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Posttraumatic stress hyperarousal symptoms mediate the relationship between childhood exposure to violence and subsequent alcohol misuse in Mi'kmaq youth

Article (PDF Available) inJournal of Traumatic Stress 24(5):566-574 · October 2011with160 Reads
DOI: 10.1002/jts.20677 · Source: PubMed
Marc Zahradnik at Gilmour Psychological Services
  • 7.02
  • Gilmour Psychological Services
Sherry H Stewart at Dalhousie University
  • 44.77
  • Dalhousie University
Simon B. Sherry at Dalhousie University
  • 36.59
  • Dalhousie University
Christine Wekerle at McMaster University
  • 35.25
  • McMaster University
Abstract
This study was part of a school-based collaborative research project with a Canadian Mi'kmaq community that examined the potential role of posttraumatic stress (PTS) symptom clusters in mediating the relationship between childhood exposure to violence (EV) and alcohol misuse in a sample of Mi'kmaq adolescents (N = 166). The study employed a cross-sectional design and used several well-validated self-report questionnaires. Path analytic results showed that when each PTS symptom cluster was independently investigated for mediating effects while controlling for depressive symptoms, age, and gender, only the PTS hyperarousal symptom cluster fully mediated the EV-alcohol misuse relationship. Results are discussed within the context of previous theory and research on the topic of PTS as a mediator between EV and alcohol misuse.
Journal of Traumatic Stress, Vol. 24, No. 5, October 2011, pp. 566–574 (C
2011)
Posttraumatic Stress Hyperarousal Symptoms Mediate
the Relationship Between Childhood Exposure
to Violence and Subsequent Alcohol Misuse
in Mi’kmaq Youth
Marc Zahradnik, Sherry H. Stewart, and Simon B. Sherry
Dalhousie University
Doreen Stevens
Mount Saint Vincent University
Christine Wekerle
McMaster University
This study was part of a school-based collaborative research project with a Canadian Mi’kmaq community that
examined the potential role of posttraumatic stress (PTS) symptom clusters in mediating the relationship between
childhood exposure to violence (EV) and alcohol misuse in a sample of Mi’kmaq adolescents (N=166). The
study employed a cross-sectional design and used several well-validated self-report questionnaires. Path analytic
results showed that when each PTS symptom cluster was independently investigated for mediating effects while
controlling for depressive symptoms, age, and gender, only the PTS hyperarousal symptom cluster fully mediated
the EV–alcohol misuse relationship. Results are discussed within the context of previous theory and research on
the topic of PTS as a mediator between EV and alcohol misuse.
Interpersonal violence, whether experienced directly or indi-
rectly, especially during childhood, can either precipitate the on-
set of posttraumatic stress disorder (PTSD) or act as a risk factor
that later increases the odds of developing PTSD after subsequent
traumas (Brewin, Andrews, & Valentine, 2000). Unfortunately,
youth exposure to violence (EV) is not rare. Two American studies
(Finkelhor, Ormrod, Turnery, & Hamby, 2005; Hanson et al.,
Marc Zahradnik, Department of Psychology, Dalhousie University; Sherry H. Stewart, De-
partments of Psychology, Psychiatry, and Community Health and Epidemiology, Dalhousie
University; Simon B. Sherry, Departments of Psychology and Psychiatry, Dalhousie Univer-
sity; Doreen Stevens, Department of Education, Mount Saint Vincent University; Christine
Wekerle, Department of Pediatrics, McMaster University.
This project was supported in part by a Canadian Institutes of Health Research New Emerging
Team (CIHR NET) grant held by Christine Wekerle and Sherry Stewart, a CIHR-Institute
of Aboriginal Peoples Health (CIHR-IAPH)-funded Aboriginal Capacity and a Develop-
mental Research Environment (ACADRE) research allowance held by Marc Zahradnik. Marc
Zahradnik was also funded by an Atlantic Aboriginal Health Research Program(AAHRP) grad-
uate student award followed by a NovaScotia Health Research Foundation (NSHRF) graduate
student award. Sherry Stewart was supported through a Killam Research Professorship from
the Dalhousie University Faculty of Science at the time this research was conducted. Christine
Wekerle is supported through an Ontario Women’s Health Council/CIHR Mid-Career Award.
Correspondence concerning this article should be addressed to Sherry Stewart, Depart-
ment of Psychology, Dalhousie University; Halifax, Nova Scotia; B3H 4J1, Canada. E-mail:
sherry.stewart@dal.ca
C
2011 International Society for Traumatic Stress Studies. View this article online at
wileyonlinelibrary.com DOI: 10.1002/jts.20677
2008) using nationally representative samples of youth suggest
that one fifth to one half of all children and adolescents have ex-
perienced a physical assault, a little over one third have witnessed
violence perpetrated toward another, and almost one tenth have
been sexually victimized. These figures are particularly alarming
because EV increases the risk of developing PTSD over-and-above
other types of traumatic events (Kessler, Sonnega, Bromet, Hughes,
& Nelson, 1995; Kilpatrick et al., 2000). Furthermore, not only
is EV more likely to result in PTSD or become a risk factor for
the later onset of PTSD after a subsequent trauma, but EV is
also more likely to predict the development of PTSD with comor-
bid substance misuse (Wekerle & Wall, 2002). This study refers
to both posttraumatic stress disorder (PTSD) and posttraumatic
stress (PTS) symptoms of PTSD. The term PTSD is used when
referring to the literature that employed this diagnostic label, but
as we did not measure diagnostic status in this study, we employ
the term PTS when referring to the construct we have measured.
There are well-documented relationships between childhood
maltreatment and both PTSD and alcohol abuse/dependence
(Langeland, Draijer, Nel, & van den Brink, 2004). Moreover,
much of the research indicates that PTSD symptoms and alco-
hol misuse are commonly “comorbid” (Stewart, 1996)—that is,
they occur together in the same individuals far more commonly
than can be explained by chance. Studies show that the lifetime
566
Mediating Effect of Posttraumatic Stress Hyperarousal Symptoms 567
prevalence rate of having an alcohol-use disorder (abuse or de-
pendence) for those with PTSD ranges from 21.6 to 51.9% but
only from 8.1 to 34.4% for those without PTSD (Breslau, Davis,
Peterson, & Schultz, 1997; Kessler et al., 1995).
Although there are a number of possible explanations for the
comorbidity of PTSD and alcohol abuse/dependence, many re-
searchers suggest that those with PTSD misuse alcohol (or other
substances) to self-medicate their PTSD symptoms (De Bellis,
2002; Chilcoat & Breslau, 1998; Stewart, Mitchell, Wright, &
Loba, 2004). The self-medication theory argues that central ner-
vous system depressants like alcohol may help attenuate certain
fear/startle responses as well as the intrusive memories that are
characteristic of PTSD (Jacobsen, Southwick, & Kosten, 2001).
The relationship between PTSD symptoms and alcohol misuse
can become further complicated by a process known as mutual
maintenance (Stewart, Pihl, Conrod, & Dongier, 1998). Although
an individual receives initial PTSD symptom relief immediately
following the consumption of alcohol, once its effects have worn
off the PTSD symptoms return. Some of those symptoms, partic-
ularly hyperarousal, can return with even greater severity, largely
due to the physiological arousal relating to withdrawal from cen-
tral nervous system depressants like alcohol (Jacobsen et al., 2001).
This maintenance or intensification of PTSD symptoms then re-
sets the stage for continued alcohol misuse, potentially causing
further dysregulation of biological stress response systems (De
Bellis, 2002), and interfering with the body’s natural habitu-
ation to traumatic memories. In this way, alcohol misuse can
actually serve to maintain PTSD symptoms in the longer term
creating a vicious cycle between PTSD symptoms and alcohol
misuse.
In essence, the self-medication/mutual maintenance theories
suggest that PTSD acts as a mediating variable, that is, a variable
that intervenes and helps explain the relationship between trauma
exposure and subsequent alcohol misuse. Previous studies that
attempted to show the role of PTSD as a mediator between a trau-
matic event and later alcohol misuse have shown weak to moderate
support (Epstein, Saunders, Kilpatrick, & Resnick, 1998; White &
Widom, 2008; Zlotnick et al., 2006) though a couple have shown
no support (Prigerson, Maciejewski, & Rosenheck, 2002; Ullman,
Filipas, Townsend, & Starzynski; 2005). However, none of these
studies examined the potential mediating role of the individual
PTSD symptom clusters.
In light of the relationships between the PTSD symptom clus-
ters of hyperarousal (McFall, MacKay, & Donovan, 1992; Stewart,
Conrod, Pihl, & Dongier, 1999; Stewart et al., 2004), reexperienc-
ing (McFall et al., 1992; Read, Brown, & Kahler, 2004; Simons,
Gaher, Jacobs, Meyer, & Johnson-Jimenez, 2005) and avoidance
and numbing (Sullivan & Holt, 2008; Taft et al., 2007) with al-
cohol misuse, it is important to examine the potential mediating
role of each PTSD symptom cluster because the self-medication
model would predict that individuals exposed to violence might be
drinking to cope with any of these symptoms (Stewart, 1996). An
important variable to control for in the trauma–alcohol misuse re-
lationship is depressive symptoms, however, because of the strong
relationships found between depressive symptoms and EV, depres-
sive symptoms and alcohol misuse, and depressive symptoms and
PTSD (Kessler, Davis, & Kendler, 1997; Kilpatrick et al., 2003).
The present study is also novel in that this is the first attempt
we know of to address this issue in both an adolescent sample
and in partnership with an Aboriginal community. Although the
literature is scant, there is evidence to attest to the fact that some
North American Aboriginal communities are facing severe issues
that involve high rates of EV, PTSD, depressive symptoms, and
alcohol misuse. For example, the Canadian Aboriginal People’s
Survey reported that 73% of Aboriginal respondents reported that
alcohol was a problem in their community (Statistics Canada,
1991). From the same survey, 44% of respondents indicated that
family violence was a problem in their community, while just over
half indicated that both physical and sexual abuse were problems
as well (Statistics Canada, 1991). Another study showed that ap-
proximately 40% of a sample of 234 American Indians reported
exposure to severe child maltreatment, which was most strongly
associated with PTSD over other psychological disorders (Duran
et al., 2004). Boyd-Ball, Manson, Noonan, and Beals (2006) ex-
amined the relationship between trauma exposure and alcohol-use
disorders in a sample of American Indian adolescents and young
adults. Compared to nontraumatized youth, youth that reported
three or more severe traumas were 3.6 times more likely to have
a lifetime diagnosis of an alcohol-use disorder, and that interper-
sonal violence compared to other traumas was more predictive
of having a lifetime diagnosis of an alcohol-use disorder (Boyd-
Ball et al., 2006); however, they did not examine the potential
influence of PTSD. Other studies with American Indian popu-
lations have linked both childhood physical and sexual assault to
both depressive symptoms and subsequent alcohol misuse (Libby
et al., 2004, 2005). With respect to alcohol consumption, a re-
cent literature review concluded that rates of alcohol use among
American Indians and Alaskan Natives are higher than in the gen-
eral population for both adults and adolescents, and that Native
adolescents experience more negative consequences of their drink-
ing than other adolescents (Szlemko, Wood, & Jumper-Thurman,
2006). Thus, by working in partnership with a Mi’kmaq com-
munity (see Zahradnik et al., 2007), we attempted to address the
question of PTS mediation with a community that is not alone in
struggling with the issues highlighted.
We hypothesized that adolescents with higher amounts of EV
would be more likely to develop PTS symptoms, and these PTS
symptoms would in turn more likely lead to alcohol misuse, even
after controlling for the influence of depressive symptoms. Con-
sistent with current studies on how best to organize PTSD symp-
tom clusters (Asmundson et al., 2000; King, Leskin, King, &
Weathers, 1998; Stewart et al., 1999) we specified four sepa-
rate path models—hyperarousal, reexperiencing, numbing, and
avoidance—in which it was predicted that in each model EV
Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.
568 Zahradnik et al.
Exposure to
violence
Depressive
symptoms
.41
PTS
hyperarousal .31
Alcohol
misuse
.40
.19
.54
.27
.19
.19
Figure 1. The structural model involving posttraumatic stress (PTS) hyperarousal. Black arrows represent significant paths (i.e., p<.05).
Grey arrows represent nonsignificant paths. Rectangles represent manifest variables. Path coefficients are standardized. Italicized numbers
(e.g., .31) positioned in the upper right hand of endogenous variables (e.g., alcohol misuse) represent the proportion of variance explained
by associated exogenous variables. In the interest of clarity, error terms and demographic variables are not displayed.
would be indirectly related to alcohol misuse through one of our
four PTS symptom clusters. See Figure 1 for an example of the
hypothesized mediational model for PTS hyperarousal.
METHOD
Participants and Procedure
There are approximately 25,000 Mi’kmaq living in Nova Scotia.
The Mi’kmaq makeup about 2.6% of the provincial population
and there are 35 reserves administered by 13 self-governing com-
munities. The community of focus in the current study is one of
the larger communities; but given this community’s request for
anonymity, identifying information cannot be provided. A more
general description of the community and the steps involved in
acquiring community consent and participation in the research
process is available (Zahradnik et al., 2007; Zahradnik et al., 2010).
The sample was drawn from the community’s school-attending
youth, and data were collected in both the spring and the fall of
2006. Across the two schools, 166 students participated in the
study, which is just over half of those that were eligible to partic-
ipate. With respect to gender, there were 91 female students and
75 male students. Ages ranged from 14 to 18 years (M=16.69,
SD =1.39), with most students (77.7%) being 16 years of age or
older, the age at which according to Nova Scotian law (Children
and Family Services Act, 1990) a child can choose whether she
or he wishes to report a case of abuse where she or he alone was
the victim. The self-reported education level ranged from Grades
8–12 (M=9.91, SD =1.05).
Measures
Physical, sexual, and emotional abuse/exposure to domestic
violence was measured with the Childhood Experience of
Violence Questionnaire (CEVQ; Walsh, MacMillan, Trocm´
e,
Jamieson, & Boyle, 2008), an 18-item self-report measure of
childhood EV for use with children/youth 12–18 years. The
CEVQ collects information about whether abuse has been ex-
perienced and if so, about the severity (measured continu-
ously), onset, and duration of abuse experienced. The reli-
ability coefficient for this measure in our sample was high
(α=.92).
Posttraumatic stress symptoms were measured with the Child
PTSD Symptom scale (CPSS; Foa, Johnson, Feeny, & Tread-
well, 2001). The CPSS is a 17-item self-report measure designed
to tap each of the three symptom clusters of PTSD accord-
ing to the Diagnostic and Statistical Manual of Mental Disorders
(4th ed.; DSM-IV; American Psychiatric Association, 1994)—
reexperiencing, avoidance/numbing, and hyperarousal—in
children/youth from ages 8–18 years. In this sample, two of the
CPSS subscales (Numbing and Reexperiencing) had unaccept-
ably low Cronbach’s α(below .60) because of three problematic
items: two items from the Numbing subscale (Item 8: traumatic
episode-related memory problems, and Item 12: having a sense of a
foreshortened future), and one item from the Reexperiencing sub-
scale (Item 4: emotional reactivity to triggers). We did not include
these items in our subscale totals. Research on PTSD has identi-
fied these two numbing items as problematic (King et al., 1998).
Thus, it is not unusual for some researchers to also drop these
items from their studies (Palyo, Clapp, Beck, Grant, & Marques,
2008). Furthermore, we felt it was justified to drop the reexperi-
encing item because its low internal consistency can be interpreted
within the context of other findings that suggest that First Na-
tions people are more likely to experience their anxiety somatically
than emotionally (Barker-Collo, 1999). Thus, our four subscales
were as follows: Reexperiencing (four items; e.g., nightmares; α=
.72), Hyperarousal (five items; e.g., exaggerated startle response;
α=.63), Avoidance (two items; e.g., avoiding thinking about
Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.
Mediating Effect of Posttraumatic Stress Hyperarousal Symptoms 569
the trauma; α=.71), and Emotional Numbing (three items; e.g.,
feeling emotionally numb; α=.73).
The 20-item Centre for Epidemiological Studies Depression
Scale (CESD; Radloff, 1977) was used to measure depressive
symptoms. The CESD has been used previously with adolescents
(Radloff, 1991). Summing all items yields one overall score ranging
from 20 to 80 that reflects depressive symptom severity (present
sample α=.84). This scale has been well-validated in differ-
ent samples of Aboriginal adolescents (Manson, Ackerson, Dick,
Bar´
on, & Fleming, 1990; Thrane, Witbeck, Hoyt, & Shelley,
2004).
Evidence suggests measuring the problems that arise as di-
rect consequences of alcohol consumption is a good indicator
of alcohol-use disorders in youth (White & Labouvie, 1989);
therefore, the Rutgers Alcohol Problem Index (RAPI; White &
Labouvie, 1989) was used to measure alcohol misuse. The RAPI is a
well-validated 23-item self-report measure that assesses adolescent
problem drinking symptoms. It has been validated in community,
clinical, and First Nations samples (Noel et al., 2010; White &
Labouvie, 1989; Winters, 1999). Responses were summed across
the 23 items (α=.97), as recommended by the authors of the
RAPI, to yield a composite score that takes problem frequency into
account (cf. Winters, 1999). Forty percent of the participants re-
ported not drinking and were given a score of zero for this measure.
Analysis
Path analysis was conducted with AMOS 7.0 (Arbuckle, 2006).
Goodness-of-fit of structural models was evaluated via multiple
indices. Adequate fit is indicated by a chi-square-to-degrees of free-
dom ratio (χ2/df ) around 2, an incremental fit index (IFI) and a
comparative fit index (CFI) around .95, and a root-mean-square
error of approximation (RMSEA) around .08 (Kline, 2005). The
RMSEA values are reported with 95% confidence intervals (95%
CIs). Given concerns about multivariate nonnormality in our data,
we used bootstrapping to address the possible effect of multivariate
nonnormality in our path models (Schumacker & Lomax, 2010).
All paths in each of the four path models examining the poten-
tial mediating role of the PTS symptom clusters were reexamined
using bootstrapping procedures. Paths generated using bootstrap-
ping were virtually identical to the results shown in Figure 1 and
summarized in text, suggesting multivariate nonnormality had lit-
tle or no influence on the results. Bootstrapping estimates are not
presented in the main text because such estimates are excessively
strict if significant deviations from multivariate normality are not
present (Nevitt & Hancock, 2001). In sum, bootstrapping proce-
dures suggested the results were not unduly influenced by possible
deviations from multivariate normality.
Mallinckrodt, Abraham, Wei, and Russell (2006) assert that
a significant indirect effect suggests mediation has occurred. The
significance levels of all indirect effects were tested using random
sampling with replacement to generate 20,000 (n=166) boot-
strap samples. Bootstrapping allowed us to estimate bias-corrected
standard errors for our indirect effects. Confidence intervals were
also calculated, and indirect effects were considered significant
(p<.05) if the 95% CI for these indirect effects did not contain
zero.
RESULTS
With respect to EV, based on the CEVQ’s more stringent defi-
nitions of physical and sexual abuse (Walsh et al., 2008), 47%
of the sample reported physical abuse, 34.3% of the sample re-
ported sexual abuse, and 57.8% of the sample reported either
physical or sexual abuse. Exposure to violence was moderately cor-
related with all four PTS symptoms, depressive symptoms, and
alcohol misuse (see Table 1 for correlations, means, and stan-
dard deviations). Furthermore, both depressive symptoms and all
four PTS symptoms were correlated with alcohol misuse. Age
correlated with EV, PTS hyperarousal, PTS avoidance and al-
cohol misuse, and gender correlated with PTS reexperiencing and
Tab l e 1. Bivariate Correlations Among Variables, Means, and Standard Deviations
Variables MSD1234567 8 9
1. EV 14.38 13.15 – .41∗∗∗ .47∗∗∗ .44∗∗∗ .45∗∗∗ .42∗∗∗ .18* .11 .41∗∗∗
2. PTS Hyperarousal 5.27 3.35 .52∗∗∗ .44∗∗∗ .59∗∗∗ .62∗∗∗ .16* .12 .49∗∗∗
3. PTS Reexperiencing 2.67 2.49 .63∗∗∗ .59∗∗∗ .56∗∗∗ .10 .21** .31∗∗∗
4. PTS Avoidance 1.75 1.79 .57∗∗∗ .47∗∗∗ .17* .11 .25∗∗∗
5. PTS Numbing 2.42 2.42 .70∗∗∗ .07 .11 .33∗∗∗
6. Depressive Symptoms 19.07 19.89 .06 .22** .45∗∗∗
7. Age 16.69 1.39 .13 .26∗∗∗
8. Gender .03
9. Alcohol Misuse 9.65 11.06
Note.N=166 with 91 males and 75 females. EV =Exposure to violence; PTS =posttraumatic stress.
p<.05. ∗∗ p<.01. ∗∗∗ p<.001.
Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.
570 Zahradnik et al.
Tab l e 2. Model Fit Indices for Structural Models Testing the Indirect Effects of Exposure to Violence on Alcohol Misuse
Through PTS Symptoms
Structural models χ2χ2/df IFI CFI RMSEA 95% CI
Hyperarousal 15.25 2.18 .96 .96 .09 [0.00, 0.15]
Reexperiencing 14.43 2.06 .96 .96 .08 [0.00, 0.15]
Avoidance 14.85 2.12 .95 .95 .08 [0.00, 0.15]
Numbing 13.80 1.97 .97 .97 .08 [0.00, 0.15]
Note. PTS =Posttraumatic stress; IFI =incremental fit index; CFI =comparative fit index; RMSEA =root-mean-square error of approximation; CI =confidence interval.
depressive symptoms. To account for their potential influence, age,
gender, and depressive symptoms were included as covariates in all
structural models involving PTS symptom clusters as potential
mediators.
Fit indices for path models appear in Table 2. All four models
fit the data reasonably well. However, when controlling for the ef-
fects of depressive symptoms in each of the four models, only one
of the models, the PTS hyperarousal model, resulted in a signifi-
cant relationship between the potential mediator and the outcome
variable (β=.27,p=.06; see Figure 1). For each of the other
three models there were no significant relationships between the
PTS symptom cluster and alcohol misuse once depressive symp-
toms were controlled for: reexperiencing (β=−.02,p=.85),
avoidance (β=−.06, p=.17), and numbing (β=−.04,p=
.681). In contrast, the pathways from depressive symptoms to al-
cohol misuse were significant in these models (βs=.35, .36, and
.37, respectively). Consequently, only the indirect effect of EV
on alcohol misuse through PTS hyperarousal was significant (see
Table 3.
In summary, all four of the PTS symptom cluster models ade-
quately fit the data. As hypothesized, PTS hyperarousal symptoms
involved a significant indirect effect; however, indirect effects were
not observed for the three other PTS symptom cluster models.
DISCUSSION
Although prior studies have examined the role of PTSD as a me-
diating variable between some form of EV and alcohol misuse
(Epstein et al., 1998; White & Widom, 2008; Zlotnick et al.,
2006), this is the first study of which we are aware to examine the
contribution of specific PTS symptom dimensions while control-
ling for depressive symptoms, which are known to be related to all
three aforementioned variables (Kilpatrick et al., 2003). It is also
the first study we know of to provide support for the PTS-specific
self-medication hypothesis by demonstrating mediation in a sam-
ple of Mi’kmaq (First Nation) adolescents. Our findings supported
an indirect relationship of EV to alcohol misuse through PTS hy-
perarousal symptoms, but not any of the other PTS symptoms.
That hyperarousal symptoms fully mediated the relation be-
tween EV and alcohol misuse is consistent with research linking
PTSD hyperarousal symptoms to alcohol misuse (McFall et al.,
1992, Simons et al., 2005, Stewart et al., 1999). With respect
to the other PTS symptoms, although at the univariate level of
analysis these symptom clusters were related to alcohol misuse,
contrary to our hypothesis, they did not explain the relationship
between EV and alcohol misuse after controlling for the influence
of depressive symptoms. Although these null results were contrary
Tab l e 3. Bootstrap Analyses for Indirect Effects of PTS Symptoms Between Exposure to Violence and Alcohol Misuse
Bootstrap estimates
SE for 95% CI for
Hypothesized Unstandardized Standardized standardized standardized
indirect indirect indirect indirect indirect effect
effect effect effect effect (lower, upper)
PTS hyperarousal .042 .051 .028 [0.010, 0.126]
PTS reexperiencing .004 .004 .031 [0.075, 0.051]
PTS avoidance .014 .017 .027 [0.075, 0.034]
PTS numbing .007 .008 .021 [0.057, 0.030]
Note.PTS=Posttraumatic stress; CI =confidence interval; SE =bias-corrected standard error.
Confidence intervals excluding zero are significant (i.e., p<.05).
Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.
Mediating Effect of Posttraumatic Stress Hyperarousal Symptoms 571
to our hypothesis, we note not all studies examining the relation-
ships between the PTSD symptoms and alcohol misuse report a
significant univariate relationship (Stewart et al., 1999), let alone
a multivariate one. Alternatively, other PTS symptoms, like reex-
periencing symptoms, might better explain why EV can lead to
misuse of drugs other than alcohol (McFall et al., 1992). Thus,
future research might also use illicit drug use and/or misuse of pre-
scription medications as outcomes, but researchers are cautioned
not to group arousal-enhancing and arousal-dampening drugs to-
gether as mediation findings may be specific to arousal-dampening
drugs (Stewart & Conrod, 2008).
The results of our study are consistent with other research in
this area. For example, our sample had comparable but higher rates
of abuse to a large community-based study of high risk adolescents
that examined the impact of abuse before age 10 on subsequent
drinking, and found that abuse increased the risk of ever using al-
cohol, preteen-first-age alcoholic drink, and binge drinking (Ham-
burger, Leeb, & Swahn, 2008). This study also makes several novel
contributions. Our study is the first we know to examine the me-
diating effects of specific PTS symptom clusters, as opposed to
examining the PTS construct as a whole (Prigerson et al., 2002;
Ullman et al., 2005; White & Widom, 2008; Zlotnick et al.,
2006). Furthermore, we show that even when controlling for the
role of depressive symptoms—a construct with strong associations
to alcohol misuse—PTS hyperarousal symptoms better explain
the link between EV and alcohol misuse. In other words, those
youth with a history of EV were more likely to misuse alcohol in
relation to their hyperarousal symptoms (i.e., perhaps to dampen
these symptoms) regardless of whether or not they would meet all
the necessary criteria for a diagnosis of PTSD. Our results are also
consistent with the theory of mutual maintenance in which bouts
of alcohol consumption, used to dampen hyperarousal symptoms,
can actually, by way of alcohol withdrawal, increase the severity of
these very symptoms (Jacobsen et al., 2001); however, our design
cannot make causal assertions.
Our study found support for mediation effects of PTS symp-
toms in a sample of adolescents, and it is rare to examine this
question in a First Nations community. This is important because
it is common for First Nations’ communities, and North Ameri-
can Aboriginal communities more generally, given their history of
colonization and cultural discontinuity (Kirmayer, Brass, & Tait,
2000), to be struggling with a variety of social issues (e.g., suicide,
fetal alcohol syndrome, community violence, and child maltreat-
ment) that are related to problematic alcohol use.
The results of this study might be of interest to Aboriginal com-
munities looking to better understand a specific pathway that can
lead to problematic alcohol use in their youth. The results of this
study, however, must be understood and interpreted within the
greater socioeconomic determinants of problematic alcohol use in
Aboriginal communities, determinants that include poverty, un-
employment, poor health, low educational levels, and low or absent
community economic development (Health Canada, 1998).
A limitation of our study was that it was a school-based study
that used a nonrandom sample. Consequently, the sample is not
representative of the whole community and may not generalize
to those youth who are not enrolled in school, and who may
be dealing with more severe sequelae of EV. Another important
caveat is that this study relied on a cross-sectional design. Thus,
inferences made about mediation and causation, given the lack
of information about temporal sequencing, are not dispositive.
This being said, most empirical evidence suggests trauma and PTS
symptoms precede alcohol misuse in the majority of comorbid
cases (Bremner, Southwick, Darnell, & Charney, 1996; Chilcoat
& Menard, 2003). Also of note, stressful life events are common
in many First Nations communities (e.g., youth suicides or motor
vehicle accidents). Thus, the expression of PTS symptoms as they
were captured in this study may not be solely attributable to EV.
Although face-to-face interviews are an ideal way to disentangle
the chronologies of multiple traumas as they relate to the devel-
opment of PTS, our use of anonymous self-report measures made
this impossible. Furthermore, our sample size precluded us from
examining the models with pure cases of one form of abuse (e.g.,
sexual abuse alone); however, two separate studies have now con-
firmed that the relationship to alcohol use from both childhood
sexual abuse (Epstein et al., 1998) and physical abuse (Zlotnick
et al., 2006) is mediated by PTSD. Our sample size also limited our
ability to examine all four PTS symptoms and covariates simulta-
neously within the same path model. Given the strong relationship
between these four variables, such an analysis is recommended in
the future.
Another limitation is that we measured depressive symptoms
with the CES-D, which some argue is better conceived of as a
measure of general distress, given research showing the CES-D
measures anxious in addition to depressive symptoms (Fechner-
Bates, Coyne, & Schwenk, 1994). Thus, future inquiries into this
topic might use a purer measure of depressive symptoms. Also of
note, White and Widom (2008) suggest that stressful life events,
and not PTSD symptoms, fully mediate the relationship between
early abuse/neglect and subsequent alcohol problems. Thus, fu-
ture studies should examine the interplay between factors that
contribute to stressful life events (e.g., chaotic interpersonal rela-
tionships at home) and PTS symptoms. We were also not able to
control for parental alcohol use, a variable that is strongly related
to problematic drinking in adolescents (Shin, Edwards, & Heeren,
2009). The literature on adolescent misuse of alcohol, however,
also suggests childhood maltreatment is related to adolescent prob-
lem drinking even after controlling for parental alcoholism (Harter,
2000; Shin et al., 2009).
Finally, our study did not directly measure motivations to con-
sume alcohol, and measuring explicit motivation is important
because drinking to cope (Cooper, 1994) is strongly related to
PTSD and alcohol misuse (Dixon, Leen-Feldner, Ham, Faldner,
Lewis, & 2009; Kaysen et al., 2007). Measuring a construct like
drinking motives could provide more direct evidence of intentional
Journal of Traumatic Stress DOI 10.1002/jts. Published on behalf of the International Society for Traumatic Stress Studies.
572 Zahradnik et al.
self-medication, particularly because self-medication is a dynamic
process and researchers are only beginning to analyze the fluc-
tuating interplay between both sets of symptoms across time
(Ouimette, Read, Wade, & Tirone, 2010). Ultimately then, future
studies would be strengthened by using a prospective design with a
direct measure of drinking motives, and with a sample large enough
to evaluate all symptoms simultaneously, and to explore the model
for both genders and specific types of abuse, while controlling for
parental alcohol consumption and the potential mediating role of
stressful life events.
The results nonetheless have important clinical implications.
For individuals with both PTS hyperarousal symptoms and
alcohol-use problems, clinicians should give consideration to
whether or not a trauma-specific therapy that reduces hyperarousal
symptoms should be used as an adjunct to treatment for the alco-
hol misuse. A treatment like imaginal exposure therapy might be
useful because it has been demonstrated to decrease all three DSM-
IV symptom domains (Robertson, Humphreys, & Ray, 2004).
In keeping with best practice guidelines, individuals who meet
the diagnostic criteria for both PTSD and an alcohol-use dis-
order should receive an integrated treatment approach (Health
Canada, Centre for Addiction and Mental Health, 2002) that tar-
gets the functional relationship between both disorders (Zahradnik
& Stewart, 2008). An integrated treatment approach to treating
PTSD-alcohol use comorbidity is important given that unremitted
PTSD is implicated in deleterious substance use disorder outcomes
(Read et al., 2004). As such, treatments that only focus on the
alcohol/substance use disorder and not the PTSD symptoms will
likely be less effective in the long term. Therefore, individuals with
both disorders will likely benefit from services in which mental
health and addiction services are working together.
Overall, this study offers support for a more specific version
of the trauma-PTS/PTSD-alcohol self-medication model by high-
lighting the importance of hyperarousal symptoms. After control-
ling for age, gender, and depressive symptoms, our results suggest
that for these Mi’kmaq adolescents, it is hyperarousal symptoms,
and hyperarousal symptoms alone, that explain the relationship
between EV and alcohol misuse. Thus, future research in this area
should consider the role of specific PTSD symptom clusters, and
not just the construct of PTSD as a whole.
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  • ... Indeed, PTSD is often seen as a disorder of chronic emotion dysregulation in which the individual fluctuates between intense hyperaroused states and emotional numbing/dissociation (). Symptoms of hyperarousal may contribute to increased anger, hostility, violent or aggressive behaviors toward self and others (Barrett, Teesson, & Mills, 2014), and substance abuse (Zahradnik, Stewart, Sherry, Stevens, & Wekerle, 2011), all of which may increase one's risk for contact with the criminal justice system. In a compounding manner, acute substance use may exacerbate psychological symptoms and disinhibit behavioral controls, leading to an increased likelihood of antisocial behavior and violence (Ogloff, Talevski, Lemphers, Wood, & Simmons, 2015). ...
    ... In this sample, exposure to increasing numbers of traumas contributed to greater odds of arrest, as much as 62% for each additional trauma exposure. Cumulative trauma exposure is associated with a wide range of psychological reactions including PTSD (Breslau, 2009), SUD (Khantzian, 1997; Mills et al., 2006; Stewart et al., 1998), depression (Breslau, 2009), and a multitude of associated deficits in emotional and interpersonal regulation (Barrett et al., 2014; Calhoun et al., 2005; Weiss et al., 2012; Zahradnik et al., 2011), which collectively may contribute to behaviors that confer greater risk for criminal justice involvement. Agnew and colleagues proposed that traumas are strain inducing because of their high intensity and the perceived injustice of the acts (Agnew, 2006Agnew, , 2012 Hay & Evans, 2006). ...
    ... Indeed, key symptoms of PTSD such as hyperarousal, hypervigilance, and emotional numbing/dissociation may all contribute to criminal behaviors placing one at risk for criminal justice involvement (). For example, the hyperarousal symptoms of PTSD may contribute to increased anger, hostility, violent or aggressive behaviors toward self and others (Barrett et al., 2014), and substance abuse (Zahradnik et al., 2011), all of which may increase one's risk for contact with the criminal justice involvement. In a sample of 241 veterans with chronic PTSD, Calhoun and colleagues (2005) found that veterans who had been arrested at least once had higher levels of depression and hostility, were more violent and more likely to use illicit substances, and had difficulty maintaining relationships than veterans who had not been arrested at all. ...
  • ... However, other studies suggest that hyperarousal symptoms are related to AUD, ND or measures of alcohol and nicotine use in addition or instead of emotional numbing symptoms . This could be shown particularly for the risk of alcohol use (Zahradnik, Stewart, Sherry, Stevens, & Wekerle, 2011) without, and for alcohol use problems (Taft et al., 2007) and ND (Greenberg et al., 2012) with consideration of other symptom clusters. This finding is often explained by a relieving effect of alcohol and nicotine use on tension, anxiety and stress (Beckham et al., 1997Beckham et al., , 2008 Bradford, Shapiro, & Curtin, 2013) which could make subjects with hyperarousal symptoms more vulnerable to AUD and ND. ...
    ... Only one of the abovementioned studies on the relation between PTSD symptom clusters fully controlled for Axis-I comorbidity (Greenberg et al., 2012). Other studies only controlled for depression (Cook et al., 2009; Joseph et al., 2012; Weaver & Etzel, 2003; Zahradnik et al., 2011) or did not consider comorbidity at all (Baschnagel et al., 2008; Kirby et al., 2008; Pietrzak et al., 2010; Taft et al., 2007). As these studies have been conducted in different samples with varying probabilities of comorbid disorders (e.g. ...
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