CILR

Co-Occurring Posttraumatic Stress and Substance Use: Emerging Research on Correlates, Mechanisms, and Treatments—Introduction to the

Special Issue

Anka A. Vujanovic University of Houston

Marcel O. Bonn-Miller VA Palo Alto Health Care System, Palo Alto, California, and

University of Pennsylvania Perelman School of Medicine

Nancy M. Petry University of Connecticut Health Center

Posttraumatic stress disorder (PTSD) and substance use disorders (SUD) are complex psychiatric conditions that commonly co-occur. Despite the well-established prevalence of this diagnostic comor- bidity, much less is known about underlying etiological and maintenance processes or most effective treatment avenues. The comorbidity is complex, difficult to treat, and marked by a more costly and chronic clinical course, when compared with either disorder alone. Therefore, this Special Issue is devoted to highlighting recent, theory-driven, scientifically rigorous, and clinically applicable advances in our understanding of the PTSD-SUD comorbidity across various populations. Emerging psychological science on PTSD-SUD is profiled, and biological, psychological, and social processes implicated in etiology and maintenance are highlighted along with promising innovations in treatment. The articles range in methodology from more basic to applied, exemplifying a translational spectrum of research as each article presents meaningful clinical implications and future research directions. This introductory article describes the articles in this Special Issue and how they can inform the field.

Keywords: addiction, posttraumatic stress, PTSD, substance use, trauma

Posttraumatic stress disorder (PTSD) and substance use disor- ders (SUD) are complex psychiatric conditions that commonly co-occur (e.g., McCauley, Killeen, Gros, Brady, & Back, 2012), presenting enormous suffering to those affected and an immense challenge to clinical scientists and practitioners. Indeed, rates of trauma exposure among adults with SUD are estimated to be as high as 95% (e.g., Dansky, Saladin, Brady, Kilpatrick, & Resnick, 1995; Reynolds et al., 2005), depending on the substance class studied. Following, among individuals with SUD, the prevalence of lifetime PTSD is estimated to be between 26 and 52%, while the

prevalence of current PTSD is estimated to be 15% to 42% (Dragan & Lis-Turlejska, 2007; Driessen et al., 2008; Mills, Tees- son, Ross, & Peters, 2006; Reynolds, Hinchliffe, Asamoah, & Kouimtsidis, 2011; Reynolds et al., 2005; Schäfer et al., 2010). Conversely, among individuals with PTSD, the prevalence of co-occurring SUD, including alcohol use disorder (AUD), is esti- mated to be between 36% and 52%, substantially higher than general population rates (Mills et al., 2006; Pietrzak, Goldstein, Southwick, & Grant, 2011).

The development of a deeper understanding of this comorbidity is critical, as the co-occurrence of PTSD and SUD presents a severe clinical and public health concern. The comorbidity is complex, difficult-to-treat, and marked by a more costly and chronic clinical course, when compared to either disorder alone (e.g., McCauley et al., 2012; Mills et al., 2006; Schäfer & Najavits, 2007). People with PTSD-SUD comorbidity, relative to those with just one of these conditions, demonstrate worse treatment out- comes, less improvement during treatment, more legal problems, increased risk for experiencing violence, poorer social functioning, more severe physical health problems, and higher rates of suicide attempts (e.g., Foa & Williams, 2010; McCauley et al., 2012). Moreover, PTSD, including subclinical PTSD symptomatology (e.g., Norman, Tate, Anderson, & Brown, 2007), is predictive of stronger drug cravings (Coffey et al., 2002; Saladin et al., 2003) and withdrawal symptoms (Boden, Babson, Vujanovic, Short, & Bonn-Miller, 2013) as well as a greater tendency to use substances to alleviate negative mood states (e.g., Back, Brady, Jaanimägi, &

Editor’s Note. This is an introduction to the special issue “Co-Occurring Posttraumatic Stress and Substance Use: Emerging Research on Correlates, Mechanisms, and Treatments.” Please see the Table of Contents here: http://psycnet.apa.org/journals/adb/30/7.—NMP

This article was published Online First October 27, 2016. Anka A. Vujanovic, Department of Psychology, University of Houston;

Marcel O. Bonn-Miller, Center of Excellence in Substance Abuse Treat- ment and Education, VA Palo Alto Health Care System, Palo Alto, Cali- fornia, and Department of Psychiatry, University of Pennsylvania Perel- man School of Medicine; Nancy M. Petry, Department of Psychiatry, University of Connecticut Health Center.

Correspondence concerning this article should be addressed to Anka A. Vujanovic, Trauma and Stress Studies Center, University of Houston, 3695 Cullen Boulevard, 126 Heyne Building, Houston, TX 77204. E-mail: [email protected]

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Psychology of Addictive Behaviors © 2016 American Psychological Association 2016, Vol. 30, No. 7, 713–719 0893-164X/16/$12.00 http://dx.doi.org/10.1037/adb0000222

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Jackson, 2006; Chilcoat & Breslau, 1998; Jacobsen, Southwick, & Kosten, 2001).

However, the majority of patients with PTSD and SUD only receive SUD treatment (Najavits, Sullivan, Schmitz, Weiss, & Lee, 2004; Young, Rosen, & Finney, 2005), contrary to most patients’ preferences (Back, Brady, Jackson, Salstrom, & Zinzow, 2005; Brown, Stout, & Gannon-Rowley, 1998; R. A. Brown et al., 1998). In addition, adults in treatment for SUD are commonly not even assessed for PTSD or offered trauma-informed interventions, and vice versa (e.g., Bujarski et al., 2016; Mills et al., 2006; Reynolds et al., 2005). To date, there is no consensus regarding ‘best practice guidelines,’ and most treatment-seeking individuals with PTSD- SUD are passed between PTSD and SUD treatment services with little care coordination (Roberts, Roberts, Jones, & Bisson, 2015). Based on recent meta-analytic evidence, there is promise in the preliminary efficacy of individualized integrated trauma-focused therapy plus evidence-based SUD interventions (Roberts et al., 2015), but effect sizes are small, and trials are plagued by high rates of attrition attributable—at least in part—to the high levels of avoidance, distress, and functional impairment inherent to these populations (e.g., Miles, Smith, Maieritsch, & Ahearn, 2015; Sza- franski, Gros, Menefee, Wanner, & Norton, 2014). Thus, more innovative and creative treatment solutions are imperative.

In an effort to improve upon the prevention and treatment of PTSD-SUD, empirical work has increasingly focused on underly- ing factors that contribute to their joint etiology and maintenance. At least three basic etiological pathways have been established (Stewart & Conrod, 2003): (a) individuals with PTSD develop SUD in the aftermath of trauma as an attempt to self-medicate the painful and intense emotionality associated with PTSD (‘self- medication model’; Khantzian, 1999; Reed, Anthony, & Breslau, 2007); (b) individuals with SUD, by virtue of lifestyles that inher- ently place them at increased risk of violence and harm, are at increased risk of experiencing trauma and subsequently develop- ing PTSD (‘high-risk hypothesis’; e.g., Acierno, Resnick, Kilpat- rick, Saunders, & Best, 1999; Bonin, Norton, Asmundson, Dicur- zio, & Pidlubney, 2000; Chilcoat & Breslau, 1998; Kaysen, Neighbors, Martell, Fossos, & Larimer, 2006; North et al., 1999); (c) the disorders develop concurrently, in the aftermath of trauma, attributable to common underlying biopsychosocial processes (‘shared liability model’; e.g., Breslau, Davis, Andreski, Peterson, & Schultz, 1997; Cottler et al., 2011; Fassino et al., 2004; Krueger & Markon, 2006; Wolf et al., 2010); and (d) individuals with SUD tend to experience increased anxiety and arousal secondary to chronic substance use (e.g., withdrawal symptoms), and this arousal coupled with poor coping, may increase risk for develop- ing PTSD in the aftermath of trauma (‘susceptibility model’; e.g., Jacobsen et al., 2001; Sharkansky, Brief, Peirce, Meehan, & Man- nix, 1999; Stewart, Conrod, Samoluk, Pihl, & Dongier, 2000). The self-medication pathway is perhaps the most well-known, well- supported, and well-studied (e.g., Coffey et al., 2002; O’Hare & Sherrer, 2011; Saladin et al., 2003; Simpson, Stappenbeck, Varra, Moore, & Kaysen, 2012; Waldrop, Back, Verduin, & Brady, 2007). However, the extant literature leaves many questions un- answered about biological, cognitive-affective, or social factors or processes influencing proclivity toward self-medication or the complex interplay of factors increasing vulnerability for and main- taining PTSD-SUD comorbidity, more generally. Furthermore, it should be noted that once both conditions (PTSD and SUD)

manifest, they may influence each other over time. For example, some studies have observed and suggested a gradient of effect, whereby when one condition improves or worsens, the other conditions follows suit (Back, Brady, Jaanimägi, et al., 2006; Back, Brady, Sonne, & Verduin, 2006; Brown, Stout, & Gannon- Rowley, 1998; Coffey, Schumacher, Brady, & Cotton, 2007; Kev- orkian et al., 2015; Simpson et al., 2012). Other studies suggest that PTSD symptomatology typically is not influenced by changes in substance use (e.g., Back, Brady, Sonne, et al., 2006), whereas substance use is impacted by changes in PTSD symptoms (Hien et al., 2010). Thus, a solid understanding of disorder comaintenance is of utmost importance to successful treatment efforts.

Special Issue Aims

This Special Issue is focused on highlighting recent, scientifi- cally rigorous, clinically applicable advances in our understanding of the PTSD-SUD comorbidity across various populations, includ- ing military veterans, college students, community-recruited adults, and adults in residential treatment for SUD. The Special Issue profiles emerging theory-driven science on PTSD-SUD spe- cifically with regard to the biological, psychological, and social processes implicated in etiology and maintenance as well as prom- ising innovations in treatment approach. Featured topics include the neural correlates of PTSD and SUD, the role of substance use motives in the perpetuation of PTSD-SUD comorbidity, associa- tions of social support with PTSD and SUD, correlates of help- seeking and self-medication in trauma-exposed adults, and a novel treatment approach for PTSD-SUD. The seven articles comprising this Special Issue thus provide an excellent overview of the current state of the field and begin to offer answers to some of the important questions that will ultimately move this field forward and closer to effective treatment and prevention programs. Studies range from more basic to applied, underscoring the translational framework that is necessary for the development and refinement of effective prevention and intervention strategies.

Special Issue Articles

Neurocognitive Correlates

This Special Issue begins with a human neuroimaging study by Simons and colleagues (p. 720) that aimed to understand under- lying neural mechanisms involved in the maintenance of PTSD- AUD comorbidity. One hundred recent military veterans were presented with masked fearful or happy faces, followed by an emotional Stroop task with negative, neutral, and combat-relevant words, while inside a functional MRI (fMRI) scanner. Because of their centrality to emotional processing, particularly in terms of fear and anxiety, responding in three primary areas of the brain was of interest: the dorsal anterior cingulate cortex (ACC), the rostral ACC, and the amygdala. Though differential reactivity was not observed in response to the masked faces task, evidence from the Stroop task supported a gradient effect, where greater severity of combat exposure was associated with hyper-activation in the dorsal and rostral ACC in response to combat-relevant Stroop words. Conversely, predeployment drinking was associated with hypo-reactivity in the dorsal ACC. These findings combine to highlight the dorsal ACC as a mechanism that may explain why

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alcohol is used as a coping strategy by individuals with PTSD: it may decrease hyper-activation of the dorsal ACC resulting from PTSD reexperiencing symptoms. Though other substances may serve to dampen the effects of PTSD through alternative mecha- nisms (e.g., endocannabinoid receptors; Neumeister, Seidel, Ra- gen, & Pietrzak, 2015), this study identifies a potential pathway for the development and maintenance of AUD among those with PTSD. Future work would benefit from replicating these findings within the context of prospective designs.

Complementary to the work of Simons and colleagues, Gorka and colleagues (pp. 720, 733) in this Special Issue examined the impact of PTSD-AUD on defensive reactivity, or aversive re- sponding to trauma and non-trauma-related stimuli (e.g., Fani et al., 2012; Shin et al., 2004). Because individuals with PTSD tend to respond with greater defensive reactivity, those with PTSD and AUD may be especially prone to defensive reactivity because of their tendency to use alcohol to avoid negative emotional states and dampen defensive reactivity (e.g., Baker, Piper, McCarthy, Majeskie, & Fiore, 2004; Yeater, Austin, Green, & Smith, 2010). Thus, Gorka et al. examined the impact of PTSD-AUD, as com- pared with PTSD without AUD and control participants (absence of PTSD and/or SUD), on defensive reactivity in 66 military veterans. Participants completed a flanker task. Those with PTSD- without AUD had significantly larger error related negativity (ERN), an event-related component that reflects defensive reactiv- ity to errors, as compared with those with PTSD without AUD. Neither the PTSD-AUD nor PTSD-without AUD groups differed significantly from the control group, indicating that defensive reactivity to errors does not distinguish between PTSD and non- PTSD groups. Results suggest that PTSD-AUD might represent a neurobiologically unique subtype of PTSD, and the presence of AUD might exacerbate defensive reactivity to errors in those with PTSD. Because defensive reactivity is conceptualized as a leading factor underlying PTSD and AUD comorbidity and a potential treatment target, future studies are necessary to disentangle tem- poral relations among these variables. Defensive reactivity may be a risk factor for onset of AUD, an artifact of chronic PTSD and alcohol use, or both. Furthermore, studies are needed to examine how individual differences in responding to perceived threat may correlate with neurobiological mechanisms to contribute to the etiology and maintenance of PTSD-SUD.

Substance Use Motives

Two articles in this Special Issue examine substance use mo- tives in PTSD-SUD. Indeed, the advancement of our understand- ing of individuals’ motivations for substance use can illuminate risk and maintenance pathways for this comorbidity and inform treatment developments. First, Metrik et al. (p. 743) examined the mediating roles of coping with negative affect, situational anxiety, and sleep, in the association between PTSD and major depressive disorder (MDD) and three cannabis use outcomes: (a) cannabis use frequency, (b) cannabis problems, and (c) cannabis use disorder (CUD). Participants were 301 U.S. military veterans. Whereas PTSD was significantly associated with only cannabis use and CUD, MDD was significantly associated with each of the three cannabis use outcomes. Both PTSD and MDD were associated with coping with negative affect, situational anxiety, and sleep. In separate single mediator models, there were significant indirect

effects of PTSD and MDD through each use motive on cannabis use frequency and CUD, and there was a significant indirect effect of MDD through each use motive on cannabis problems. In mul- tiple mediator models, sleep motives were the most robust signif- icant mediating factor underlying the relations between both PTSD and MDD with cannabis use and increased risk of CUD. These findings highlight the potential importance of incorporating sleep and coping interventions into PTSD-SUD interventions. More longitudinal and experimental studies are necessary to better un- derstand the temporal relations among these variables. Advancing our understanding of these complex relations can help to inform not only intervention efforts but also preventive interventions aimed at decreasing risk of developing PTSD or SUD following trauma.

Second, Berenz et al. (p. 755) explore the role of anxiety sensitivity, a cognitive factor defined as the fear of anxiety and related sensations (McNally, 2002), in the association between PTSD and alcohol use coping motives in 295 undergraduate stu- dents with histories of interpersonal trauma and current alcohol use; approximately 22.8% of participants screened positive for PTSD on the PTSD Checklist for Diagnostic and Statistical Man- ual of Mental Disorders, fifth edition (DSM–5; Blevins, Weathers, Davis, Witte, & Domino, 2015) and approximately half of partic- ipants scored within the range of (self-reported) moderate alcohol problems. The main effects of both anxiety sensitivity and PTSD symptom severity were significantly associated with greater alco- hol use coping motives, above and beyond covariates. In addition, anxiety sensitivity significantly moderated the association between PTSD symptom severity and alcohol use coping motives. Elevated PTSD symptoms were related to higher coping motives only among those individuals with high anxiety sensitivity. This study has important clinical implications for college student populations with interpersonal trauma histories and clinical or subclinical symptoms of PTSD, as PTSD symptoms following assault may increase motivation for coping-oriented alcohol use. Anxiety sen- sitivity is malleable via cognitive– behavioral intervention, and anxiety sensitivity reduction interventions might prevent problem- atic alcohol use in high-risk college student populations exposed to trauma. It is important for future work to examine the relations among anxiety sensitivity, PTSD symptomatology, and alcohol use longitudinally to better determine directionality of the ob- served relations. In addition, future work might focus upon testing the efficacy of either stand-alone or adjunctive anxiety sensitivity reduction interventions, provided alongside PTSD treatment, in decreasing the potential negative outcomes following interpersonal trauma.

Social Support, Help-Seeking, and Self-Medication

The protective effects of social support following trauma have been well-documented (e.g., Kilpatrick et al., 2007; Pietrzak, Goldstein, Malley, Rivers, & Southwick, 2010), and social support is related to better PTSD treatment outcomes (Price et al., 2013). In this Special Issue, Gros and colleagues (p. 764) extend prior literature to provide the first investigation of the associations of social support with PTSD and co-occurring SUD among a sample of 171 U.S. military veterans seeking treatment for PTSD-SUD. The majority of participants (76.5%) were diagnosed with PTSD and alcohol dependence (73.3%), and approximately 38.9% also

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715POSTTRAUMATIC STRESS AND SUBSTANCE

met criteria for current drug dependence. Higher levels of social support were associated with less severe PTSD symptomatology in veterans with PTSD-SUD. However, social support was positively associated with alcohol use, elucidating several explanatory path- ways: (a) the sample was comprised of a relatively younger sample of OEF/OIF/OND veterans, highlighting potential differences be- tween eras of service or contextual shifts in relations between alcohol use and social support over time; (b) because young adults are more likely to consume alcohol to enhance social enjoyment (Gruenewald, Remer, & LaScala, 2014), this sample of veterans may have been more likely to engage in drinking for social reward; and/or (c) measurement of social support in the literature is highly diverse, highlighting the importance of replication and extension of these findings with other social support measures and among more representative veteran samples. This line of inquiry has important clinical implications, because enhancement of social support via intervention could be incorporated into extant PTSD- SUD interventions to improve outcomes. Indeed, Gros et al. un- derscore the importance of considering social support in PTSD- SUD as not only a risk or protective factor for PTSD or SUD but also a potential intervention target to improve treatment outcomes and quality of life.

However, perhaps equally as important as informing the devel- opment and refinement of evidence-based treatments is better understanding correlates of help-seeking behaviors among relevant populations. In this Special Issue, Sheerin and colleagues (p. 771) investigated the correlates of help-seeking and self-medication in Norwegian adults with histories of trauma. The study presents a population-based sample of 2,794 individuals, of whom 307 adults endorsing at least one symptom of PTSD and were eligible. Help- seeking, defined as telling a medical doctor or other professional about problems that occurred as a result of the trauma, was endorsed at higher rates by adults with PTSD and lower rates in adults with alcohol use disorders (AUD). Self-medication, defined as the use of drugs or alcohol for trauma-related problems, was more likely to be endorsed by those with PTSD versus those without PTSD. PTSD was associated with a greater than fourfold increased likelihood of self-medication and twofold increased like- lihood of help-seeking (2.29), whereas AUD was associated with decreased likelihood of help-seeking. Indeed, approximately 50% of individuals with PTSD did not endorse help-seeking but a significant portion of those reported using substance to manage symptoms. This study provides an important step in understanding correlates of help-seeking and self-medication, while laying the groundwork for future work to investigate correlates of help- seeking and self-medication in adults with various types of trauma exposure to examine the role of socioeconomic disparities and/or racial/ethnic differences in help-seeking and self-medication. The overarching roles of experiential avoidance, guilt or shame, socio- cultural and contextual factors, such as financial strain and health care access, as well as mental health and substance use stigma on treatment-seeking and engagement as well as availability and use of substances for symptom management and cannot be underesti- mated.

Treatment Development

The literature on treatment for PTSD-SUD is lacking ‘best practice guidelines.’ Current research suggests trauma-focused

therapies plus evidence-based therapies for SUD have demon- strated the most efficacy. Results of a recent meta-analysis on PTSD-SUD treatments (Roberts et al., 2015), however, suggest small effect sizes and call for more treatment development re- search. In this Special Issue, Coffey and colleagues (p. 778) provide an illustrative example of evidence-based treatment devel- opment, as they report upon the results of a randomized controlled clinical trial (RCT), wherein they tested the efficacy of two ver- sions of prolonged exposure therapy (PE; Foa, Hembree, & Roth- baum, 2007), one of the leading evidence-based interventions for PTSD (Foa, Keane, Friedman, & Cohen, 2008), in combination with standard SUD treatment in a sample of 126 adults in a community residential SUD facility. The study included three treatment arms: (a) a modified version of prolonged exposure (mPE), (b) mPE administered after a 90-min trauma-focused mo- tivational enhancement session (mPE � MET � PTSD), and (c) a Healthy Lifestyles Sessions (HLS) control condition, comprising 9 to 12 sessions of health-related education. All treatment conditions were paired with 6 weeks of traditional, 12-Step residential SUD treatment programming. Results indicate that mPE yielded signif- icantly greater improvement in PTSD and depressive symptom- atology as well as greater clinically significant improvements in trauma symptoms and substance use outcomes, as compared with HLS. Individuals across conditions reported more than 85% days of abstinence at 6-month follow-up. However, no significant between-groups differences were found with regard to substance outcomes, including craving. This study adds to growing support for the use of PE in the treatment of PTSD-SUD, demonstrating the effectiveness and safety of mPE and the feasibility of offering PTSD and SUD treatments concurrently but with different thera- pists. However, Coffey et al. note lower completion rates in the mPE conditions (60 –62.2%), as compared with the HLS condition (87.8%), and the mPE � MET-PTSD condition did not enhance mPE retention, as compared with the mPE condition. These find- ings suggest that offering PE to individuals in residential SUD treatment has the potential to yield positive outcomes especially in the context of PTSD symptomology, but more work needs to be done to increase treatment completion and to better understand patients’ reasons for dropping out (e.g., symptom improvement or lack of tolerance for the treatment modality).

Conclusions

The seven articles featured in this Special Issue advance our understanding of the PTSD-SUD comorbidity both theoretically and methodologically. These articles showcase several innovative scientific approaches, including functional imaging, experimental paradigms, correlational designs, and RCTs, to studying this com- plex comorbidity. However, much more research is needed, par- ticularly longitudinal and experimental studies, to improve our understanding of temporal relations among variables of interest and the biological and genetic/epigenetic underpinnings of use motives, help-seeking, or treatment engagement and completion. More studies are needed on adolescents and adults, civilian and veteran populations, as well as socioeconomically and racially diverse individuals with various SUDs, including cannabis, co- caine, opioids, and amphetamines. Unanswered questions and un- explored topics abound. A theory-driven, methodologically rigor- ous approach is the best avenue to gaining knowledge on this

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complex, difficult-to-treat comorbidity, and only knowledge will be able to ameliorate the immeasurable suffering and burden endured by so many.

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Received August 29, 2016 Accepted August 30, 2016 �

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