Fehon, McGalshan, & Southwick, 2000; Sonne, Back, Zuniga,
Section Summary Randall, & Brady, 2003; for reviews see Langeland, van den
Brink, & Draijer, 2005, and Ouimette & Brown, 2003). Although
The literature suggests that the higher PTSD risk in females may most individuals use many different types of coping simulta-
be attributable in part to the observed higher rates of acute emo- neously, making it difficult to isolate the unique effects, research
tional and dissociative trauma reactions in women and to funda- indicates that avoidance behaviors, and more particularly escape–
mental sex or gender differences in neurobiological factors that avoidance coping, constitute significant predictors of posttrau-
contribute to the phenomenon of peritraumatic dissociation. Fur- matic morbidity (e.g., Chang et al., 2003; Charlton & Thompson,
ther traumatic stress research is needed to seek support for the 1996; Marmar et al., 1996). Avoidance coping has been found to
hypothesis that sensitized dissociative systems are more common be conducive to symptom development and, hence, predictive of
in females and that sensitized hyperarousal systems are more PTSD severity (e.g., Bryant & Harvey, 1995; Bryant et al., 2000).
common in males and to determine how certain symptoms and Other evidence links passive, avoidance-based coping to peritrau-
disorders, PTSD in particular, relate to those systems. Although matic dissociation (Koopman et al., 2004; Marmar et al., 1996),
there is evidence indicating sex differences in the acute neuroen- which for its part has been implicated in higher levels of PTSD
docrine stress response, the current information is insufficient to symptoms (Koopman et al., 1994) and higher rates of PTSD
draw conclusions about the specificity of the neuroendocrine sys- diagnosis (Shalev, Peri, Canetti, & Schreiber, 1996). Dissociation
tem in explaining female–male differences in acute trauma re- has further been linked to a greater likelihood of engaging in
sponses. The sympathetic nervous system or other neurotransmit- dangerous and irrelevant passive actions in response to an acute
ter systems could likewise contribute to women’s higher PTSD traumatic event (Koopman, Classen, & Spiegel, 1996).
risk. Additional research is needed to evaluate gender-specific In the light of the available information, Peirce and colleagues
acute response patterns to threat and to investigate whether gender- (2002) have hypothesized that differences in coping styles might
specific PTSD subgroups exist—in particular, arousal-related and provide a plausible basis to account for gender differences in
PTSD. Avoidant styles, in particular, might alter the usual pattern extreme demands of the stressor. This raises the need to review the
of physiological reactivity and neuroendocrine response in the empirical evidence for further gender differences in the psychobi-
body (see also Olff et al., 2005a). Only very few studies have ological stress response system. This section describes some of the
actually examined gender effects in coping after traumatic events other known gender differences in neurohormone and neurotrans-
(Gavrilovic et al., 2003; Slusarcick, Ursano, Fullerton, & Dinneen, mitter systems that seem important to understanding female–male
1999; Ullman & Filipas, 2005). These findings suggest that differences in maladaptive stress responses that can contribute to
women and men tend to apply different mechanisms of stress the development of PTSD. We examine the effects of HPA-axis
reduction. The observed gender differences seem consistent with hormones, the neuropeptide hormone oxytocin, and female sex
the socialization hypothesis (Miller & Kirsch, 1987), which pro- hormones. Given the tremendous complexity of psychobiological
poses that females are socialized to use more passive and emotion- responses to stress, the information we provide is highly selective.
focused coping behaviors and males are socialized to use more
active, instrumental behaviors. The few studies that have con- HPA Axis
nected gender role characteristics to PTSD support this argument
(Norris et al., 2001; Sciancalepore & Motta, 2004). Their findings Sex differences in reactivity to psychological stress have been
raise the possibility that gender role expectations or cultural influ- reported in the general stress literature with regard to the HPA
ences may be related to female–male differences in coping and axis. Empirical studies for humans show equivocal results (e.g.,
even to PTSD risk. Support for this assumption can be found in the Kemp et al., 2004; Kirschbaum, Kudielka, Gaab, Schommer, &
general psychological literature on links between gender role so- Hellhammer, 1999; Matthews, Gump, & Owens, 2001; Seeman,
cialization practices and general personality development. Stress Singer, Wilkinson, & McEwen, 2001; Traustadottir, Bosch, &
responding in women with a masculine or androgynous gender Matt, 2003; see also Biondi & Picardi, 1999; Kudielka & Kirsch-
role orientation would result in a better adaptability and flexibility baum, 2005). In particular, this literature indicates that adult
to face difficult life circumstances than in feminine women (e.g., women between puberty and menopause usually show lower HPA-
Cheng, 2005; Thomas & Reznikoff, 1984). Consistent with the axis responses than men of the same age. However, the HPA
proposed conceptual model, there are findings suggesting that it is response is higher in the luteal phase of the menstrual cycle, when,
the lack of masculine instrumentality in the personality, not the for example, poststress cortisol levels approach those of men.
feminine role per se, that is implicated in mental illness in women After menopause, there is usually an increase in the HPA response
(Thomas & Reznikoff, 1984). It remains to be elucidated whether in women (Kudielka & Kirschbaum, 2005). It has been argued that
traumatized women with a more prototypic masculine arousal- biological sex differences like these may contribute to the greater
related pattern of stress responding show neuroendocrine re- vulnerability of females to stress (Young, 1998). As described
sponses more commonly seen in traumatized men and, at least in earlier in this article, HPA-axis dysregulation may be associated
some cases, a lower vulnerability to develop PTSD. Clearly further with an elevated risk for PTSD. Findings among newborns (Buske-
research is needed to explore gender-specific coping processes as Kirschbaum et al., 2004; Davis & Emory, 1995) and prepubertal
potential sources of differential neuroendocrinological stress re- children (e.g., Rosmalen et al., 2005) also suggest that gender
sponses. As argued above, greater knowledge of gender differ- should be included as a potential confounder when studying the
ences in psychological processes, particularly cognitive appraisal relationship between cortisol and psychopathology. The few data
and coping, and how they relate to the acute neuroendocrine stress available in children seem to point towards similar gender differ-
response should aid in developing gender-specific preventive and ences in cortisol responses as found in adults (e.g., Dahl et al.,
therapeutic interventions that can modulate HPA-axis responses 1992; Rosmalen et al., 2005). Early sex differences may have
(see e.g., Gaab, Rohleder, Nater, & Ehlert, 2005; Hammerfald, implications for stress reactivity in later life (Dienstbier, 1989).
Ehlert, & Gaab, 2004). Because the HPA axis represents the “final effector” in the mod-
There is compelling evidence from diverse sources that women ulation of stress response, a large number of preclinical and clin-
use less effective combinations of coping strategies than men, with ical studies have attempted to define a direct link between sex-
a preponderance of avoidance- and emotion-focused strategies but related differences in key elements of this system and the higher
also palliative behaviors like drinking. Avoidance-focused forms female susceptibility to stress and stress-related psychopathology
of coping have been linked to the higher occurrence of peritrau- (see e.g., Kudielka & Kirschbaum, 2005; Rasmusson & Friedman,
matic dissociation in women. Other evidence suggests a relation- 2002; Seeman et al., 2001; van Oers et al., 1998).
ship between gender role characteristics and male–female differ- With regard to traumatic stress, preclinical research has shown
ences in stress coping, which could be reflected in the gender sex differences in HPA-axis reactivity and behavior in rats ex-
differences in PTSD rates. Further research is needed to confirm posed to a traumatic footshock, which was followed by situational
the latter hypothesis. reminders more than 2 months after the footshock; only the female
animals showed an enhanced corticosterone negative feedback
Other Gender Differences in Psychobiological (Louvart, Maccari, Ducrocq, Thomas, & Darnaudery, 2005).
Stress Responses These findings are consistent with evidence from human studies
that have linked greater HPA-axis feedback sensitivity to PTSD
Our framework proposes (see “Neuroendocrine Response” at (for a review, see Yehuda, 2002). In particular, during cognitive or
the lower center of the model in Figure 1) that the activation of the psychological challenges, PTSD patients display elevated cortisol
stress response system is a psychobiological phenomenon. The levels (Bremner et al., 2003; Elzinga et al., 2003). It is interesting,
subject perceives and appraises the traumatic event and instinc- however, that these effects are not found in samples with only male
tively activates the biological response in accordance with the subjects (Liberzon et al., 1999). In addition, although there was
large variability in basal cortisol levels across studies, a recent ently and have evolved differentially to support these different
meta-analysis performed in our group showed a significant trend behaviors (S. E. Taylor et al., 2000). This model proposes that
of lower cortisol levels in female PTSD patients compared with women in stressful situations may use a tend-and-befriend re-
controls, whereas no such effect was seen in male patients (Mee- sponse—mediated by the “bonding” hormone oxytocin in conjunc-
wisse et al., 2006). The typical dysregulation of the HPA axis tion with female reproductive hormones (mainly estrogen) and
associated with PTSD with lower basal levels and increased re- endogenous opioids—rather than the fight-or-flight response that
sponses to stressful challenge, therefore, seems to be observed is often assumed (Bateup, Booth, Shirtcliff, & Granger, 2002;
more consistently in female patients compared with female con- Kivlighan, Granger, & Booth, 2005; S. E. Taylor et al., 2000;
trols. Studies specifically designed to test these sex differences in Tops, 2004). The theory is that women may be more specifically
the HPA axis have yet to be done. adapted to mounting a type of stress response that has evolved to
It has been argued that HPA-axis hormones could theoretically maximize the survival of self and offspring. This oxytocin-
be conducive to PTSD development through their complex and mediated tend-and-befriend response might, for example, protect
simultaneous interactions with memory formation and retrieval women against overconsolidation of memories surrounding child-
(Buchanan & Lovallo, 2001; Schelling et al., 2001; Schelling, birth, thus explaining the rarity of posttraumatic symptoms in
Roozendaal, & de Quervain, 2004). It has been shown that cortisol postpartum women (van der Kolk, 1994). The tend-and-befriend
modulates emotionally influenced memory and that the relation- response implies that women respond to stress by displaying
ship between stress-induced cortisol levels and memory differs nurturing behaviors to shield them from harm and by affiliating
between women and men (Wolff, Schommer, Hellhammer, Mc- with social groups to reduce risk. Preclinical research has impli-
Ewen, & Kirschbaum, 2001; see also Wolff, 2003). It should be cated central pathways for oxytocin in the neurobiology of anxiety
noted that—apart from being due to sex differences—the incon- and social behaviors (e.g., Francis, Young, Meaney, & Insel, 2002;
sistent patterns of HPA-axis abnormalities in PTSD (including Nair, Gutman, Davis, & Young, 2005). Higher levels of oxytocin
reduced responsiveness to glucocorticoids or insufficient glucocor- are associated with decreases in anxiety and stress, increases in
ticoid signaling) could be attributable to the methods of measuring positive social interactions and parental care, and facilitation of
cortisol levels; age of the subjects (pediatric vs. adult PTSD); extinction of conditioned avoidance behavior (Uvnäs-Moberg,
subjects’ genetic backgrounds; length of time since the original 1997, 1998). Oxytocin thus seems to have a calming and comfort-
trauma exposure (acute vs. long-standing PTSD); trauma history; ing effect, but the mechanisms through which it modulates auto-
coping phase; use of nicotine, alcohol, drugs or medication; and, in nomic fear responses are still unclear (Huber, Veinante, & Stroop,
women, menstrual or reproductive state (e.g., Laudenslager, 1988; 2005).
McCleerly, Bhagwagar, Smith, Goodwin, & Cowen, 2000; Nicol- Of particular relevance for the present article is that patterns of
son, 2004; Seeman et al., 2001; Sher, Oquendo, Galfalvy, Cooper, attachment and caregiving responses and the associated increased
& Mann, 2004; see also Rasmusson, Vythilingham, & Morgan, levels of oxytocin serve to suppress both sympathetic arousal and
2003). Although type of trauma exposure (often sexual abuse in HPA responses to stress. Higher oxytocin levels have also been
female-only studies) cannot sufficiently explain gender differences associated with faster HPA recovery in women after an acute stress
in PTSD prevalence, it may contribute to sex differences in HPA- laboratory challenge (Taylor, Klein, Greendale, & Seeman, 1999,
axis reactivity. Other researchers have suggested that low cortisol manuscript cited in S. E. Taylor et al., 2000, p. 416). Conceivably,
levels are associated with specific dimensions of PTSD symptom- they might also diminish people’s risk of developing PTSD after
atology like emotional numbing (Hawk et al., 2000). trauma.
The reviewed literature suggests that females are more sensitive Numerous variables can affect oxytocin levels. Determining
than males to prolonged changes in the corticosterone response to how closely PTSD might be associated with alterations or dys-
stress. Clearly, HPA-axis alterations (including cortisol levels) are functions in oxytocin metabolism will require careful consider-
complex and may have implications for different aspects of PTSD, ation of all such issues. Oxytocin levels can be increased by close
including the risk of developing the disorder, specific features of it relationships and social support and reduced by sad emotions or
(such as comorbid depression), or its time course (Friedman & social isolation (S. E. Taylor et al., 2000). A recent study showed
McEwen, 2004; Yehuda, 2002). Future research will need to an increase in oxytocin levels in females in response to positive
determine whether different biologic variants of PTSD exist with affiliative behaviors (Light, Grewen, & Amico, 2005). Preliminary
relatively similar phenotypic expressions but that may account for findings in healthy adults now also suggest that women with
different facets of the neuroendocrinology of PTSD (Yehuda, positive affect may inhibit the basal release of cortisol more
2002). Because sex differences in physiological stress reactivity efficiently than men with positive affect (Polk, Cohen, Doyle,
under both acute and chronic conditions could potentially provide Skoner, & Kirschbaum, 2005), presumably because they develop
underlying explanations for the gender differences in PTSD rates, higher levels of oxytocin. On the negative side, it has been shown
future research should include both sexes. that exposure to early adverse social experiences like childhood
neglect may disrupt the normal development of the oxytocin
Oxytocin system in children and thereby a mechanism critical to the regu-
lation of emotional behaviors (A. B. Fries, Ziegler, Kurian, Jacoris,
Theoretical models on biological sex differences in human & Pollak, 2005). The study of A. B. Fries and colleagues demon-
stress response may provide frameworks to better understand strated that children who had experienced early neglect did not
gender differences in the prevalence of a number of psychiatric show the expected hormonal reactivity—an increase in oxytocin
disorders. In terms of more general stress response, one argument levels—years later that typically emerges between young children
has been that females and males handle stressful situations differ- and familiar adults who provide care and protection. Thus, chronic
oxytocin dysfunction can occur in people who have experienced stress (Da Silva, 1999). HPA-axis responses are especially aggra-
adverse social circumstances early in life; that is, oxytocin levels vated when estrogens remain elevated for longer periods of time
can remain lower compared with levels in persons not exposed to because of chronic stress. Clearly, damage can result if stress
early adversity. Low oxytocin levels could therefore represent an hormones are overproduced or not shut off when they are no
index of risk for stress-related disorders and may even figure in the longer needed (McEwen, 2000). Chronic constant elevation of the
secondary biological alterations that ultimately lead to PTSD. It glucocorticoid hormone cortisol can lead to damage to brain struc-
remains to be elucidated whether the effects of early social cir- tures, inefficient cognitive appraisal of events (Erickson, Drevets,
cumstances, such as variations in maternal care, on the oxytocin & Schulkin, 2003), and an increase in behaviors like freezing and
neuropeptide system have a particular impact on girls, as suggested passive avoidance (e.g., Koolhaas et al., 1999). Thus, female sex
by findings from two animal studies (Francis et al., 2002; hormones appear to affect not just the overall cortisol responses
Yamamoto, Carter, & Cushing, 2006). but also the recovery process. This implies that women are more
Returning now to the considerations in our conceptual frame- likely than men to suffer delayed recovery from the deleterious
work, what is particularly interesting about the reviewed findings consequences of stress. We have seen that rapid shutoff of the
on oxytocin is the clear association between levels of this neu- stress response is important for trauma recovery. Findings suggest-
ropeptide and the availability and experience of social support (see ing delayed recovery in women are consistent with results of stress
also Neumann, 2002). Although little is known as yet about the studies indicating that women’s stress levels unwind much more
oxytocin-mediated response to trauma, an inability to seek social slowly than men’s (e.g., Frankenhaeuser et al., 1989; Lundberg,
support after trauma is a factor that significantly predicts PTSD, as 2005).
evidenced in meta-analyses (Brewin et al., 2000; Ozer et al., 2003).
In addition, the repeated observation that a lack of social support Section Summary
is more strongly related to the development of posttraumatic stress
symptoms in women than in men (e.g., Ahern et al., 2004; B. Women appear to have more sensitized HPA systems than men.
Andrews, Brewin, & Rose, 2003; Weismann et al., 2005) is com- Both the oxytocin-mediated responses to trauma and the influence
patible with the idea that oxytocin-mediated response to trauma of sex hormones on HPA-axis regulation could be of specific
may be of specific benefit to women. These results in human relevance to women. The findings suggest that women are more
populations are consistent with animal studies reporting that social vulnerable than men to developing posttrauma symptoms and may
support had a favorable influence on stress sensitivity, particularly take longer to recover from them. Future work should continue to
in female rats, whereas it did not enhance stress coping in male rats explore how sex differences in the neurohormone or neurotrans-
(e.g., Westenbroek et al., 2003). Another gender-dependent differ- mitter systems contribute to gender differences in stress reactivity.
ence in oxytocin function has been shown in healthy subjects:
increased oxytocin responses in women, but not in men, to Gender, PTSD, and Comorbidity
m-chlorophenylpiperazine, a serotonin 5-HT2c receptor agonist
(Bagdy & Arato, 1998). All these observed gender differences The final box of our conceptual model (“PTSD/Depression/
could render traumatized women more vulnerable to depression Addiction” at the lower right in Figure 1) concerns mental health
and PTSD (see Rasmusson & Friedman, 2002). Overall, then, the outcomes of traumatic-stress-coping pathways. In addition to
findings reviewed here suggest that PTSD in women may be PTSD, many other forms of posttrauma psychopathology can
associated with a compromised social-coping or tend-and-befriend develop, as well as subjective health complaints (medically unex-
response. This means that providing social support may be partic- plained symptoms) and nonpsychiatric morbidity such as immune
ularly beneficial for traumatized women (Kimerling, Prins, We- system-related disorders. It is important to have information on the
strup, & Lee, 2004). Future research needs to test whether indi- impact that gender-related phenomena can have on the clinical
viduals with stress-related disorders, and PTSD in particular, have manifestations of PTSD, including comorbid psychiatric and phys-
characteristic dysfunctions in oxytocin metabolism. ical conditions. The many variations of stress-related illness may
complicate the interpretation of psychobiological outcome data
Female Sex Hormones and impede trauma assessment (for reviews of gender differences
in psychiatric and medical comorbidity in PTSD, see Kimerling,
Many of the major neurotransmitter or neurohormone systems 2004, and Kimerling et al., 2004).
implicated in PTSD (including the serotonin, norepinephrine, do- In women, PTSD has been linked to major depression,
pamine, gamma aminobutyric acid, and HPA systems) are subject substance-use disorders, other anxiety disorders, somatoform dis-
to modulation by female sex hormones (see Vasterling & Brewin, orders, dissociative disorders, eating disorders, and personality
2005). Women’s greater biological complexity compared with disorders, especially of the borderline type. In men, it has been
men’s implies substantial gender-related differences in HPA-axis linked to substance-use disorders, major depression, other anxiety
regulation. The HPA axis and the female reproductive system are disorders, and personality disorders, especially the antisocial type
complexly intertwined. Because females have greater variations in (e.g., Brady, Killeen, Brewerton, & Lucerni, 2000; Kessler et al.,
neuroendocrine responses because of their reproductive cycle, 1995). PTSD and major depressive disorder (MDD) are twice as
their data often present confusing patterns of results. All the same, common in females as in males (Kessler et al., 1995); both disor-
sex hormones have been implicated as key factors in the higher ders are associated with HPA-axis dysregulation. Findings of
liability of females to psychopathology (McEwen, 1999; Young, HPA-axis hyperactivity have been reported with some consistency
1998). Preclinical research clearly demonstrates that androgens in women with concurrent PTSD and MDD (e.g., Young &
inhibit and estrogens enhance the HPA-axis responsiveness to Breslau, 2004). Comorbidity, particularly with MDD, may be one
of the factors contributing to the divergent results involving cor- Gender differences have also recently been reported in the
tisol levels in PTSD studies. More broadly, such findings highlight nonpsychiatric morbidity associated with PTSD (Kimerling,
the need for biological studies to explore lifetime comorbidity, 2004). Although no findings are yet available on gender effects in
particularly with respect to gender differences. the immune response to stressors (Segerstrom & Miller, 2004),
Alcohol-use disorders are another condition that is frequently such information could be valuable for explaining the already
comorbid with PTSD (e.g., Kessler et al., 1995; see also Ouimette observed gender differences in medical conditions associated with
& Brown, 2003). It is interesting that in the literature about this PTSD, such as chronic fatigue syndrome or fibromyalgia. Asso-
type of comorbidity, some evidence has emerged about possible ciations have been described between these conditions and HPA-
gender differences in the functional relationship between PTSD axis abnormalities (e.g., Cleare, O’Keane, & Miell, 2004). As we
and alcohol-use disorder. Although men show higher absolute have seen, the perception and appraisal of stressors and the various
levels of comorbid alcohol use, more women start drinking exces- types of stress-coping responses involve the sympathetic nervous
sively after trauma (Clark et al., 1995, 1997; Deykin & Buka, system and the HPA axis in different ways, and both these systems
1997; Lipschitz et al., 2000; Najavits, Weiss, & Shaw, 1997). affect immune response. Research on laboratory stressors has
shown a link between cognitive appraisal and immune function,
PTSD symptomatology appears to be one of the factors contrib-

uting to alcohol-use disorders in women who report experiences of with low perceived controllability of the stressor associated with
childhood sexual or physical abuse or adult rape (Darves-Bornoz, decreases in immune functioning (e.g., Brosschot et al., 1998; Olff,
Delmotte, Benhamou, Degiovanni, & Gaillard, 1996; Epstein, 1999; Sieber et al., 1992). The disturbed regulation of the HPA
Saunders, Kilpatrick, & Resnick, 1998; Najavits et al., 1997). The axis and the SAM system in PTSD suggests that immune function
literature also indicates that women with these comorbid condi- may logically be dysregulated too. Support for this is found in the
tions are more likely than men to have PTSD as their primary literature. Enhanced cellular immune response has been shown in
diagnosis and that their typical drinking pattern is more likely to be women with chronic PTSD related to childhood abuse (Altemus,
episodic binge drinking than habitual heavy drinking (see Cloitre, & Dhabhar, 2003). More generally, neuroimmunological
Ouimette & Brown, 2003). alterations have been demonstrated in patients with current PTSD
In addition, psychological dissociation in response to childhood (enhanced immunological functions) and in patients in remission
from PTSD (immunosuppression; Burges Watson, Muller, Jones,
trauma has been found to be more common in adult women,
& Bradley, 1993; G. F. Solomon, Segerstrom, Grohr, Kemeny, &
whereas chemical dissociation (as through alcohol use) appears
Fahey, 1997; see Vermetten & Bremner, 2002). Given the mod-
more common in men reporting childhood trauma (Langeland,
erating role that coping presumably has on immune function after
Draijer, & van den Brink, 2002; Langeland et al., 2005). Men may
stress, further research is clearly warranted to identify possible
be compensating for a lack of psychological dissociation by using
gender differences among trauma victims in the area of psycho-
alcohol to create some kind of substance-induced dissociation as a
neuroimmunology (Dougall & Baum, 2004; Stowell, Kiecolt-
similar numbing or soothing coping strategy with trauma-related
Glaser, & Glaser, 2001).
distress (Langeland et al., 2002; Langeland et al., 2005). Study
Compelling evidence exists for gender differences in both the
findings in fact suggest that two different forms of PTSD could
psychiatric and the nonpsychiatric morbidity associated with
exist with respect to pathological dissociation in alcohol-
PTSD. Women may be more vulnerable than men to comorbidity
dependent subjects: an anxious subtype (possibly more common in between trauma-related symptoms (particularly posttraumatic
men) and a dissociative subtype (possibly more common in wom- stress symptoms and dissociation) and alcohol abuse. In view of
en; Langeland et al., 2005). The existence of a distinct anxious the different underlying neurobiological mechanisms that could be
subtype of PTSD in early traumatized male alcohol-dependent involved, the evaluation of gender-specific clinical profiles should
patients reporting profound phobic avoidance and little psycholog- be considered to aid in interpreting psychobiological outcome data.
ical dissociation has been shown (Langeland et al., 2002, Lange-
land, Draijer, & van den Brink, 2004; Langeland, van den Brink,
& Draijer, 2004).
Gender Differences in Traumatic Stress Coping: Heuristic
On the whole, the reviewed findings suggest that the mecha- Model and Clinical Implications
nisms linking traumatic stress and alcohol use may indeed be The information on gender differences documented here is
gender specific. The neurobiological response patterns we have summarized in the gender-differentiated traumatic-stress-coping
described above as potentially gender specific— hyperarousal ver- model (see Figure 2). The literature review has shown that factors
sus dissociative— could be implicated here, representing different related to the trauma exposure itself may partially explain gender
pathways to PTSD. Recent research on sexually abused children effects in PTSD. Although men have higher overall rates of trauma
has identified independent pathways to PTSD related to anxiety exposure than women, women more often experience particular
and/or arousal responses and dissociative reactions (Kaplow, types of traumas, such as rape and childhood sexual abuse, that
Dodge, Amaya-Jackson, & Saxe, 2005). Because the neurobiology may help to account for the higher PTSD rates observed in women.
of hyperarousal is distinct from that of dissociation, the gender- Trauma exposure at a younger age could also be a more significant
specific comorbidity patterns can provide critical insights for the risk factor for women than for men. More profound explanations
interpretation of psychobiological outcome data. In a more general for women’s apparent higher vulnerability to PTSD include
sense, the findings underline the relevance of assessing alcohol use gender-specific cognitive appraisal and coping processes. Subjec-
in traumatized populations, especially in women reporting early tive appraisals of traumatic events have been shown to be far
interpersonal violence, as well as the need for comprehensive stronger predictors of PTSD than the objective characteristics of
psychiatric evaluation of all traumatized individuals with PTSD. those events. The higher levels of negative threat appraisal and of
Personal, social & cultural factors

(e.g.genetics, trauma history,
gender role orientation)
coping
F: less effective social support
combinations F: greater effects
defense
;
t er y F:
l m as an mor
e n ta dp ee
n s trum ht F: tend-and-befriend, all
iat motio
M: -or- fli
i g ive
freezing, passive avoidance n
t (e. -focu
figh g.
alc sed
F:more cognitive defense oh
o l)
Psychological & biological Health outcomes:

Exposure: response:
F: more anxiety, horror F: higher PTSD rate
M: more overall Appraisal: more subjective distress F: more other anxiety,
exposure more (peritraumatic) dissociation depressive &
F: more high impact eventss F: higher perception dissociative disorders,
F: more exposure at of threat and loss F: sensitized dissociative system somatization,
younger age of control, more HPA axis dysregluation alcohol abuse
more negative appraisals oxytocin, estrogens, endog. opioids M: more aggressive
M: sensitized hyperarousal system behaviors, hypervigilence
higher SNS activity chemical dissociation
Figure 2. Gender-differentiated traumatic-stress-coping model. F ⫽ females; M ⫽ males; HPA ⫽ hypothal-

amic–pituitary–adrenocortical; endog ⫽ endogenous; SNS ⫽ sympathetic nervous system; PTSD ⫽ posttrau-
matic stress disorder.
perceived loss of control seen in women may thus contribute to sures of negative cognitive appraisals and acute stress reactions
their higher PTSD prevalence. Women also appear more likely to including peritraumatic dissociation, coping styles, alcohol use,
use avoidant and emotion-focused coping, both of which are and social support. Specific therapeutic techniques that ought to be
associated with a heightened risk of PTSD. Other sources of of particular benefit to women would include installing more
explained variance in the prevalence rate are female–male differ- positive appraisals or cognitions, reinterpreting the event and its
ences in acute physiological, emotional, and dissociative reactions consequences, learning more effective combinations of coping
to trauma and women’s more frequent negative appraisals of acute skills (or new skills) to manage extreme stress without resorting to
symptoms. Neurobiological data also suggest that HPA-axis dys- dissociation or alcohol use, and enhancing social resources to help
regulations may be more common in women with PTSD than in cope with trauma. Psychotherapeutic approaches such as cognitive
men with PTSD. Women with PTSD appear to more often report behavioral therapy, and in particular brief eclectic psychotherapy
dissociative symptoms, whereas men with PTSD are more likely to (Lindauer et al., 2005), address these key issues. Novel pharma-
report hyperarousal-related symptoms. Lack of social support after cological interventions that reduce acute psychobiological re-
the trauma and the trauma-related use of alcohol may be more sponses to trauma, such as the use of beta-blockers like propran-
crucial in the development of posttrauma psychopathology in olol (which blocks the noradrenergic response), may also be of
women than in men, probably because of their specific effects on interest because they can reduce immediate threat appraisal and,
female neuroendocrine responses to the trauma. All these factors hence, the likelihood of sustained dissociation and emergent PTSD
together, in combination with personal, social, and cultural factors symptoms (Famularo, Kinsherff, & Fenton, 1988; Pitman et al.,
such as gender role orientation, may be hypothesized to increase 2002; F. Taylor & Cahill, 2002; Vaiva, Ducrocq, Jezequel, Brunet,
the female risk for developing a range of posttrauma psychopa- & Marmar, 2003). Rapid assessment of peritraumatic dissociation
thology, including PTSD, depression, addiction, or other psychi- and pharmacological treatment of these symptoms may be partic-
atric and physical disorders. ularly important for women. Selective serotonin reuptake inhibi-
Given the inconsistencies in the literature, it is not yet possible tors treatment might be a supportive strategy in combination with
to determine which specific alterations in the neuroendocrine cognitive training in stress management for alcohol-dependent
system will be involved in the development of PTSD at an indi- patients with less severe alcohol dependence and early onset PTSD
vidual level. It is unlikely that individual stress vulnerability can be (Back, Jackson, Sonne, & Brady, 2005; Brady et al., 2005). As
fully explained by gender-related differences in hormone levels. suggested above, this subtype of alcohol-dependent individuals
Other factors will probably play a role too, such as genetic back- with primary PTSD will consist mostly of women. Further re-
ground, age, and pretrauma history including interactions between search on gender differences in psychobiological factors in stress-
these factors. related disorders would stimulate development of improved
Taken altogether, the findings suggest that the assessment of gender-specific psychosocial and pharmacological treatment op-
psychological trauma and PTSD in women should include mea- tions. A more specific focus would be to investigate gender-related
factors in differential treatment response; this could result in References

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Psychological Bulletin Copyright 2007 by the American Psychological Association

2007, Vol. 133, No. 2, 183–204 0033-2909/07/$12.00 DOI: 10.1037/0033-2909.133.2.183

Gender Differences in Posttraumatic Stress Disorder

Miranda Olff Willie Langeland

Nel Draijer Berthold P. R. Gersons

person has to “fight or flee” or has to exert effort to control a

Personal, social & cultural factors

coping social support

Figure 1. Traumatic-stress-coping model. HPA ⫽ hypothalamic–pituitary–adrenocortical; SNS ⫽ sympathetic

that men have a broadly higher risk of being exposed to potentially

ment options, including gender-specific interventions. After syn-

Helzer et al. (1987) USA 2,493 1.00 1.3 0.5

Note. PTSD ⫽ posttraumatic stress disorder.

the negative effects of childhood sexual abuse, whereas boys may

It has been suggested that gender differences in brain engage-

whereas others do not develop it even after horrific traumas like

Lower basal cortisol levels have been reported in patients with

PTSD symptomatology appears to be one of the factors contrib-

Personal, social & cultural factors

Psychological & biological Health outcomes:

Figure 2. Gender-differentiated traumatic-stress-coping model. F ⫽ females; M ⫽ males; HPA ⫽ hypothal-

factors in differential treatment response; this could result in References

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nal study of combat stress reactions. Journal of Traumatic Stress, 4,

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