Co-Occurring Disorders and Addiction


1. Describe and define co-occurring disorders.

2. Describe the evaluation process.

3. Identify mental disorders and when to refer for further evaluation

4. Identify and describe co-occurring treatment options.

Terms Associated with Substance Related Disorders

Substance Abuse, Substance Dependence, and Substance-Induced Disorders

The standard use of these terms derives from the DSM-IV-TR, within which substance-related disorders are divided into substance use disorders and substance-induced disorders. Substance use disorders are further divided into substance abuse and substance dependence.

There are 11 categories of substance use disorders (e.g., disorders related to alcohol, cannabis, cocaine, opioids, nicotine), which are separated by criteria into abuse and dependence. The term “substance abuse” has come to be used informally to refer to both abuse and dependence. By and large, the terms “substance dependence” and “addiction” have come to mean the same thing, though debate exists about the interchangeable use of these terms. Finally, the system of care for substance-related disorders is usually referred to as the substance abuse treatment system.

Substance-induced disorders are important to consider in a discussion of COD. Although they actually represent the direct result of substance use, their presentation can be clinically identical to other mental disorders. Therefore, individuals with substance-induced disorders must be included in COD planning and service delivery.

Terms Associated with Mental Disorders

The standard use of terms for non–substance-related mental disorders also derives from the DSM-IV-TR. These terms are used throughout the medical, social service, and behavioral health fields. The major relevant disorders for COD include schizophrenia and other psychotic disorders, mood disorders, anxiety disorders, and personality disorders (see Table 2). While several disorders listed in the DSM-IV-TR may (and frequently do) co-exist with COD, they are excluded from the definition of co-occurring disorders because other service sectors have traditionally been responsible for caring for persons with these disorders (e.g., developmentally disabled) or the qualities of the disorder are not typically responsive to behavioral health interventions (e.g., dementia). In these instances, the costs of providing care typically come from sources outside the behavioral health system. For example, the elderly person with Alzheimer’s dementia and alcohol abuse will typically have service authorized by medical care organizations, while the adolescent with developmental disability and cannabis abuse will have services financed through State disability monies.

Over the past few decades, practitioners and researchers increasingly have recognized the link between substance abuse and mental disorders. Research has provided a more in-depth understanding of co-occurring substance use and mental disorders—how common they are, the multiple problems they create, and the impact they have on treatment and treatment outcome. As knowledge of cooccurring disorders (COD) continues to evolve, new challenges arise: How do we treat specific populations such as the homeless and those in our criminal justice system? What is the role of housing? What about those with specific mental disorders such as posttraumatic stress disorder? Where is the best locus for treatment? Can we build an integrated system of care? The main purpose of this TIP is to provide addiction counselors and other practitioners with this state-of-the-art information on the rapidly advancing field of co-occurring substance use and mental disorders.

Following a discussion of the evolving field of co-occurring disorders, this chapter addresses the developments that led to this TIP. It then describes the scope of this TIP (both what is included and what is excluded by design), its intended audience, and the basic approach that has guided the selection of strategies, techniques, and models highlighted in the text. The organization of the TIP is laid out for the reader, with the components of each chapter and appendix described in an effort to help users of the TIP quickly locate subjects of immediate interest.

Major Relevant Categories of Mental Disorders for COD

Schizophrenia and other psychotic disorders

Mood disorders

Anxiety disorders

Somatoform disorders

Factitious disorders

Dissociative disorders

Sexual and gender identity disorders

Eating disorders

Sleep disorders

Impulse-control disorders

Adjustment disorders

Personality disorders

Distinctions Between Mental Disorders and Serious Mental Illnesses

Normal, and even exaggerated, responses to stressful experiences should not be confused with a diagnosable mental disorder. Only when intense emotions, thoughts, and/or behaviors occur over extended periods of time and result in impairment in functioning are they considered mental disorders. Nonetheless, clients with substance use disorders will seek services for severe or acute symptoms that do not meet diagnostic criteria for a mental disorder. Like persons with substance-induced disorders, these individuals must be included in COD planning and service delivery because their symptoms require screening, assessment, and treatment planning. Mental disorders are characterized by:

The nature and severity of symptoms

The duration of symptoms

The extent to which symptoms interfere with one’s ability to carry out daily routines, succeed at work or school, and form and keep meaningful interpersonal relationships

The Evolving Field of Co-Occurring Disorders

Today’s emphasis on the relationship between substance use and mental disorders dates to the late 1970s, when practitioners increasingly became aware of the implications of these disorders, when occurring together, for treatment outcomes. The association between depression and substance abuse was particularly striking and became the subject of several early studies (e.g., Woody and Blaine 1979). In the 1980s and 1990s, however, both the substance abuse and mental health communities found that a wide range of mental disorders were associated with substance abuse, not just depression (e.g., De Leon 1989; Pepper et al. 1981; Rounsaville et al. 1982b; Sciacca 1991). During this period, studies conducted in substance abuse programs typically reported that 50 to 75 percent of clients had some type of co-occurring mental disorder (although not usually a severe mental disorder) while studies in mental health settings reported that between 20 and 50 percent of their clients had a co-occurring substance use disorder. (See Sacks et al. 1997b for a summary of studies and Compton et al. 2000 for a more recent study.)

The multiple studies reflect the extent to which COD constitutes a clinical concern. At the same time, however, these studies varied in that they (1) were conducted in an array of settings and on a range of sample sizes from 68 to 20,291, (2) used different measures and criteria for determining a disorder, and (3) reported on different time periods (i.e., either lifetime or current, or both). This diversity in reporting can produce differing estimates and suggests a need to address the broad range of survey and analytic strategies used to generate estimates. Further work to clarify the type, severity, and clinical significance of cooccurring disorders can contribute to an improved understanding of the phenomenon and treatment. Nevertheless, it is important that, in spite of those differences, there is a consistency in reporting significant rates of disorder across all studies.

Researchers not only found a link between substance abuse and mental illness, they also found the dramatic impact the complicating presence of substance abuse may have on the course of treatment for mental illness. One study of 121 clients with psychoses found that those with substance abuse problems (36 percent) spent twice as many days in the hospital over the 2 years prior to treatment as clients without substance abuse problems (Crome 1999; Menezes et al. 1996). These clients often have poorer outcomes, such as higher rates of HIV infection, relapse, rehospitalization, depression, and suicide risk (Drake et al. 1998b; Office of the Surgeon General 1999).

Just as the field of treatment for substance use and mental disorders has evolved to become more precise, so too has the terminology used to describe people with both substance use and mental disorders. The term co-occurring disorders replaces the terms dual disorder or dual diagnosis. These latter terms, though used commonly to refer to the combination of substance use and mental disorders, are confusing in that they also refer to other combinations of disorders (such as mental disorders and mental retardation). Furthermore, the terms suggest that there are only two disorders occurring at the same time, when in fact there may be more. For purposes of this TIP, co-occurring disorders refers to co-occurring substance use (abuse or dependence) and mental disorders. Clients said to have co-occurring disorders have one or more disorders relating to the use of alcohol and/or other drugs of abuse as well as one or more mental disorders. A diagnosis of cooccurring disorders occurs when at least one disorder of each type can be established independent of the other and is not simply a cluster of symptoms resulting from the one disorder.

New models and strategies are receiving attention and encouraging treatment innovation (Anderson 1997; De Leon 1996; Miller 1994a; Minkoff 1989; National Advisory Council [NAC] 1997; Onken et al. 1997; Osher and Drake 1996). Reflecting the increased interest in issues surrounding effective treatment for this population, the American Society of Addiction Medicine (ASAM) added substantial new sections on clients with COD to an update of its patient placement criteria. These sections refine criteria both for placing clients with COD in treatment and for establishing and operating programs to provide services for such clients (ASAM 2001).

These efforts are slowly changing the way that the public, policymakers, and substance abuse counselors view mental illness. Still, stigma attached to mental illness remains. One topic worth mentioning is the public perception that people with mental illness are dangerous and pose a risk of violence. However, stu dies have shown that the public’s fear is greater than the actual risk, and that often, people with mental disorders are not particularly violent; it is when substance abuse is added that violence can ensue. For example, Steadman et al. (1998) found that substance abuse symptoms significantly raised the rate of violence in both individuals with mental illness and those without mental illness. This research adds support to the importance of treating both mental illness and substance abuse.

In recent years, dissemination of knowledge has been widespread. Numerous books and hundreds of articles have been published, from counseling manuals and instruction (Evans and Sullivan 2001; Pepper and Massaro 1995) to database analysis of linkage among treatment systems and payors (Coffey et al. 2001). Several annual “dual diagnosis” conferences emerged. One of the most longstanding is the annual conference on The Person With Mental Illness and Substance Abuse, hosted by MCP Hahnemann University (now Drexel University), which began in 1988.

In spite of these developments, individuals with substance use and mental disorders commonly appear at facilities that are not prepared to treat them. They may be treated for one disorder without consideration of the other disorder, often “bouncing” from one type of treatment to another as symptoms of one disorder or another become predominant. Sometimes they simply “fall through the cracks” and do not receive needed treatment. This TIP captures the current state-of-the-art treatment strategies to assist counselors and treatment agencies in providing appropriate services to clients with COD.

(1) COD are common in the general adult population, though many individuals with COD go untreated.

National surveys suggest COD are common in the adult population. For example, the National Survey on Drug Use and Health (NSDUH) reports that in 2002, 4 million adults met the criteria for both serious mental illness (SMI) and substance dependence and abuse. NSDUH information is based on a sample of 67,500 American civilians aged 12 or older in noninstitutionalized settings (Office of Applied Studies [OAS] 2003b). The NSDUH defined SMI as having at some time during the past year a diagnosable mental, behavioral, or emotional disorder that met the criteria specified in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) (American Psychiatric Association 1994) and resulted in functional impairment that substantially interfered with or limited one or more major life activities. The NSDUH classification scheme was not diagnosis specific, but function specific. Results from the survey are highlighted below.

• SMI is highly correlated with substance dependence or abuse. Among adults with SMI in 2002, 23.2 percent were dependent on or abused alcohol or illicit drugs, while the rate among adults without SMI was only 8.2 percent. Among adults with substance dependence or abuse, 20.4 percent had SMI; the rate of SMI was 7 percent among adults who were not dependent on or abusing a substance.

•Among adults who used an illicit drug in the past year, 17.1 percent had SMI in that year, while the rate was 6.9 percent among adults who did not use an illicit drug. Conversely, among adults with SMI, 28.9 percent used an illicit drug in the past year while the rate was 12.7 percent among those without SMI (OAS 2003b).

28.8 percent were binge drinkers, while 23.9 percent of adults with no SMI were binge drinkers. Earlier, the National Comorbidity Study (NCS) reported 1991 information on mental disorders and substance abuse or dependence in a sample of 8,098 American civilians aged 15 to 54 in noninstitutionalized settings. Figure 1-1 shows estimates from the NCS of the comparative number of any alcohol, drug abuse, or mental disorder (52 million), any mental disorder (40 million), any substance abuse/dependence disorder (20 million), and both mental disorder and substance abuse/dependence (8 million) in the past year.

Homeless populations

Data on the increasing rates of co-occurring mental and sub stance use disorders in home­ less populations are now available (North et al. 2004). North and colleagues estimate that rates of co-occurring Axis I and substance use disorders among females who are homeless increased from 14.3 percent in 1990 to 36.7 percent in 2000 and that rates among men who are homeless increased from 23.2 percent in 1990 to 32.2 percent in 2000.

North and colleagues also compared data collected in their 2000 study with estimates from ECA data collected in the early 1980s. They found that alcohol and drug use for both males and females rose considerably over the 2 decades. In 2000, 84 percent of the men who were homeless and 58 percent of the women who were homeless had a substance use disorder (North et al. 2004). The article reports an increase in bipolar disorder from 1990 to 2000 and an increase in major depression from 1980 to 2000. (Major depression accounted for the majority of all Axis I non-substance disorders.) The authors also noted that non-Axis I antisocial personality disorder (APD) appeared to change little from 1980 to 2000, with 10 to 20 percent of women who were homeless and 20 to 25 percent of men who were homeless receiving APD diagnoses in both time periods (North et al. 2004).

The increased prevalence of COD among people who are homeless and the need to provide services to this growing population has led to treatment innovations and research on service delivery. One of the main challenges is how to engage this group in treatment. CMHS’s Access to Community Care and Effective Services and Supports initiative, which supported programs in nine States over a 5-year period, indicated the effectiveness of integrated systems, including the value of street outreach (Lam and Rosenheck 1999; Rosenheck et al. 1998). Both systems integration and comprehensive services, such as Assertive Community Treatment (ACT) and Intensive Case Management (ICM), were seen as essential and effective (Integrating Systems of Care 1999; Winarski and Dubus 1994). (See chapter 6 for a discussion of these approaches.)


The Bureau of Justice Statistics estimates that “at midyear 1998, an estimated 283,800 mentally ill offenders were incarcerated in the Nation’s prisons and jails” (Ditton 1999, p. 1). Surveys by the Bureau found that “16 percent of State prison inmates, 7 percent of Federal inmates, and 16 percent of those in local jails reported either a mental condition or an overnight stay in a mental hospital” (Ditton 1999). In addition, an estimated 547,800 probationers—16 percent—said they had had a mental condition or stayed overnight in a mental hospital at some point in their lifetime (Ditton 1999).

The Office of National Drug Control Policy (ONDCP) emphasized that “the fastest and most cost-effective way to reduce the demand for illicit drugs is to treat chronic, hard core drug users” (ONDCP 1995, p. 53). These “hard core users” are in need of COD services. The NTIES study reported that, when given the choice to rate their desire for certain services as “not important,” “somewhat important,” or “very important,” 37 percent of a population that was predominantly criminaljustice–involved rated mental health services as “very important” (Karageorge 2000).

The substance abuse treatment and mental health services communities have been called on to provide, or assist in providing, treatment to these individuals. This requires the integration of substance abuse treatment and mental health services and the combination of these approaches with those that address criminal thinking and behavior, while attending to both public health and public safety concerns.

HIV/AIDS and infectious diseases

The association between psychological dysfunction and a tendency to engage in highrisk behaviors (Joe et al. 1991; Simpson et al. 1993) suggests that it is important to integrate HIV/AIDS prevention and treatment with substance abuse treatment and mental health services for the COD population. Advances in the treatment of HIV/AIDS (such as antiretroviral combination therapy, including protease inhibitors) and the improved outcomes resulting from such therapies potentially will extend the survival of those with HIV/AIDS and co-occurring disorders. This will extend their requirement for continued mental health and substance abuse services. For persons with COD who also have HIV/AIDS or other infectious diseases (e.g., hepatitis C), primary medical care should be integrated with COD treatment. To be successful, this treatment should include an emphasis on treatment adherence (see chapter 7 for one such model).

Trauma and PTSD

Many persons with substance use disorders have experienced trauma, often as a result of abuse. A significant number of them have the recognized mental disorder known as PTSD. Recent studies have demonstrated strong connections between trauma and addictions, including the possibility that childhood abuse plays a part in the development of substance use disorders (Anderson et al. 2002; Brady et al. 2000; Chilcoat and Breslau 1998b; Jacobsen et al. 2001). Although substance abuse treatment clinicians have counseled these clients for years, new treatment strategies for PTSD and trauma have expanded treatment options (see chapter 8 and appendix D). The forthcoming TIP Substance Abuse Treatment and Trauma will explore these issues in depth (CSAT in development d).

Changes in Treatment Delivery

The substance abuse treatment field has recognized the importance of COD programming. In 1995, only 37 percent of the substance use disorder treatment programs reporting data to the Substance Abuse and Mental Health Services Administration (SAMHSA) offered COD programming. By 1997, this percentage had increased to almost half (data not shown).

According to 2002 N-SSATS data, the number of programs for COD peaked in 1999, followed by a slight decline in 2000 that remained constant in 2002. This tracked the number of substance use disorder treatment providers, which also peaked in 1999. In 1999, there were 15,239 substance abuse treatment programs reporting to SAMHSA; in 2000, there were 13,428; in 2002, there were 13,720 (OAS 2003a). Figure 1-3 shows that the number of programs for people with COD decreased slightly from 1999 to 2000, from 6,818 to 6,696, but remained constant in 2002 at 6,696 (OAS 2003a). However, the ratio between the total number of substance abuse treatment programs and those offering COD programming has been relatively stable since 1997, increasing slightly from 44.7 percent in 1999 to 49.9 percent in 2000, and then remaining roughly constant at 48.8 percent in 2002.

An important consideration for the public mental health and substance abuse delivery systems is the recognition that not all people with emotional problems are candidates for care within the public mental health system. Because many States prioritize the funding of mental health slots by providing access to those who meet the criteria for the most severe and persistent mental illnesses, it is important for treatment providers to recognize the criteria that their State jurisdiction uses to provide care. For example, a treatment program may be aware that a person has psychological symptoms signifying stress, a diagnosable mental disorder, a serious mental disorder, a severe and persistent mental disorder, or, finally, a severe and persistent mental disorder with disability. From the point of view of the behavioral healthcare delivery system, these distinctions are important. In a State that restricts the use of its Federal community mental health services dollars to those with severe and persistent mental illness, a person not meeting the criteria for that condition may not be eligible for mental health services.

If a client/consumer has a primary substance abuse problem and a “non-eligible” mental disorder—that is, a disorder that cannot by regulation or law be treated in a public mental health program—then all providers should be aware of this. The difference between ideal care and available care is critical to the utility of this TIP. Furthermore, during periods of financial difficulty, the prospect of additional resources being created to address complex problems is not likely. Thus, an integrated care framework is preferred in this TIP. An integrated framework recognizes that quality evidence-based individualized care can be provided within a behavioral health delivery system using existing resources and partnerships.

Integrated care as a priority for people with severe and persistent mental illness

For those with severe and persistent mental illness, integrated treatment, as originally articulated by Minkoff (1989), emphasized the correspondence between the treatment models for mental illness and addiction in a residential setting. The model stressed a parallel view of recovery, concomitant treatment of mental illness and substance abuse, application of treatment stages, and the use of strategies from both the mental health and substance abuse treatment fields. During the last decade, integrated treatment has continued to evolve, and several models have been described (Drake and Mueser 1996b; Lehman and Dixon 1995; Minkoff and Drake 1991; Solomon et al. 1993).

For the purposes of this TIP, integrated treatment refers more broadly to any mechanism by which treatment interventions for COD are combined within the context of a primary treatment relationship or service setting. Integrated treatment is a means of coordinating substance abuse and mental health interventions to treat the whole person more effectively. In a review of mental health centerbased research for clients with serious and persistent mental illness, Drake and colleagues (1998b) concluded that comprehensive, integrated treatment, “especially when delivered for 18 months or longer, resulted in significant reductions of substance abuse and, in some cases, in substantial rates of remission, as well as reductions in hospital use and/or improvements in other outcomes” (p. 601). Several studies based in substance abuse treatment centers addressing a range of COD have demonstrated better treatment retention and outcome when mental health services were integrated onsite (Charney et al. 2001; McLellan et al. 1993; Saxon and Calsyn 1995; Weisner et al. 2001).

An integrated care framework supports the provision of some assessment and treatment wherever the client enters the treatment system, ensures that arrangements to facilitate consultations are in place to respond to client issues for which a provider does not have inhouse expertise, and encourages all counselors and programs to develop increased competency in treating individuals with COD. Several States have received Community Action Grants from SAMHSA to develop comprehensive continuous integrated systems of care. It is especially important that appropriate substance abuse and mental health services for clients with COD be designed specifically for the substance abuse treatment system—a system that addresses a wide range of COD, not mainly those with severe and persistent mental illness.

Development of effective approaches, models, and strategies

Treatment approaches are emerging with demonstrated effectiveness in achieving positive outcomes for clients with COD. These include a variety of promising treatment approaches that provide comprehensive integrated treatment. Successful strategies with important implications for clients with COD also include interventions based on addiction work in contingency management, cognitive– behavioral therapy, relapse prevention, and motivational interviewing. In fact, it is now possible to identify “guiding principles” and “fundamental elements” for COD treatment in COD settings that are common to a variety of approaches.

Pharmacological advances

Pharmacological advances over the past decade have produced antipsychotic, antidepressant, anticonvulsant, and other medications with greater effectiveness and fewer side effects (see appendix F for a listing of medications). With the support available from better medication regimens, many people who once would have been too unstable for substance abuse treatment, or institutionalized with a poor prognosis, have been able to lead more functional lives. To meet the needs of this population, the substance abuse treatment counselor needs both greater understanding of the signs and symptoms of mental illness and greater capacity for consultation with trained mental healthcare providers. As substance abuse treatment counselors learn more about mental illness, they are better able to partner with mental health counselors to design effective treatment for both types of disorders. Such partnerships benefit mental health agencies as well, helping them enhance their ability to treat clients with substance abuse issues.

Increasingly, substance abuse treatment counselors and programs have come to appreciate the importance of providing medication to control symptoms as an essential part of treatment. The counselor has an important role in describing client behavior and symptoms to ensure that proper medication is prescribed when needed. The peer community also is a powerful tool that can be employed to support and monitor medication adherence. Support from mutual self-help groups can include learning about the effects of medication and learning to accept medication as part of recovery. Monitoring involves clients learning from and reflecting on their own and others’ reactions, thoughts, and feelings about the ways medications affect them, both positively as symptoms are alleviated, and negatively as unwanted side effects may occur.

This chapter reviews and defines many of the terms that are applied commonly to co-occurring substance use and mental disorders (COD). Discussion points include how different terms have emerged, the contexts in which various classification systems are likely to be used, and why many of the specific terms and classification systems used throughout this TIP were chosen.

After a review of basic terminology related to substance use (including the distinction between abuse and dependence) and a brief description of mental disorders, the chapter discusses terms related to clients. A key point is the importance of using person-centered terminology as a way of acknowledging each client’s individuality. The chapter notes the many terms that may be used to describe co-occurring disorders, reviews the terms related to treatment and programs, and concludes with an overview of terms that describe the systems of care within which treatment occurs and programs operate.

The addiction counselor should be aware that the terminology and classifications introduced in this chapter, though important and useful, were developed by different groups for different purposes. Therefore, these terms do not necessarily form a seamless picture or work smoothly together. Nevertheless, they are useful and appropriate when used in the intended context.

Personality Disorders

These are the disorders most commonly seen by the addiction counselor and in quadrant III substance abuse treatment settings (see Figure 2-1 for a depiction of the four quadrants). Individuals with personality disorders have symptoms and personality traits that are enduring and play a major role in most, if not all, aspects of the person’s life. These individuals have personality traits that are persistent and cause impairment in social or occupational functioning or cause personal distress. Symptoms are evident in their thoughts (ways of looking at the world, thinking about self or others), emotions (appropriateness, intensity, and range), interpersonal functioning (relationships and interpersonal skills), and impulse control.

Personality disorders are listed in the DSMIV under three distinct areas, referred to as “clusters.” The clusters are listed below with the types of symptoms or traits seen in that category. The specific personality disorders included in each cluster also are listed. For personality disorders that do not fit any of the specific disorders, the diagnosis of “personality disorder not otherwise specified” is used.

Cluster A: Hallmark traits of this cluster involve odd or eccentric behavior. It includes paranoid, schizoid, and schizotypal personality disorders.

Cluster B: Hallmark traits of this cluster involve dramatic, emotional, or erratic behavior. It includes antisocial, borderline, histrionic, and narcissistic personality disorders.

Cluster C: Hallmark traits of this cluster involve anxious, fearful behavior. It includes avoidant, dependent, and obsessive-compulsive personality disorders.

The prevalence of co-occurring substance abuse and antisocial personality disorder is high (Flynn et al. 1997). In fact, much of substance abuse treatment is targeted to those with antisocial personality disorders and substance abuse treatment alone has been especially effective for these disorders.

client has a mood disorder, these feelings or emotions are experienced to the extreme. Many people with substance use disorders also have a co-occurring mood disorder and tend to use a variety of drugs in association with their mood disorder. There are several types of mood disorders, including depression, mania, and bipolar disorder.

Depression. Instead of just feeling “down,” the client might not be able to work or function at home, might feel suicidal, lose his or her appetite, and feel very tired or fatigued. Other symptoms can include loss of interest, weight changes, changes in sleep and appetite, feelings of worthlessness, loss of concentration, and recurrent thoughts of death.

Mania. This includes feelings that are toward the opposite extreme of depression. There might be an excess of energy where sleep is not needed for days at a time. The client may be feeling “on top of the world,” and during this time, the client’s decisionmaking process might be significantly impaired and expansive and he may experience irritability and have aggressive outbursts, although he might think such outbursts are perfectly rational.

Bipolar. A person with bipolar disorder cycles between episodes of mania and depression. These episodes are characterized by a distinct period of abnormally elevated, expansive, or irritable mood. Symptoms may include inflated self-esteem or grandiosity, decreased need for sleep, being more talkative than usual, flight of ideas or a feeling that one’s thoughts are racing, distractibility, increase in goal-directed activity, excessive involvement in pleasurable activities that have a high potential for painful consequences (sexual indiscretions, buying sprees, etc.). Excessive use of alcohol is common during periods of mania.

Anxiety disorders. As with mood disorders, anxiety is something that everyone feels now and then, but anxiety disorders exist when anxiety symptoms reach the point of frequency and intensity that they cause significant impairment. In addiction treatment populations, the most common anxiety syndrome seen is that associated with early recovery, which can be a mix of substance withdrawal and learning to live without the use of drugs or alcohol. This improves with time and addiction treatment. However, other anxiety disorders that may occur, but need particular assessment and treatment, are social phobia (fear of appearing or speaking in front of groups), panic disorder (recurrent panic attacks that usually last a few hours, cause great fear, and make it hard to breathe), and posttraumatic stress disorders (which cause recurrent nightmares, anxiety, depression, and the experience of reliving the traumatic issues).

Terms Related to Clients Person-Centered Terminology

In recent years, consumer advocacy groups have expressed concerns related to how clients are classified. Many take exception to terminology that seems to put them in a “box” with a label that follows them through life, that does not capture the fullness of their identities. A person with COD also may be a mother, a plumber, a pianist, a student, or a person with diabetes, to cite just a few examples. Referring to an individual as a person who has a specific disorder—a person with depression rather than “a depressive,” a person with schizophrenia rather than “a schizophrenic,” or a person who uses heroin rather than “an addict” is more acceptable to many clients because it implies that they have many characteristics besides a stigmatized illness, and therefore that they are not defined by this illness.

Integrated Interventions

Integrated interventions are specific treatment strategies or therapeutic techniques in which interventions for both disorders are combined in a single session or interaction, or in a series of interactions or multiple sessions. Integrated interventions can include a wide range of techniques. Some examples include

Episodes of Treatment

An individual with COD may participate in recurrent episodes of treatment involving acute stabilization (e.g., crisis intervention, detoxification, psychiatric hospitalization) and specific ongoing treatment (e.g., mental-health–supported housing, mental-health day treatment, or substance abuse residential treatment). It is important to recognize the reality that clients engage in a series of treatment episodes, since many individuals with COD progress gradually through repeated involvement in treatment.

Integrated Treatment

Integrated treatment refers broadly to any mechanism by which treatment interventions for COD are combined within the context of a primary treatment relationship or service setting. Integrated treatment is a means of actively combining interventions intended to address substance use and mental disorders in order to treat both disorders, related problems, and the whole person more effectively.

Culturally Competent Treatment

One definition of cultural competence refers to “the capacity of a service provider or of an organization to understand and work effectively with the cultural beliefs and practices of persons from a given ethnic/racial group” (Castro et al. 1999, p. 504). Treatment providers working with individuals with COD should view these clients and their treatment in the context of their language, culture, ethnicity, geographic area, socioeconomic status, gender, age, sexual orientation, religion, spirituality, and any physical or cognitive disabilities. For a full discussion of cultural issues in treatment for persons with substance use disorders, see the forthcoming TIP Improving Cultural Competence in Substance Abuse Treatment (CSAT in development a).

Cultural factors that may have an impact on treatment include heritage, history and experience, beliefs, traditions, values, customs, behaviors, institutions, and ways of communicating. The client’s culture may include distinctive ways of understanding disease or disorder, including mental and substance use disorders, which the provider needs to understand. Referencing a model of disease that is familiar to the client can help communication and enhance treatment. The counselor acquires cultural knowledge by becoming aware of the cultural factors that are important to a particular ethnic group or client.

Cultural competence may be viewed as a continuum on which, through learning, the provider increases his or her understanding and effectiveness with different ethnic groups. Various researchers have described the markers on this continuum (Castro et al. 1999; Cross 1988; Kim et al. 1992). The continuum moves from cultural destructiveness, in which an individual regards other cultures as inferior to the dominant culture, through cultural incapacity and blindness to the more positive attitudes and greater levels of skill described below:

•Cultural sensitivity is being “open to working with issues of culture and diversity” (Castro et al. 1999, p. 505). Viewed as a point on the continuum, however, a culturally sensitive individual has limited cultural knowledge and may still think in terms of stereotypes.

•Cultural competence, when viewed as the next stage on this continuum, includes an ability to “examine and understand nuances” and exercise “full cultural empathy.” This enables the counselor to “understand the client from the client’s own cultural perspective”.

•Cultural proficiency is the highest level of cultural capacity. In addition to understanding nuances of culture in even greater depth, the culturally proficient counselor also is working to advance the field through leadership, research, and outreach.

It is important to remember that clients, not counselors, define what is culturally relevant to them. It is possible to damage the relationship with a client by making assumptions, however well intentioned, about the client’s cultural identity. For example, a client of Hispanic origin may be a third-generation United States citizen, fully acculturated, who feels little or no connection with her Hispanic heritage. A counselor who assumes this client shares the beliefs and values of many Hispanic cultures would be making an erroneous generalization. Similarly, it is helpful to remember that all of us represent multiple cultures. Clients are not simply African– American, white, or Asian. A client who is a 20-year-old African-American man from the rural south may identify, to some extent, with youth, rural south, or African-American cultural elements—or may, instead, identify more strongly with another cultural element, such as his faith, that is not readily apparent. Counselors are advised to open a respectful dialog with clients around the cultural elements that have significance to them.

Integrated Counselor Competencies

A counselor has integrated competencies if he or she has the specific attitudes, values, knowledge, and skills needed to provide appropriate services to individuals with COD in the context of his or her actual job and program setting. Just as other types of integration exist on a continuum, so too does integrated competency. Some interventions and/or programs require clinicians only to have basic competency in welcoming, screening, assessing, and identifying treatment needs of individuals with COD. Other interventions, programs, or job functions (e.g., those of supervisory staff) may require more advanced integrated competency. The more complex or unstable the client, the more formal mechanisms are required to coordinate the various staff members working with that client in order to provide effective integrated treatment.

A number of service delivery systems are moving toward identification of a required basic level of integrated competency for all clinicians in the mental health and substance abuse treatment systems. Many States also are developing curricula for initial and ongoing training and supervision to help clinicians achieve these competencies. Other State systems (e.g., Illinois) have created career ladders and certification pathways to encourage clinicians to achieve higher levels of integrated competency and to reward them for this achievement. (See chapter 3 for a full discussion of counselor competencies.)

Terms Related to Programs

A program is a formally organized array of services and interventions provided in a coherent manner at a specific level or levels of care in order to address the needs of particular target populations. Each program has its own staff competencies, policies, and procedures. Programs may be operated directly by public funders (e.g., States and counties) or by privately funded agencies. An individual agency may operate many different programs. Some agencies operate only mental health programs, some operate only substance abuse treatment programs, and some do both. An individual, licensed healthcare practitioner (such as a psychiatrist or psychologist) may offer her or his own integrated treatment services as an independent practitioner.

Key Programs

Mental health-based programs

A mental health program is an organized array of services and interventions with a primary focus on treating mental disorders, whether by providing acute stabilization or ongoing treatment. These programs may exist in a variety of settings, such as traditional outpatient mental health centers (including outpatient clinics and psychosocial rehabilitation programs) or more intensive inpatient treatment units.

Many mental health programs treat significant numbers of individuals with COD. Programs that are more advanced in treating persons with COD may offer a variety of interventions for substance use disorders (e.g., motivational interviewing, substance abuse counseling, skills training) within the context of the ongoing mental health treatment.

Substance abuse treatment programs

A substance abuse treatment program is an organized array of services and interventions with a primary focus on treating substance use disorders, providing both acute stabilization and ongoing treatment. Substance abuse treatment programs that are more advanced in treating persons with COD may offer a variety of interventions for mental disorders (e.g., psychopharmacology, symptom management training) within the context of the ongoing substance abuse treatment.


Screening and Basic Assessment for COD  

This section provides an overview of the screening and assessment process for COD. In carrying out these processes, counselors should understand the limitations of their licensure or certification authority to diagnose or assess mental disorders. Generally, however, collecting assessment information is a legitimate and legal activity even for unlicensed providers, provided that they do not use diagnostic labels as conclusions or opinions about the client. Information gathered in this way is needed to ensure the client is placed in the most appropriate treatment setting (as discussed later in this chapter) and to assist in providing mental disorder care that addresses each disorder.

In addition, there are a number of circumstances that can affect validity and test responses that may not be obvious to the beginning counselor, such as the manner in which instructions are given to the client, the setting where the screening or assessment takes place, privacy (or the lack thereof), and trust and rapport between the client and counselor. Throughout the process it is important to be sensitive to cultural context and to the different presentations of both substance use and mental disorders that may occur in various cultures.


Screening is a formal process of testing to determine whether a client does or does not warrant further attention at the current time in regard to a particular disorder and, in this context, the possibility of a co-occurring substance use or mental disorder. The screening process for COD seeks to answer a “yes” or “no” question: Does the substance abuse (or mental health) client being screened show signs of a possible mental health (or substance abuse) problem? Note that the screening process does not necessarily identify what kind of problem the person might have or how serious it might be, but determines whether or not further assessment is warranted. A screening process can be designed so that it can be conducted by counselors using their basic counseling skills. There are seldom any legal or professional restraints on who can be trained to conduct a screening.

Screening processes always should define a protocol for determining which clients screen positive and for ensuring that those clients receive a thorough assessment. That is, a professionally designed screening process establishes precisely how any screening tools or questions are to be scored and indicates what constitutes scoring positive for a particular possible problem (often called “establishing cut-off scores”). Additionally, the screening protocol details exactly what takes place after a client scores in the positive range and provides the necessary standard forms to be used to document both the results of all later assessments and that each staff member has carried out his or her responsibilities in the process.

So, what can a substance abuse treatment counselor do in terms of screening? All counselors can be trained to screen for COD. This screening often entails having a client respond to a specific set of questions, scoring those questions according to how the counselor was trained, and then taking the next “yes” or “no” step in the process depending on the results and the design of the screening process. In substance abuse treatment or mental health service settings, every counselor or clinician who conducts intake or assessment should be able to screen for the most common COD and know how to implement the protocol for obtaining COD assessment information and recommendations.

Basic Assessment

While both screening and assessment are ways of gathering information about the client in order to better treat him, assessment differs from screening in the following way:

•Screening is a process for evaluating the possible presence of a particular problem.

•Assessment is a process for defining the nature of that problem and developing specific treatment recommendations for addressing the problem.

A basic assessment consists of gathering key information and engaging in a process with the client that enables the counselor to understand the client’s readiness for change, problem areas, COD diagnosis(es), disabilities, and strengths. An assessment typically involves a clinical examination of the functioning and well-being of the client and includes a number of tests and written and oral exercises. The COD diagnosis is established by referral to a psychiatrist, clinical psychologist, or other qualified healthcare professional. Assessment of the client with COD is an ongoing process that should be repeated over time to capture the changing nature of the client’s status. Intake information consists of

It is essential for treatment planning that the counselor organize the collected information in a way that helps identify established mental disorder diagnoses and current treatment. Careful attention to the characteristics of past episodes of substance abuse and abstinence with regard to mental health symptoms, impairments, diagnoses, and treatments can illuminate the role of substance abuse in maintaining, worsening, and/or interfering with the treatment of any mental disorder. Understanding a client’s mental health symptoms and impairments that persist during periods of abstinence of 30 days or more can be useful, particularly in understanding what the client copes with even when the acute effects of substance use are not present. For any period of abstinence that lasts a month or longer, the counselor can ask the client about mental health treatment and/or substance abuse treatment—what seemed to work, what did the client like or dislike, and why? On the other hand, if mental health symptoms (even suicidality or hallucinations) resolve in less than 30 days with abstinence from substances, then these symptoms are most likely substance induced and the best treatment is maintaining abstinence from substances.

The counselor also can ask what the mental health “ups and downs” are like for the client. That is, what is it like for the client when he or she gets worse (or “destabilizes”)? What—in detail—has happened in the past? And, what about getting better (“stabilizing”)—how does the client usually experience that? Clinician and client together should try to understand the specific effects that substances have had on that individual’s mental health symptoms, including the possible triggering of psychiatric symptoms by substance use. Clinicians also should attempt to document the diagnosis of a mental disorder, when it has been established, and determine diagnosis through referral when it has not been established. The consensus panel notes that many, if not most, individuals with COD have well-established diagnoses when they enter substance abuse treatment and encourages counselors to find out about any known diagnoses.

Treatment Planning

A comprehensive assessment serves as the basis for an individualized treatment plan. Appropriate treatment plans and treatment interventions can be quite complex, depending on what might be discovered in each domain. This leads to another fundamental principle:

•There is no single, correct intervention or program for individuals with COD. Rather, the appropriate treatment plan must be matched to individual needs according to these multiple considerations.

The Assessment Process

This chapter is organized around 12 specific steps in the assessment process. Through these steps, the counselor seeks to accomplish the following aims:

•To obtain a more detailed chronological history of past mental symptoms, diagnosis, treatment, and impairment, particularly before the onset of substance abuse, and during periods of extended abstinence.

•To obtain a more detailed description of current strengths, supports, limitations, skill deficits, and cultural barriers related to following the recommended treatment regimen for any disorder or problem.

•To determine stage of change for each problem, and identify external contingencies that might help to promote treatment adherence.

Note that although the steps appear sequential, in fact some of them could occur simultaneously or in a different order, depending on the situation. It is particularly important to identify and attend to any acute safety needs, which often have to be addressed before a more comprehensive assessment process can occur. Sometimes, however, components of the assessment process are essential to address the client’s specific safety needs. For example, if a person is homeless, more information on that person’s mental status, resources, and overall situation is required to address that priority appropriately. Finally, it must be recognized that while the assessment seeks to identify individual needs and vulnerabilities as quickly as possible to initiate appropriate treatment, assessment is an ongoing process: As treatment proceeds and as other changes occur in the client’s life and mental status, counselors must actively seek current information rather than proceed on assumptions that might be no longer valid.

In the following discussion, validated assessment tools that are available to assist in this process are discussed with regard to their utility for counselors. There are a number of tools that are required by various States for use in their addiction systems (e.g., ASI [McLellan et al. 1992], American Society of Addiction Medicine (ASAM) Patient Placement Criteria [ASAM PPC-2R]).

Particular attention will be given to the role of these tools in the COD assessment process, suggesting strategies to reduce duplication of effort where possible. It is beyond the scope of this TIP to provide detailed instructions for administering the tools mentioned in this TIP (with the exceptions of the Mental Health

Screening Form-III [MHSF-III] and the Simple Screening Instrument for Substance Abuse [SSI-SA] in appendix H). Basic information about each instrument is given in appendix G, and readers can obtain more detailed information regarding administration and interpretation from the sources given for obtaining these instruments.

As a final point, this discussion primarily is directed toward substance abuse treatment clinicians working in substance abuse treatment settings, though many of the steps apply equally well to mental health clinicians in mental health settings. At certain key points in the discussion, particular information relevant to mental health clinicians is identified and described.

Assessment Step 1: Engage the Client

The aim is to create a safe and nonjudgmental environment in which sensitive personal issues may be discussed. Counselors should recognize that cultural issues, including the use of the client’s preferred language, play a role in creating a sense of safety and promote accurate understanding of the client’s situation and options. Such issues therefore must be addressed sensitively at the outset and throughout the assessment process.

The consensus panel identified five key concepts that underlie effective engagement during the initial clinical contact: universal access (“no wrong door”), empathic detachment, person-centered assessment, cultural sensitivity, and trauma sensitivity. All staff, as well as substance abuse treatment and mental health clinicians, in any service setting need to develop competency in engaging and welcoming individuals with COD. It is also important to note that while engagement is presented here as the first necessary step for assessment to take place, in a larger sense engagement represents an ongoing concern of the counselor—to understand the client’s experience and to keep him or her positive and engaged relative to the prospect of better health and recovery.

No wrong door

“No wrong door” refers to formal recognition by a service system that individuals with COD may enter a range of community service sites; that they are a high priority for engagement in treatment; and that proactive efforts are necessary to welcome them into treatment and prevent them from falling through the cracks. Substance abuse and mental health counselors are encouraged to identify individuals with COD, welcome them into the service system, and initiate proactive efforts to help them access appropriate treatment in the system, regardless of their initial site of presentation. The recommended attitude is as follows: The purpose of this assessment is not just to determine whether the client fits in my program, but to help the client figure out where he or she fits in the system of care, and to help him or her get there.

Empathic detachment

Empathic detachment requires the assessing clinician to

•Acknowledge that the clinician and client are working together to make decisions to support the client’s best interest

•Recognize that the clinician cannot transform the client into a different person, but can only support change that he or she is already making

•Maintain empathic connection even if the client does not seem to fit into the clinician’s expectations, treatment categories, or preferred methods of working

In the past, the attitude was that the client with COD was the exception. Today, clinicians should be prepared to demonstrate responsiveness to the requirements clients with COD present. Counselors should be careful not to label mental health symptoms immediately as caused by addiction, but instead should be comfortable with the strong possibility that a mentalhealth condition may be present independently and encourage disclosure of information that will help clarify the meaning of any COD for that client.

Person-centered assessment

Person-centered assessment emphasizes that the focus of initial contact is not on filling out a form or answering several questions or on establishing program fit, but rather on finding out what the client wants, in terms of his or her perception of the problem, what he or she wants to change, and how he or she thinks that change will occur. Mee-Lee (1998) has developed a useful guide that illustrates the types of questions that might be asked in a person-centered assessment in an addiction setting. (It should be noted, however, that this is not a validated tool.) While each step in this decision tree leads to the next, the final step can lead back to a previous step, depending on the client’s progress in treatment.

Answers to some of these important questions inevitably will change over time. As the answers change, adjustments in treatment strategies may be appropriate to help the client continue to engage in the treatment process.

Sensitivity to culture, gender, and sexual orientation

An important component of a person-centered assessment is the continual recognition that culture plays a significant role in determining the client’s view of the problem and the treatment. (For a comprehensive discussion of culturally sensitive assessment strategies in addiction settings, see the forthcoming TIP Improving Cultural Competence in Substance Abuse Treatment [CSAT in development a]). With regard to COD, clinicians must remember that ethnic cultures may differ significantly in their approach to substance use disorders and mental disorders, and that this may affect how the client presents. In addition, clients may participate in treatment cultures (12-Step recovery, Dual Recovery Self-Help, psychiatric rehabilitation) that also may affect how they view treatment. Cultural sensitivity also requires recognition of one’s own cultural perspective and a genuine spirit of inquiry into how cultural factors influence the client’s request for help. (See also chapter 2 for a discussion of culturally competent treatment.)

During the assessment process, it is important to ascertain the individual’s sexual orientation as part of the counselor’s appreciation for the client’s personal identity, living situation, and relationships. Counselors also should be aware that women often have family-related and other concerns that must be addressed to engage them in treatment, such as the need for child care. See chapter 7 of this TIP for a more extended consideration of women with COD as a population with specific needs. More information about women’s issues is provided in the forthcoming TIP Substance Abuse Treatment: Addressing the Specific Needs of Women (CSAT in development b).

Trauma sensitivity

The high prevalence of trauma in individuals with COD requires that the clinician consider the possibility of a trauma history even before the assessment begins. Trauma may include early childhood physical, sexual, or emotional abuse; experiences of rape or interpersonal violence as an adult; and traumatic experiences associated with political oppression, as might be the case in refugee or other immigrant populations. This pre-interview consideration means that the approach to the client must be sensitive to the possibility that the client has suffered previous traumatic experiences that may interfere with his or her ability to be trusting of the counselor. Clinicians who observe guardedness on the part of the client should consider the possibility of trauma and try to promote safety in the interview through providing support and gentleness, rather than trying to “break through” evasiveness that erroneously might look like resistance or denial.

Assessment Step 2: Identify and Contact Collaterals (Family, Friends, Other
Providers) To Gather Additional Information

Clients presenting for substance abuse treatment, particularly those who have current or past mental health symptoms, may be unable or unwilling to report past or present circumstances accurately. For this reason, it is recommended that all assessments include routine procedures for identifying and contacting any family and other collaterals who may have useful information to provide. Information from collaterals is valuable as a supplement to the client’s own report in all of the assessment steps listed in the remainder of this chapter. It is valuable particularly in evaluating the nature and severity of mental health symptoms when the client may be so impaired that he or she is unable to provide that information accurately. Note, however, that the process of seeking such information must be carried out strictly in accordance with applicable guidelines and laws 1 regarding confidentiality and with the client’s permission.

Assessment Step 3: Screen for and Detect Co-Occurring Disorders

Because of the high prevalence of co-occurring mental disorders in substance abuse treatment settings, and because treatment outcomes for individuals with multiple problems improve if each problem is addressed specifically, the consensus panel recommends that

•All individuals presenting for substance abuse treatment should be screened routinely for co-occurring mental disorders.

•All individuals presenting for treatment for a mental disorder should be screened routinely for any substance use disorder.

The content of the screening will vary upon the setting. Substance abuse screening in mental health settings should

•Screen for acute safety risk related to serious intoxication or withdrawal
•Screen for past and present substance use, substance related problems, and substancerelated disorders
Mental health screening has four major components in substance abuse treatment settings:
•Screen for acute safety risk: suicide, violence, inability to care for oneself, HIV and hepatitis C virus risky behaviors, and danger of physical or sexual victimization
•Screen for past and present mental health symptoms and disorders
•Screen for cognitive and learning deficits
• Regardless of the setting, all clients should be screened for past and present victimization and trauma.

Safety screening

Safety screening requires that early in the interview the clinician specifically ask the client if he or she has any immediate impulse to engage in violent or self-injurious behavior, or if the client is in any immediate danger from others. These questions should be asked directly of the client and of anyone else who is providing information. If the answer is yes, the clinician should obtain more detailed information about the nature and severity of the danger, the client’s ability to avoid the danger, the immediacy of the danger, what the client needs to do to be safe and feel safe, and any other information relevant to safety. Additional information can be gathered depending on the counselor/staff training for crisis/emergency situations and the interventions appropriate to the treatment provider’s particular setting and circumstances. Once this information is gathered, if it appears that the client is at some immediate risk, the clinician should arrange for a more in-depth risk assessment by a mental-health–trained clinician, and the client should not be left alone or unsupervised.

A variety of tools are available for use in safety screening: None of these tools is definitive for safety screening. Clinicians and programs should use one of these tools only as a starting point, and then elaborate more detailed questions to get all relevant information. Clinicians should not underestimate risk because the client is using substances actively. For example, although people who are intoxi­ cated might only seem to be making threats of  self-harm (e.g., “I’m just going to go home  and blow my head off if nobody around here can help me”), all statements about harming  oneself or others must be taken seriously. Individuals who have suicidal or aggressive impulses when intoxicated may act on those  impulses; remember, alcohol and drug abuse  are among the highest predictors of danger­ ousness to self or others—even without any  co-occurring mental disorder. Determining  which intoxicated suicidal client is “serious”  and which one is not requires a skilled mental health assessment, plus information from collaterals who know the client best. (See chapter 8 and appendix D of this TIP for a more detailed discussion of suicidality.) In addition, it is important to remember that the vast majority of people who are abusing or depen­ dent on substances will experience at least  transient symptoms of depression, anxiety, and other mental symptoms. Moreover, it may not be possible, even with a skilled clinician, to determine whether an intoxicated suicidal patient is making a serious threat of self harm; however, safety is a critical and paramount concern. A more detailed discussion of each symptom subgroup is provided in appendix D. Safety screening conducted in mental health settings is highlighted in the text box below.

Screening for past and present mental disorders

Screening for past and present mental disorders has three goals: 

3.  For  clients  with   a current  COD,  to  determine  the  nature  of  the  symptoms  that  might wax  and  wane  to  help  the  client  monitor  the symptoms,  especially  how  the  symptoms improve  or  worsen  in  response  to  medications,  “slips”  (i.e.,  substance  use),  and treatment  interventions.  For  example, clients  often  need  help  seeing  that  the  treatment  goal  of  avoiding  isolation  improves their  mood—that  when  they  call  their  sponsor  and  go  to   a meeting  they  break  the vicious  cycle  of  depressed  mood,  seclusion, dwelling  on  oneself  and  one’s  mood, increased  depression,  greater  isolation,  and so  on. A  number  of  screening,  assessment,  and treatment  planning  tools  are  available  to assist  the  substance  abuse  treatment  team. For  assessment  of  specific  disorders and/or  for  differential  diagnosis  and  treatment  planning,  there  are  literally  hundreds  of  assessment  and  treatment  planning  tools.  

Maintaining a therapeutic alliance with clients who have co-occurring disorders (COD) is important—and difficult. The first section of this chapter reviews guidelines for addressing these challenges. It stresses the importance of the counselor’s ability to manage feelings and biases that could arise when working with clients with COD (sometimes called countertransference). Together, clinicians and clients should monitor the client’s disorders by examining the status of each disorder and alerting each other to signs of relapse. The consensus panel recommends that counselors use primarily a supportive, empathic, and culturally appropriate approach when working with clients with COD. With some clients who have COD, it is important to distinguish behaviors and beliefs that are cultural in origin from those indicative of a mental disorder. Finally, counselors should increase structure and support to help their clients with COD make steady progress throughout recovery.

The second part of this chapter describes techniques effective in counseling clients with COD. One is the use of motivational enhancement consistent with the client’s specific stage of recovery. This strategy is helpful even for clients whose mental disorder is severe. Other strategies include contingency management, relapse prevention, and cognitive–behavioral techniques. For clients with functional deficits in areas such as understanding instructions, repetition and skill-building strategies can aid progress. Finally, 12-Step and other dual recovery mutual self-help groups have value as a means of supporting individuals with COD in the abstinent life. Clinicians often play an important role in facilitating the participation of these clients in such groups. This chapter will provide a basic overview of how counselors can apply each of these strategies to their clients who have COD. The material in this chapter is consistent with national or State consensus practice guidelines for COD treatment, and consonant with many of their recommendations.

The purpose of this chapter is to describe for the addiction counselor and other practitioners how these guidelines and techniques, many of which are useful in the treatment of substance abuse or as general treatment principles, can be modified specifically and applied to people with COD. These guidelines and techniques are particularly relevant in working with clients in quadrants II and III. Additionally, this chapter contains Advice to the Counselor boxes to highlight the most immediate practical guidance (for a full listing of these boxes see the table of contents).

Guidelines for a Successful Therapeutic

Relationship With a Client Who Has COD

The following section reviews seven guidelines that have been found to be particularly helpful in forming a therapeutic relationship with clients who have COD (see text box below).

General. Research suggests that a therapeutic alliance is “one of the most robust predictors of treatment outcome” in psychotherapy (Najavits et al. 2000, p. 2172). Some studies in the substance abuse treatment field also have found associations between the strength of the therapeutic alliance and counseling effectiveness. One research team found that both clinician and client ratings of the alliance were strong predictors of alcoholic outpatients’ treatment participation in treatment, drinking behavior during treatment, and drinking behavior at a 12-month followup, even after controlling for a variety of other sources of variance (Connors et al. 1997). Similarly, Luborsky and colleagues (1985) found that the development of a “helping alliance” was correlated with positive outcomes.

A number of researchers have verified that clients are more responsive when the therapist acts consistently as a nurturing and nonjudgmental ally (Frank and Gunderson 1990; Luborsky et al. 1997; Siris and Docherty 1990; Ziedonis and D’Avanzo 1998). For example, in a study of clients with opioid dependence and psychopathology, Petry and Bickel (1999) found that among clients with moderate to severe psychiatric problems, fewer than 25 percent of those with weak therapeutic alliances completed treatment, while more than 75 percent of those with strong therapeutic alliances completed treatment. In this study, they did not find the strength of the therapeutic alliance to be related to treatment completion among clients with few psychiatric symptoms.

Challenges for the clinician

General. The clinician’s ease in working toward a therapeutic alliance also is affected by his or her comfort level in working with the client. Substance abuse counselors may find some clients with significant mental illnesses or severe substance use disorders to be threatening or unsettling. It is therefore important to recognize certain patterns that invite these feelings and not to let them interfere with the client’s treatment. This discomfort may be due to a lack of experience, training, or mentoring. Likewise, some mental health clinicians may feel uncomfortable or intimidated by clients with substance use disorders. Clinicians who experience difficulty forming a therapeutic alliance with clients with COD are advised to consider whether this is related to the client’s difficulties; to a limitation in the clinician’s own experience and skills; to demographic differences between the clinician and the client in areas such as age, gender, education, race, or ethnicity; or to issues involving countertransference (see the discussion of countertransference below). A consultation with a supervisor or peer to discuss this issue is important. Often these reactions can be overcome with further experience, training, supervision, and mentoring.

Individuals with COD often experience demoralization and despair because of the complexity of having two problems and the difficulty of achieving treatment success. Inspiring hope often is a necessary precursor for the client to give up short-term relief in exchange for long-term work with some uncertainty as to timeframe and benefit.

Challenges in working with clients with serious mental and substance use disorders. Achieving a therapeutic alliance with clients with serious mental illness and substance use disorders can be challenging. According to Ziedonis and D’Avanzo (1998), many people who abuse substances also may have some antisocial traits. Such individuals are “less amenable to psychological and pharmacological interventions and avoid contact with the mental health treatment staff.” Therefore, it is reasonable to conclude that “the dually diagnosed are less likely to develop a positive therapeutic alliance than non–substanceabusing patients with schizophrenia…”

Individuals with both schizophrenia and a substance use disorder may be particularly challenging to treat. These individuals “present and maintain a less involved and more distant stance in relation to the therapist than do non–substance-abusing individuals with schizophrenia”

The presence or level of these deficits may vary widely for people living with schizophrenia, and also may vary significantly for that individual within the course of his illness and the course of his lifetime. While “this configuration of interpersonal style suggests that developing a therapeutic alliance can be difficult,” Ziedonis and D’Avanzo insist, “working with the dually diagnosed requires a primary focus on the therapeutic alliance” (Ziedonis and D’Avanzo 1998, p. 444).

For all clients with co-occurring disorders, the therapeutic relationship must build on the capacity that does exist. These clients often need the therapeutic alliance to foster not only their engagement in treatment but as the cornerstone of the entire recovery process. Once established, the therapeutic alliance is rewarding for both client and clinician and facilitates their participation in a full range of therapeutic activities; documentation of these types of interactions provides an advantage in risk management.

Maintain a Recovery Perspective

Varied meanings of “recovery”

The word “recovery” has different meanings in different contexts. Substance abuse treatment clinicians may think of a person who has changed his or her substance abuse behavior as being “in recovery” for the rest of his or her life (although not necessarily in formal treatment forever). Mental health clinicians, on the other hand, may think of recovery as a process in which the client moves toward specific behavioral goals through a series of stages. Recovery is assessed by whether or not these goals are achieved. For persons involved with 12-Step programs, recovery implies not only abstinence from drugs or alcohol but also a commitment to “work the steps,” which includes changing the way they interact with others and taking responsibility for their actions. Consumers with mental disorders may see recovery as the process of reclaiming a meaningful life beyond mental disorder, with symptom control and positive life activity.

While “recovery” has many meanings, generally, it is recognized that recovery does not refer solely to a change in substance use, but also to a change in an unhealthy way of living. Markers such as improved health, better ability to care for oneself and others, a higher degree of independence, and enhanced selfworth are all indicators of progress in the recovery process.

Implications of the recovery perspective

The recovery perspective as developed in the substance abuse field has two main features:
(1) It acknowledges that recovery is a long-term process of internal change, and (2) it recognizes that these internal changes proceed through various stages (see De Leon 1996 and Prochaska et al. 1992 for a detailed description).
The recovery perspective generates at least two main principles for practice:

  1. Develop a treatment plan that provides for continuity of care over time. In preparing this plan, the clinician should recognize that treatment may occur in different settings over time (e.g., residential, outpatient) and that much of the recovery process is client-driven and occurs typically outside of or following professional treatment (e.g., through participation in mutual self-help groups) and the counselor should reinforce long-term participation in these constantly available settings.
Devise treatment interventions that are specific to the tasks and challenges faced at each stage of the COD recovery process. The use of treatment interventions that are specific to the tasks and challenges faced at each stage of the COD recovery process enables the clinician (whether within the substance abuse or mental health treatment system) to use sensible stepwise approaches in developing and using treatment protocols. In addition, markers that are unique to individuals— such as those related to their cultural, social, or spiritual context—should be considered. It is therefore important to engage the client in defining markers of progress that are meaningful to

Stages of change and stages of treatment

Working within the recovery perspective requires a thorough understanding of the interrelationship between stages of change (see De Leon 1996 and Prochaska et al. 1992) and stages of treatment (see section on motivational enhancement below for a description of the stages of change; see also TIP 35, Enhancing Motivation for Change in Substance Abuse Treatment [Center for Substance Abuse Treatment (CSAT) 1999b]). De Leon has developed a measure of motivation for change and readiness for treatment— The Circumstances, Motivation and Readiness Scales—and provided scores for samples of persons with COD (De Leon et al. 2000a). De Leon has demonstrated the relationship between these scales and retention in nificant others. As observed by the American Association of Community Psychiatrists (AACP), the strong client empowerment movement within the mental health field is a cornerstone for recovery:

Pessimistic attitudes about people with COD represent major barriers to successful system change and to effective treatment interventions ... recovery is defined as a process by which a person with persistent, possibly disabling disorders, recovers self-esteem, selfworth, pride, dignity, and meaning, through increasing his or her ability to maintain stabilization of the disorders and maximizing functioning within the constraints of the disorders. As a general principle, every person, regardless of the severity and disability associated with each disorder, is entitled to experience the promise and hope of dual recovery, and is considered to have the potential to achieve dual recovery (AACP 2000b).

Continuous support

Another implication of the recovery perspective is the need for continuing support for recovery. This means the provider encourages clients to build a support network that offers respect, acceptance, and appreciation. For example, an important element of long-term participation in Alcoholics Anonymous (AA) is the offering of a place of belonging or a “home.” AA accomplishes this supportive environment without producing overdependence because the client is expected to contribute, as well as receive, support.

Continuity of treatment

An emphasis on continuity of treatment also flows from a recovery perspective. Continuity of treatment implies that the services provided by the program are constant, and a client might remain a consumer of substance abuse or mental health services indefinitely. Treatment continuity for individuals with COD begins with proper and thorough identification, assessment, and diagnosis. It includes easy and early access to the appropriate service providers “...through multiple episodes of acute and subacute treatment independent of any particular setting or locus of care” (AACP 2000b).

Manage Countertransference

Though somewhat dated and infrequently used in the COD literature, the concept of “countertransference” is useful for understanding how the clinician’s past experience can influence current attitudes toward a particular client. “Transference” describes the process whereby clients project attitudes, feelings, reactions, and images from the past onto the clinician. For example, the client may regard the clinician as an “authoritative father,” “know-it-all older brother,” or “interfering mother.” Once considered a technical error, countertransference now is understood to be part of the treatment experience for the clinician.

Particularly when working with multiple and complicated problems, clinicians are vulnerable to the same feelings of pessimism, despair, anger, and the desire to abandon treatment as the client. Inexperienced clinicians often are confused and ashamed when faced with feelings of anger and resentment that can result from situations where there is a relative absence of gratification from working with clients with these disorders (Cramer 2002). Less experienced practitioners may have more difficulty identifying countertransference, accessing feelings evoked by interactions with a client, naming them, and working to keep these feelings from interfering with the counseling relationship.

Both substance use disorders and mental disorders are illnesses that are stigmatized by the general public. These same attitudes can be present among clinicians. Mental health clinicians who usually do not treat persons with substance abuse issues may not have worked out their own response to the disorder, which can influence their interactions with the client. Similarly, substance abuse treatment clinicians may not be aware of their own reactions to persons with specific mental disorders and may have difficulty preventing these reactions from influencing treatment. The clinician’s negative attitudes or beliefs may be communicated, directly or subtly, to the client. For example: “I was depressed too, but I never took medications for it—I just worked the steps
and got over it. So why should this guy need medication?”

Such feelings often are related to burnout and are exacerbated by the long time required to see progress in many clients with COD. For example, one study found that therapists’ attitudes toward their substance abuse clients tended to become more negative over time, though the increasing negativity was found to be less extreme for substance abuse counselors without graduate degrees who used the 12 steps to inform their counseling approach than for psychotherapists with graduate training who participated in the study (Najavits et al. 1995). (For a full discussion of countertransference in substance abuse treatment see Powell and Brodsky 1993.)

Cultural issues also may arouse strong and often unspoken feelings and, therefore, generate transference and countertransference. Although counselors working with clients in their area of expertise may be familiar with countertransference issues, working with an unfamiliar population will introduce different kinds and combinations of feelings.

The clinician is advised to understand and be familiar with some of the issues related to countertransference and strategies to manage it. Such countertransference issues are particularly important when working with persons with COD because many receiving therapy from a mental health services provider, it is especially important for the substance abuse counselor to participate in the development of the treatment plan and to monitor psychiatric symptoms. At a minimum, the clinician should be knowledgeable about the overall treatment plan to permit reinforcement of the mental health part of the plan as well as the part specific to recovery from addiction.

It is equally important that the client participate in the development of the treatment plan. For example, for a client who has both bipolar disorder and alcoholism, and who is receiving treatment at both a substance abuse treatment agency and a local mental health center, the treatment plan might include individual substance abuse treatment counseling, medication management, and group therapy. In another example, the substance abuse treatment clinician may assist in medication monitoring of a person taking lithium. The clinician can ask such questions as, “How are your meds doing? Are you remembering to take them? Are you having any problems with them? Do you need to check in with the prescribing doctor?” It also is prudent to ask the client to bring in all medications and ask the client how he is taking them, when, how much, and if medication is helping and how. Clinicians should help educate clients about the effects of medication, teach clients to monitor themselves (if possible), and consult with clients’ physicians whenever appropriate.

Status of symptoms

Substance abuse counselors need to have a method by which to monitor changes in severity and number of symptoms over time. For example, most clients present for substance abuse treatment with some degree of anxiety or depressive symptoms. As discussed in chapters 2 and 4, these symptoms are referred to as substance induced if caused by substances and resolved within 30 days of abstinence. Substance-induced symptoms tend to follow the “teeter totter” principle of “what goes up, must come down,” and vice versa—so that after a run of amphetamine or cocaine the individual will appear fatigued and depressed, while after using depressants such as alcohol or opioids, the individual more likely will appear agitated and anxious. These “teeter totter” symptoms are substance withdrawal effects and usually are seen for days or weeks. They may be followed by a substance-related depression (which can be seen as a neurotransmitter depletion state), which should begin to improve within a few weeks. If depressive or other symptoms persist, then a co-occurring (additional) mental disorder is likely, and the differential diagnostic process ensues. These symptoms may be appropriate target symptoms for establishing a diagnosis or determining treatment choices (medication, therapy, etc.). Clients using methamphetamines may present with psychotic symptoms that require medications.

A number of different tools are available to substance abuse treatment providers to help monitor psychiatric symptoms. Some tools are simply questions and require no formal instrument. For example, to gauge the status of depression quickly, ask the client: “On a scale of 0 to 10, how depressed are you? (0 is your best day, 10 is your worst).” This simple scale, used from session to session, can provide much useful information. Adherence to prescribed medication also should be monitored by asking the client regularly for information about its use and effect.

To identify changes, it is important to track symptoms that the client mentions at the onset of treatment from week to week. The clinician should keep track of any suggestions made to the client to alleviate symptoms to determine whether the client followed through, and if so, with what result. For example: “Last week you mentioned low appetite, sleeplessness, and a sense of hopelessness. Are these symptoms better or worse now?”

Use Supportive and Empathic Counseling

Definition and importance

A supportive and empathic counseling style is one of the keys to establishing an effective therapeutic alliance. According to Ormont, empathy is the ability to “experience another person’s feeling or attitude while still holding on to our own attitude and outlook”; it is the foundation adults use for relating to and interacting with other adults (Ormont 1999, p. 145). The clinician’s empathy enables clients to begin to recognize and own their feelings, an essential step toward managing them and learning to empathize with the feelings of others. However, this type of counseling must be used consistently over time to keep the alliance intact. This caveat often is critical for clients with COD, who usually have lower motivation to address either their mental or substance abuse problems, have greater difficulty understanding and relating to other people, and need even more understanding and support to make a major lifestyle change such as adopting abstinence. Support and empathy on the clinician’s part can help maintain the therapeutic alliance, increase client motivation, assist with medication adherence, model behavior that can help the client build more productive relationships, and support the client as he or she makes a major life transition.

Confrontation and empathy

The overall utility of confrontational techniques is well accepted in the substance abuse literature. It is used widely in substance abuse treatment programs, including those surveyed in the Drug Abuse Treatment Outcomes Study in which the effectiveness of such programs was demonstrated. Confrontation is a form of interpersonal exchange in which individuals present to each other their observations of, and reactions to, behaviors and attitudes that are matters of concern and should change (De Leon 2000b).

In substance abuse treatment counseling, some tension always is felt between being empathic and supportive, and having to handle minimization, evasion, dishonesty, and denial. However, a counselor can be empathic and firm at the same time. This is especially true when working with clients with COD. The heart of confrontation is not the aggressive breaking down of the client and his or her defenses, but feedback on behavior and the compelling appeal to the client for personal honesty, truthfulness in interacting with others, and responsible behavior. A straightforward and factual presentation of conflicting material or of problematic behavior in an inquisitive and caring manner can be both “confrontative” and caring. The ability to do this well and with balance often is critical in maintaining the therapeutic alliance with a client who has COD. Chapter 6 includes a more complete discussion of confrontation including a definition, description of its application, and suggested modifications for using this technique with clients who have COD.

Employ Culturally Appropriate Methods

Understanding the client’s cultural background

It is well known that population shifts are resulting in increasing numbers of minority racial and ethnic groups in the United States. Each geographic area has its own cultural mix, and providers are advised to learn as much as possible about the cultures represented in their treatment populations. Of particular importance are the backgrounds of those served, conventions of interpersonal communication, understanding of healing, views of mental disorder, and perception of substance abuse.

To work effectively with persons of various cultural groups, the provider should learn as much as possible about characteristics of the cultural group such as communication style, interpersonal interactions, and expectations of family. For example, some cultures may tend to somaticize symptoms of mental disorders, and clients from such groups may expect the clinician to offer relief for physical complaints. The same client may be offended by too many probing, personal questions early in treatment and never return. Similarly, understanding the client’s role in the family and its cultural significance always is important (e.g., expectations of the oldest son, a daughter’s responsibilities to her parents, grandmother as matriarch).

At the same time, the clinician should not make assumptions about any client based on his or her perception of the client’s culture. The level of acculturation and the specific experiences of an individual may result in that person identifying with the dominant culture, or even other cultures. For example, a person from India adopted by American parents at an early age may know little about the cultural practices in his birth country. For such clients, it is still important to recognize the birth country and discover what this association means to the client; however, it may exert little influence on his beliefs and practices. For more detailed information about cultural issues in substance abuse treatment, see the forthcoming TIP Improving Cultural Competence in Substance Abuse Treatment.

Clients’ perceptions of substance abuse, mental disorders, and healing

Clients may have culturally driven concepts of what it means to abuse substances or to have a mental disorder, what causes these disorders, and how they may be “cured.” Clinicians are encouraged to explore these concepts with people who are familiar with the cultures represented in their client population. Counselors should be alert to differences in how their role and the healing process are perceived by persons who are of cultures other than their own.

Cultural perceptions and diagnosis

It is important to be aware of cultural and ethnic bias in diagnosis. For example, in the past some African Americans were stereotyped as having paranoid personality disorders, while women have been diagnosed frequently as being histrionic. American Indians with spiritual visions have been misdiagnosed as delusional or as having borderline or schizotypal personality disorders. Some clinicians would be likely to over diagnose obsessive-compulsive disorder among Germans or histrionic disorder in Hispanic/Latino populations. The diagnostic criteria should be tempered by sensitivity to cultural differences in behavior and emotional ing and to be “viewed by clinical staff as suffering from more severe and persistent symptomatology and as having lower psychosocial functioning.” Researchers noted “this was due in part to the chronicity of their mental disorders and persistent substance abuse, but also was magnified by cross-cultural misperceptions; for example, system bias, countertransference, or inadequate support systems” (Jerrell and Wilson 1997, p. 138).

The study also found that nonwhite clients tended to have fewer community resources available to them than white clients, and that clinicians had more difficulty connecting them with needed services. For example, staff members experienced “extraordinary difficulties in identifying willing and suitable sponsors for the young ethnic clients” in 12-Step programs (Jerrell and Wilson 1997, p. 138). To address such issues, researchers stressed the importance of developing cultural competence in staff, giving extra attention to the needs of such clients, and engaging in “more active advocacy for needed, culturally relevant services” (Jerrell and Wilson 1997, p. 139).

Increase Structure and Support

To assist clients with COD, counselors should provide an optimal amount of structure for the individual. Free time is both a trigger for substance use cravings and a negative influence for many individuals with mental disorders; therefore it is a particular issue for clients with COD. Strategies for managing free time include structuring one’s day to have meaningful activities and to avoid activities that will be risky. Clinicians often help clients to plan their time (especially weekends). Creating new pleasurable activities can both help depression and help derive “highs” from sources other than substance use. Other important activities to include are working on vocational and relationship issues.

In addition to structure, it is also important that the daily activities contain opportunities for receiving support and encouragement. Counselors should work with clients to create a healthy support system of friends, family, and activities. Increasing support, time organization, and structured activities are strategies in cognitive–behavioral therapies (see section below) for both mental disorders and substance abuse treatment.

Techniques for Working With Clients With COD

The following section reviews techniques, mainly from the substance abuse field, that have been found to be particularly helpful in the treatment of clients with substance abuse and that are being adapted for work with clients with COD (see text box below).

Provide Motivational Enhancement Consistent With the Client’s Specific Stage of Change

Definition and description

Motivational Interviewing (MI) is a “client-centered, directive method for enhancing intrinsic motivation to change by exploring and resolving ambivalence” (Miller and Rollnick 2002, p. 25). MI has proven effective in helping clients clarify goals and make commitment to change (CSAT 1999b; Miller 1996; Miller and Rollnick 2002; Rollnick and Miller 1995). This approach shows so much promise that it is one of the first two psychosocial treatments being sponsored in multisite trials in the National Institute on Drug Abuse (NIDA) Clinical Trials Network program.

As Miller and Rollnick have pointed out, MI is “a way of being with a client, not just a set of techniques for doing counseling” (Miller and Rollnick 1991, p. 62). This approach involves accepting a client’s level of motivation, whatever it is, as the only possible starting point for change. For example, if a client says she has no interest in changing her drinking amounts or frequency, but only is interested in complying with the interview to be eligible for something else (such as the right to return to work or a housing voucher), the clinician would avoid argumentation or confrontation in favor of establishing a positive rapport with the client—even remarking on the positive aspect of the client wishing to return to work or taking care of herself by obtaining housing. The clinician would seek to probe the areas in which the client does have motivation to change. The clinician is interested in eventually having an impact on the client’s drinking or drug use, but the strategy is to get to that point by working with available openings.

A variety of adaptations of MI have emerged. Examples include brief negotiation, motivational consulting, and motivational enhancement therapy (MET). MET combines the clinical style associated with MI with systematic feedback of assessment results in the hope of producing rapid, internally motivated change. For more information, see the Project MATCH Motivational Enhancement Therapy Manual (National Institute on Alcohol Abuse and Alcoholism 1994). Rollnick and other practitioners of MI find that the many variants differ widely in their reliance on the key principles and elements of MI (Miller and Rollnick 2002).

Guiding principles of motivational interviewing

The four principles outlined below guide the practice of MI (see text box p. 114). In this section, each principle is summarized. For each principle, some of the related strategies that practitioners use when applying this principle to client interactions are highlighted.

1. Expressing empathy

Miller and Rollnick state that “an empathic counseling style is one fundamental and defining characteristic of motivational interviewing” (Miller and Rollnick 2002, p. 37). The counselor refrains from judging the client; instead, through respectful, reflective listening, the counselor projects an attitude of acceptance. This acceptance of the person’s perspectives does not imply agreement. It “does not prohibit the counselor from differing with the client’s views and expressing that divergence” (Miller and Rollnick 2002, p. 37). It simply accepts the individual’s ambivalence to change as normal and expected behavior in the human family. Practitioners find that projecting acceptance rather than censure helps free the client to change (Miller and Rollnick 2002).

2. Developing discrepancies

While recognizing the client’s ambivalence to change as normal, the counselor is not neutral or ambivalent about the need for change. The counselor advances the cause of change not by insisting on it, but by helping the client perceive the discrepancy between the current situation and the client’s personal goals (such as a supportive family, successful employment, and good health). The task of the counselor is to call attention to this discrepancy between “the present state of affairs and how one wants it to be,” making it even more significant and larger in the client’s eyes. The client is therefore more likely to change, because he sees that the current behavior is impeding progress to his goals—not the counselor’s (Miller and Rollnick 2002, p. 39).

3. Rolling with resistance

Practitioners believe that “the least desirable situation, from the standpoint of evoking change, is for the counselor to advocate for change while the client argues against it” (Miller and Rollnick 2002, p. 39). The desired situation is for clients themselves to make the argument for change. Therefore, when resistance is encountered, the counselor does not oppose it outright. Instead, the counselor offers new information and alternative perspectives, giving the client respectful permission to “take what you want and leave the rest” (Miller and Rollnick 2002, p. 40).

The counselor’s response to resistance can defuse or inflame it.

4. Supporting self-efficacy

The final principle of Motivational Interviewing recognizes that an individual must believe he or she actually can make a change before attempting to do so. Therefore, the counselor offers support for the change and communicates to the client a strong sense that change is possible. Self-efficacy also can be enhanced through the use of peer role models, as well as by pointing out past and present evidence of the client’s capacity for change.

One way practitioners put this principle into action is by evoking “confidence talk” in which the client is invited to share “ideas, experiences, and perceptions that are consistent with ability to change” (Miller and Rollnick 2002, p. 113). This could involve reviewing past successes, discussing specific steps for making change happen, identifying personal strengths, and acknowledging sources of support.

“Change talk”

Clients’ positive remarks about change, or “change talk,” are the opposite of resistance. The counselor responds to any expression of desire to change with interest and encourages the client to elaborate on the statement. For example in a person with combined alcohol dependence and PTSD, the clinician might ask, “What are some other reasons why you might want to make a change?” (Miller and Rollnick 2002, p. 87). The counselor also can use reflective listening to clarify the client’s meaning and explore what is being said. It is important, however, to do this in a way that does not appear to be taking a side in the argument. This sometimes results in resistance and the client may begin to argue with the counselor instead of continuing to think about change.

“Decisional balance”

Practitioners of MI have coined the term “decisional balance” to describe a way of looking at ambivalence. Picture a seesaw, with the costs of the status quo and the benefits of change on one side, and the costs of change and the benefits of the status quo on the other (Miller and Rollnick 2002). The counselor’s role is to explore the costs and benefits of substance use with the aim of tipping the balance toward change. That change will be stronger and more likely to endure if it is owned by the client’s perception that the benefits of change are greater than the costs.

Matching motivational strategies to the client’s stage of change

The motivational strategies selected should be consistent with the client’s stage of change (summarized in Figure 5-1, p. 116). Clients could be at one stage of recovery or change for the mental disorder and another for the substance use disorder; to complicate things further, a client may be at one stage of change for one substance and another stage of change for another substance. For example, a client with combined alcohol and cocaine dependence with co-occurring panic disorder may be in the contemplation stage (i.e., aware that a problem exists and considering overcoming it, but not committed to taking action) in regard to alcohol, precontemplation (i.e., unaware that a problem exists, with no intention of changing behavior) in regard to cocaine, and action (i.e., actively modifying behavior, experiences, or environment to overcome the problem) for the panic disorder.

In each case, the clinician examines the internal and external leverage available to move the client toward healthy change. For example, a client may want to talk about her marriage, but not about the substance abuse problem. The clinician can use this as an opening; the marriage doubtless will be affected by the substance abuse, and the motivation to improve the marriage may lead to a focus on substance abuse. Evaluating a client’s motivational state necessarily is an ongoing process. It should be recognized that court mandates, rules for clients engaged in group therapy, the treatment agency’s operating restrictions, or other factors may place some barriers on how this strategy is implemented in particular situations.

Although MI is a well-accepted and commonly used strategy in the substance abuse treatment field, the issue of when it is appropriate to avoid or postpone addressing the client’s substance use is the subject of some debate. MI does make a distinction between agreeing with a client’s denial system (which is counterproductive) and sidestepping it in order to make some progress. As shown above, these motivational strategies are employed to help both clinician and client work together toward the common goal of helping the client. With practice and experience, the clinician will come to recognize when to sidestep disagreements and pursue MI and when to move forward with traditional methods with clients who are motivated sufficiently and ready for change. The details of these strategies and techniques are presented in TIP 35 (CSAT 1999b) and in Miller and Rollnick 2002.

Motivational interviewing and co-occurring disorders

Approaches based on MI have been adapted for people with COD with some initial evidence of efficacy for improved treatment engagement. In a sample of 100 inpatient clients with COD from a large university hospital, Daley and Zuckoff (1998, p. 472) found that with only one “motivational therapy” session prior to hospital discharge, “...the show rate for the initial outpatient appointment almost doubled, increasing from 35 percent to 67 percent.” In this study MI approaches were modified to focus on contrasting the goals and methods of hospital and outpatient treatment. Also, the client was invited to consider the advantages and challenges of continuing in outpatient treatment. Daley and Zuckoff’s results are relevant for people in most quadrants (see chapters 2 and 3), as the majority of their clientele are described as “public sector clients who have mood, anxiety, personality, or psychotic disorders combined with alcohol, cocaine, heroin, sedative hypnotic, cannabis, or polysubstance use disorders.”

Strategies for Working With Clients With Co-Occurring Disorders

Swanson and colleagues (1999) modified MI techniques by increasing the amount of discussion of the client’s perception of the problem and his understanding of his clinical condition. Of the 121 study participants who were selected from psychiatric inpatients at two inner-city hospitals, 93 had concomitant substance use disorders. Participants were assigned randomly to either standard treatment or standard treatment with the addition of a motivational interview. The MI focused on exploring the clients’ commitment to treatment, plans for continuing care, and understanding of their role in their own recovery.

Essentially, the therapists were attempting to elicit a motivational statement that indicated the clients’ commitment to treatment. The authors found that, whether considering the entire sample or only those with COD, study participants who received the MI were significantly more likely to attend an initial outpatient treatment session.

A Brief Overview of   Specific Mental

Disorders and Cross-Cutting Issues


This chapter provides a brief overview for working with substance abuse treatment clients who also have specific mental disorders. It is presented in concise form so that the counselor can refer to this one chapter to obtain basic information. Appendix D contains more indepth information on suicidality, nicotine dependence, and each of the disorders addressed in this chapter. The material included is not a complete review of all disorders in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), but updates the material from TIP 9 (Center for Substance Abuse Treatment 1994a) (i.e., personality disorders, mood disorders, anxiety disorders, and psychotic disorders), adding other mental disorders with special relevance to co-occurring disorders (COD) not covered in TIP 9 (i.e., attention deficit/hyperactivity disorder, posttraumatic stress disorder, eating disorders, and pathological gambling). The consensus panel acknowledges that people with COD may have multiple combinations of the various mental disorders presented in this chapter (e.g., a person with a substance use disorder, schizophrenia, and a pathological gambling problem). However, for purposes of clarity and brevity the panel chose to focus the discussion on the main disorders and not explore the multitude of possible combinations.

While suicidality is not a DSM-IV diagnosed mental disorder per se, it is a high-risk behavior associated with COD. Nicotine dependency is recognized as a disorder in DSMIV, and as such a client with nicotine dependency and a mental disorder could be considered to have a co-occurring disorder. Though this is the case, an important difference between tobacco addiction and other addictions is that tobacco’s chief effects are medical rather than behavioral, and, as such, it is not conceptualized and presented as a typical co-occurring addiction disorder. However, because of the high proportion of the COD population addicted to nicotine, as well as the devastating health consequences of tobacco use, nicotine dependency is treated as an important cross-cutting issue for people with substance use disorders and mental illness.

The discussions of suicidality and nicotine dependency highlight key information counselors should know about that disorder in combination with substance abuse. This section offers factual information (e.g., prevalence data), commonly agreed-upon clinical practices, and other general information that may be best characterized as “working formulations.”

A brief description of selected disorders and their diagnostic criteria follows. This material has been extracted from DSM-IV-TR (Text Revision, American Psychiatric Association [APA] 2000) and highlights the descriptive features, diagnostic features, and symptom clusters of each mental disorder. The consensus panel elected to take this material directly from DSM-IV-TR to provide easy access to the material that is not typically available in the substance abuse treatment field. Use of a specialized dictionary that includes terminology related to mental disorders may be needed to understand terms in the quoted material from DSM-IV-TR, though the main features of each disorder should still be clear.

Because of the greater availability of case histories from the mental health literature, the illustrative material in the next section has a greater emphasis on the mental disorder. Wherever possible case histories were selected to illustrate the interaction of the mental and substance use disorders. Finally, each section contains an Advice to the Counselor box.

The consensus panel recognizes that no one chapter can replace the comprehensive training necessary for diagnosing and treating clients with specific mental disorders cooccurring with substance use disorders and that the Advice to the Counselor understates the complexity involved in treating clients with these disorders. The Advice to the Counselor boxes are designed to distill for the counselor the main actions and approaches that they can take in working with substance abuse treatment clients who have the specific mental disorder being discussed (see the table of contents for a full listing of these boxes throughout the TIP).

The consensus panel also recognizes the chapter cannot possibly cover each mental disorder exhaustively and that addiction counselors are not expected to diagnose mental disorders. The limited goals of the panel in providing this material are to increase substance abuse treatment counselors’ familiarity with mental disorders terminology and criteria, as well as to provide advice on how to proceed with clients who demonstrate these disorders. It is also the purpose of this chapter and appendix D to stimulate further work in this area and to make this research accessible to the addiction field.

Cross-Cutting Issues


Suicidality is not a mental disorder in and of itself, but rather a high-risk behavior associated with COD, especially (though not limited to) serious mood disorders. Research shows that most people who kill themselves have a diagnosable mental or substance use disorder or both, and that the majority of them have depressive illness. Studies indicate that the most promising way to prevent suicide and suicidal behavior is through the early recognition and treatment of substance abuse and mental illnesses. This is especially true of clients who have serious depression (U.S. Public Health Service 1999). Substanceinduced or exacerbated suicidal ideations, intentions, and behaviors are an ever-present possible complication of substance use disorders, especially for clients with co-occurring mental disorders.

The topic of suicidality is critical for substance abuse treatment counselors working with clients with COD. Substance use disorders alone increase suicidality, while the added presence of some mental disorders doubles an already heightened risk. Counselors should be aware that the risk of suicide is greatest when relapse occurs after a substantial period of abstinence— especially if there is concurrent financial or psychosocial loss. Every agency that offers counseling for substance abuse also must have a clear protocol in place that addresses the recognition and treatment (or referral) of persons who may be s

Nicotine Dependence

In 2003 an estimated 29.8 percent of the general population aged 12 or older report current (past month) use of a tobacco product (National Survey on Drug Use and Health 2003c). The latest report of the Surgeon General on the Health Consequences of Smoking (U.S. Public Health Service Office of the Surgeon General 2004) provides a startling picture of the damage caused by tobacco. Tobacco smoking injures almost every organ in the body, causes many diseases, reduces health in general, and leads to reduced life span and death. Tobacco dependence also has serious consequences to nonsmokers through environmental tobacco smoke (secondhand smoke) and the negative effects on unborn children. Fortunately quitting smoking has immediate as well as longterm benefits (U.S. Public Health Service Office of the Surgeon General 2004).

Evidence suggests that people with mental disorders and/or dependency on other drugs are more likely to have a tobacco addiction. In fact, most people with a mental illness or another addiction are tobacco dependent— about 50 to 95 percent, depending on the subgroup (Anthony and Echeagaray-Wagner 2000; Centers for Disease Control and Prevention 2001; National Institute on Drug Abuse 1999a; Richter 2001; Stark and Campbell 1993b). Smokers with mental disorders consume nearly half of all the cigarettes sold in the United States (Lasser et al. 2000). A study of individuals doing well in recovery from alcohol dependence found that those who smoked lived 12 fewer years because of their tobacco dependence and the quality of their lives was affected by other tobaccocaused medical illnesses (Hurt et al. 1996).

There is increasing recognition of the importance of integrating tobacco dependence treatment and management into mental health services and addiction treatment settings. Although tobacco dependence treatment works for smokers with mental illness and other addictions, only recently have clinicians been given training to address this serious public health and addiction treatment concern. It is increasingly recognized that all clients deserve access to effective treatments for tobacco addiction, and that smokers and their families should be educated about the considerable risks of smoking as well as the benefits of tobacco dependence treatment. All current tobacco dependence clinical practice guidelines strongly recommend addressing tobacco during any clinical contact with smokers and suggest the use of one or more of the six Food and Drug Administration (FDA)approved medications as first-line treatments (e.g., bupropion SR/zyban and the nicotine patch, gum, nasal spray, inhaler, and lozenge).

Tobacco use and dependence should be assessed and documented in all clinical baseline assessments, treatment plans, and treatment efforts. A motivation-based treatment model allows for a wider range of treatment goals and interventions that match the patient’s motivation to change. Like other addictions, tobacco dependence is a chronic disease that may require multiple treatment attempts for many individuals and there is a range of effective clinical interventions, including medications, patient/family education, and stage-based psychosocial treatments. Recent evidence-based treatment guidelines have been published for the management of tobacco dependence and this information can be a primary guide for addressing tobacco. Few recognize how ignoring tobacco perpetuates the stigma associated with mental illness and addiction when some ask, “Why should tobacco be addressed in mental health or addiction settings?” or “Other than increased morbidity and mortality, why should we encourage and help this group to quit?” or “What else are they going to do if they cannot smoke?”

What counselors should know about nicotine dependence

• Tobacco dependence is common in clients with other substance use disorders and mental illnesses.
•Like patients in primary care settings, clients in mental health services and addiction treatment settings should be screened for tobacco use and encouraged to quit.
•The U.S. Public Health Service Guidelines encourage the use of the “5 A’s” (Ask, Advise, Assess, Assist, Arrange Followup) as an easy road map to guide clinicians to help their patients who smoke:

  1. Ask about tobacco use and document in chart.
  2. Advise to quit in a clear, strong, and   personal message. 
  3. Assess willingness to make a quit attempt and consider motivational interventions for the lower motivated and assist those ready to quit.
  4. Assist in a quit attempt by providing practical counseling, setting a quit date, helping them to anticipate the challenges they will face, recommending the use of tobacco dependence treatment medications, and discussing options for psychosocial treatment, including individual, group, telephone, and Internet counseling options.
  5. Arrange followup to enhance motiva­tion, support success, manage relapses, and assess medication use and the need for more intensive treatment if necessary.

•Assessment of tobacco use includes assessing the amount and type of tobacco products used (cigarettes, cigars, chew, snuff, etc.), current motivation to quit, prior quit attempts (what treatment, how long abstinent, and why relapsed), withdrawal symptoms, common triggers, social supports and barriers, and preference for treatment.
•Behavioral health professionals already have many of the skills necessary to provide tobacco dependence psychosocial interventions.
•Smokers with mental illness and/or another addiction can quit with basic tobacco dependence treatment, but may also require motivational interventions and treatment approaches that integrate medications and psychosocial treatments.
•Tobacco treatment is cost-effective, feasible, and draws on principles of addictions and co-occurring disorders treatment.
•The current U.S. Clinical Practice Guidelines indicate that all patients trying to quit smoking should use first-line pharmacotherapy, except in cases where there may be contraindications (Fiore 2000).
•Currently there are six FDA-approved treatments for tobacco dependence treatment: bupropion SR and five Nicotine Replacement Treatments (NRTs): nicotine polacrilex (gum), nicotine transdermal patch, nicotine inhaler, nicotine nasal spray, and nicotine lozenge.•Tobacco treatment medications are effective even in the absence of psychosocial treatments, but adding psychosocial treatments to medications enhances outcomes by at least 50 percent.
•Specific coping skills should be addressed to help smokers with mental or substance use disorders to cope with cravings associated with smoking cues in treatment settings where smoking is likely to be ubiquitous.
•When clients with serious mental illnesses attempt to quit smoking, watch for changes in mental status, medication side effects, and the need to lower some psychiatric medication dosages due to tobacco smoke interaction.

Personality Disorders  

These are the disorders seen most commonly by addiction counselors and in quadrant II substance abuse treatment settings. Personality disorders (PDs) are rigid, inflexible, and maladaptive behavior patterns of sufficient severity to cause internal distress or significant impairment in functioning. PDs are enduring and persistent styles of behavior and thought, rather than rare or unusual events in someone’s life. Furthermore, rather than showing these thoughts and behaviors in response to a particular set of circumstances or particular stressors, people with PDs carry with them these destructive patterns of thinking, feeling, and behaving as their way of being and interacting with the world and others.

Those who have PDs tend to have difficulty forming a genuinely positive therapeutic alliance. They tend to frame reality in terms of their own needs and perceptions and not to understand the perspectives of others. Also, most clients with PDs tend to be limited in terms of their ability to receive, accept, or benefit from corrective feedback.

A further difficulty is the strong countertransference clinicians can have in working with these clients, who are adept at “pulling others’ chains” in a variety of ways. Specific concerns will, however, vary according to the specific PD and other individual circumstances.

Borderline Personality Disorder

What counselors should know about substance abuse and borderline personality disorders

The essential feature of borderline personality disorder (BPD) is a pervasive pattern of instability of interpersonal relationships, self-image, and affects, along with marked impulsivity,that begins by early adulthood and is present in a variety of contexts. Counselors should be aware that
•People with BPD may use drugs in a variety of ways and settings.
•At the beginning of a crisis episode, a client with this disorder might take a drink or a different drug in an attempt to quell the growing sense of tension or loss of control.
•People with BPD may well use the same drugs of choice, route of administration, and frequency as the individuals with whom they are interacting.

  1. People with BPD often use substances in idiosyncratic and unpredictable patterns.
Polydrug use is common, which may involve alcohol and other sedative-hypnotics
  1. taken for self-medication.
  2. Individuals with BPD often are skilled in seeking multiple sources of medication that they favor, such as benzodiazepines. Once they are prescribed this medication in a mental health system, they may demand to be continued on the medication to avoid dangerous withdrawal.

Antisocial Personality Disorder

The two essential features of antisocial personality disorder (APD) are: (1) a pervasive disregard for and violation of the rights of others, and (2) an inability to form meaningful interpersonal relationships.

What counselors should know about substance abuse and APD

The prevalence of antisocial personality disorder and substance abuse is high:
•Much of substance abuse treatment is particularly targeted to those with APD, and substance abuse treatment alone has been particularly effective for these disorders.
•The majority of people with substance use disorders are not sociopathic except as a result of their addiction.
•Most people diagnosed as having APD are not true psychopaths—that is, predators who use manipulation, intimidation, and violence to control others and to satisfy their own needs.
•Many people with APD use substances in a polydrug pattern involving alcohol, marijuana, heroin, cocaine, and methamphetamine.
•People with APD may be excited by the illegal drug culture and may have considerable pride in their ability to thrive in the face of the dangers of that culture. They often are in trouble with the law. Those who are more effective may limit themselves to exploitative or manipulative behaviors that do not make them as vulnerable to criminal sanctions.

Case study: counseling a substance abuse treatment client with antisocial personality disorder

Mark R., a Hispanic/Latino male, was 27 years old when he was arrested for driving while intoxicated. Mark R. presented himself to the court counselor for evaluation of the possible need for substance abuse treatment. Mark R. was on time for the appointment and was slightly irritated at having to wait 20 minutes due to the counselor’s schedule. Mark R. was wearing a suit (which had seen better days) and was trying to present himself in a positive light.

Mark R. denied any “problems with alcohol” and reported having “smoked some pot as a kid.” He denied any history of suicidal thinking or behavior except for a short period following his arrest. He acknowledged that he did have a “bit of a temper” and that he took pride in the ability to “kick ass and take names” when the situation required. Mark R. denied any childhood trauma and described his mother as a “saint.” He described his father as “a real jerk” and refused to give any other information.

In describing the situation that preceded his arrest, Mark R. tended to see himself as the victim, using statements such as “The bartender should not have let me drink so much,” “I wasn’t driving that bad,” and “The cop had it in for me.” Mark R. tended to minimize his own responsibility throughout the interview. Mark R. had been married once but only briefly. His only comment about the marriage was, “She talked me into it but I got even with her.” Mark R. has no children and lives alone in a studio apartment. Mark R. has attended two meetings of Alcoholics Anonymous (AA) “a couple of years ago before I learned how to control my drinking.”

The counselor coordinates closely with the parole officer and arranges several three-way meetings. He carefully reviews details of the court contract and conditions of parole and keeps court records up to date. His work with Mark R. centers on clarifying expectations.

Discussion. It is likely that Mark R. has antisocial personality disorder. Clients with this disorder usually are very hard to engage in individual treatment and are best managed through strict limits with clear consequences. With such an individual, it is important to maximize the interaction with the court, parole officers, or other legal limit setters. This enforces the limits of treatment, and prevents the client from criticizing and blaming one agency representative to the other.

People with this disorder are best managed in group treatment that addresses both their substance abuse and antisocial personality disorder. In such groups the approach is to hold the clients responsible for their behavior and its consequences and to confront dishonest and antisocial behavior directly and firmly and stress immediate learning experiences that teach corrective responses. It is important to differentiate true antisocial personality from substance-related antisocial behavior. This can best be done by looking at how the person relates to others throughout the course of his or her life. Persons with this disorder will have evidence of antisocial behavior preceding substance use and even during periods of enforced abstinence. It also is important to recognize that people with substance-related antisocial behavior may be more likely to have major depression than other typical personality disorders. However, the type and character of depressions that may be experienced by those with true APD have been less well characterized, and their treatment is unclear.

Mood Disorders and Anxiety Disorders

Because of the striking similarities in understanding and serving clients with mood and anxiety disorders, the sections have been combined to address both disorders. (It should be noted, however, that two disorder types are separated in DSM-IV-TR [APA 2000].)
What Counselors Should Know About Mood and Anxiety Disorders and Substance Abuse

Counselors should be aware of the following:

•Approximately one quarter of United States residents are likely to have some anxiety disorder during their lifetime, and the prevalence is higher among women than men.
•About one half of individuals with a substance use disorder have an affective or anxiety disorder at some time in their lives.
•Among women with a substance use disorder, mood disorders may be prevalent. Women are more likely than men to be clinically depressed and/or to have posttraumatic stress disorder.
•Certain populations are at risk for anxiety and mood disorders (e.g., clients with HIV, clients maintained on methadone, and older adults).
•Older adults may be the group at highest risk for combined mood disorder and substance problems. Episodes of mood disturbance generally increase in frequency with age. Older adults with concurrent mood and substance use disorders tend to have more mood episodes as they get older, even when their substance use is controlled.
•Both substance use and discontinuance may be associated with depressive symptoms.
•Acute manic symptoms may be induced or mimicked by intoxication with stimulants, steroids, hallucinogens, or polydrug combinations.
•Withdrawal from depressants, opioids, and stimulants invariably includes potent anxiety symptoms. During the first months of sobriety, many people with substance use disorders may exhibit symptoms of depression that fade over time and that are related to acute withdrawal.
•Medical problems and medications can produce symptoms of anxiety and mood disorders. About a quarter of individuals who have chronic or serious general medical conditions, such as diabetes or stroke, develop major depressive disorder.
•People with co-occurring mood or anxiety disorders and a substance use disorder typically use a variety of drugs.
•Though there may be some preference for those with depression to favor stimulation and those with anxieties to favor sedation, there appears to be considerable overlap. The use of alcohol, perhaps because of its availability and legality, is ubiquitous.
•It is now believed that substance use is more often a cause of anxiety symptoms rather than an effort to cure these symptoms.
•Since mood and anxiety symptoms may result from substance use disorders, not an underlying mental disorder, careful and continuous assessment is essential.

Schizophrenia and Other Psychotic Disorders

What Counselors Should Know About Substance Abuse and Psychotic Disorders

There are different types of psychotic disorders or disorders that have psychotic features. Schizophrenia, a relatively common type of psychotic disorder, is featured in this section.
Counselors should be aware of the following:

• There is evidence of increasing use of alcohol and drugs by persons with schizophrenia (from 14 to 22 percent in the 1960s and 1970s
•There is no clear pattern of drug choice among clients with schizophrenia. Instead, it is likely that whatever substances happen to be available or in vogue will be the substances used most typically.
•What looks like resistance or denial may in reality be a manifestation of negative symptoms of schizophrenia.
•An accurate understanding of the role of substance use disorders in the client’s psychosis requires a multiple-contact, longitudinal assessment.
•Clients with a co-occurring mental disorder involving psychosis have a higher risk for self-destructive and violent behaviors.
•Clients with a co-occurring mental disorder involving psychosis are particularly vulnerable to homelessness, housing instability, victimization, poor nutrition, and inadequate financial resources.
•Both psychotic and substance use disorders tend to be chronic disorders with multiple relapses and remissions, supporting the need for long-term treatment. For clients with co-occurring disorders involving psychosis, a long-term approach is imperative.
It is important that the program philosophy be based on a multidisciplinary team approach. Ideally, team members should be cross-trained, and there should be representatives from the medical, mental health, and addiction systems. The overall goals of long-term management should include (1) providing comprehensive and integrated services for both the mental and substance use disorders, and (2) doing so with a long-term focus that addresses biopsychosocial issues in accord with a treatment plan with goals specific to a client’s situation.

Attention Deficit/ Hyperactivity Disorder (AD/HD)

What Counselors Should Know About Substance Abuse and AD/HD

The essential feature of AD/HD is a persistent pattern of inattention and/or hyperactivityimpulsivity that is displayed more frequently and more serious than is observed typically in individuals at a comparable level of development (APA 2000). Counselors should be aware of the following:
•Studies of the adult substance abuse treatment population have found AD/HD in 5 to 25 percent of persons (Clure et al. 1999; King et al. 1999; Levin et al. 1998; Schubiner et al. 2000; Weiss et al. 1998).

•Approximately one third of adults with AD/HD have histories of alcohol abuse or dependence, and approximately one in five has other drug abuse or dependence histories.
•Adults with AD/HD have been found primarily to use alcohol, with marijuana being the second most common drug of abuse.
•The history of a typical AD/HD substance abuse treatment client may show early school problems before substance abuse began.
•The client may use self-medication for AD/HD as an excuse for drug use.
•The most common attention problems in substance abuse treatment populations are secondary to short-term toxic effects of substances, and these should be substantially better with each month of sobriety.
•The presence of AD/HD complicates the treatment of substance abuse, since clients with these COD may have more difficulty engaging in treatment and learning abstinence skills, be at greater risk for relapse, and have poorer substance use outcomes.

Posttraumatic Stress Disorder (PTSD)

What Counselors Should Know About Substance Abuse and PTSD

PTSD is classified in DSM-IV-TR as one type of anxiety disorder. It is treated separately in this TIP because of its special relationship to substance abuse and the growing literature on PTSD and its treatment. The essential feature of PTSD is the development of characteristic symptoms following exposure to an extreme traumatic stressor involving direct personal experience of an event that involves actual or threatened death or serious injury, or other threat to one’s physical integrity; or witnessing an event that involves death, injury, or a threat to the physical integrity of another person; or learning about unexpected or violent death, serious harm, or threat of death or injury experienced by a family member or other close associate (APA 2000, p. 463). Counselors should be aware that

•The lifetime prevalence of PTSD among adults in the United States is about 8 percent.
•Among high-risk individuals (those who have survived rape, military combat, and captivity or ethnically or politically motivated internment and genocide), the proportion of those with PTSD ranges from one-third to one-half.
•Among clients in substance abuse treatment, PTSD is two to three times more common in women than in men.
•The rate of PTSD among people with substance use disorders is 12 to 34 percent; for women with substance use disorders, it is 30 to 59 percent (Brown and Wolfe 1994).
•Women with substance abuse problems report a lifetime history of physical and/or sexual abuse ranging from 55 to 99 percent (Najavits et al. 1997).
•Most women with this co-occurring disorder experienced childhood physical and/or sexual abuse; men with both disorders typically experienced crime victimization or war trauma.
•Clinicians are advised not to overlook the possibility of PTSD in men.
•People with PTSD and substance abuse are more likely to experience further trauma than people with substance abuse alone.
•Because repeated trauma is common in domestic violence, child abuse, and some substance-using lifestyles (e.g., the drug trade), helping the client protect against future trauma may be an important part of work in treatment.
•People with PTSD tend to abuse the most serious substances (cocaine and opioids); however, abuse of prescription medications, marijuana, and alcohol also are common.
•From the client’s perspective, PTSD symptoms are a common trigger for substance use.
•While under the influence of substances, a person may be more vulnerable to trauma—for example, a woman drinking at a bar may go home with a stranger and be assaulted.
•As a counselor, it is important to recognize, and help clients understand, that becoming abstinent from substances does not resolve PTSD; both disorders must be addressed in treatment.

Eating Disorders

What Counselors Should Know About Substance Abuse and Eating Disorders

The essential features of anorexia nervosa are that the individual refuses to maintain a minimal normal body weight, is intensely afraid of gaining weight, and exhibits a significant disturbance in the perception of the shape or size of his or her body. The essential features of bulimia nervosa are binge eating and inappropriate compensatory methods to prevent weight gain. In dealing with persons who have either disorder, counselors should be aware of the following:

  1. The prevalence of bulimia nervosa is elevated in women presenting for substance abuse treatment.
  2. Studies of individuals in inpa­tient substance abuse treatment centers (as assessed via questionnaire) suggest that approximately 15 percent of women and 1 percent of men had a DSMIII-R eating disorder (primarily bulimia nervosa) in their lifetime (Hudson et al. 1992).
  3. Substance abuse is more com­mon in bulimia nervosa than in anorexia nervosa.
  4. Individuals with eating disor­ders are significantly more likely to use stimulants and significantly less likely to use opioids than other individuals undergoing substance abuse treatment who do not have a co-occurring eating disorder.
  5. Many individuals alternate between substance abuse and eating disorders.
  6. Alcohol and drugs such as mari­juana can disinhibit appetite (i.e., remove normal restraints on eating) and increase the risk of binge eating as well as relapse in individuals with bulimia nervosa.
  • Individuals with eating disor­ders experience craving, tolerance, and withdrawal from drugs associated with purging, such as laxatives and diuretics.
  • Women with eating disorders often abuse pharmacological agents ingested for the purpose of weight loss, appetite suppression, and purging. Among these drugs are prescription and over-the-counter diet pills, laxatives, diuretics, and emetics. Nicotine and caffeine also must be considered when assessing substance abuse in women with eating disorders.
  • Several studies have suggested that the pres­ence of co-occurring substance-related disorders does not affect treatment outcome adversely for bulimia nervosa.
  • Further studies are required to assess how the presence of an eating disorder affects substance abuse treatment and how best to integrate treatment for those with both conditions. This condition is quite serious and can be fatal. Treat it accordingly.
  • Individuals with eating disorders experience urges (or cravings) for binge foods similar to urges for drugs.

Pathological Gambling  

What Counselors Should Know About Substance Abuse and Pathological Gambling

The essential feature of pathological gambling is persistent and recurrent maladaptive gambling behavior that disrupts personal, family, or vocational pursuits. Counselors should be aware that

•Prevalence data for gambling regularly makes distinctions among “pathological” gamblers (the most severe category) and levels of “problem” gambling (less severe to moderate levels of difficulty). Recent general estimates (Gerstein et al. 1999; Shaffer et al. 1997) indicate about 1 percent of the U.S. general population could be classified as having pathological gambling, according to the diagnostic criteria below. Cogent considerations regarding prevalence are given in the DSM-IV-TR regarding variations due to the availability of gambling and seemingly greater rates in certain locations (e.g., Puerto Rico, Australia), which have been reported to be as high as 7 percent. Higher prevalence rates also have been reported in adolescents and college students, ranging from 2.8 to 8 percent (APA 2000). The general past-year estimate for pathological and problem gambling combined is roughly 3 percent. This can be compared to past year estimates of alcohol abuse/dependence of 9.7 percent and drug abuse/dependence of 3.6 percent.

•The rate of co-occurrence of pathological gambling among people with substance use disorders has been reported as ranging from 9 to 30 percent and the rate of substance abuse among individuals with pathological gambling has been estimated at 25 to 63 percent.
•Among pathological gamblers, alcohol has been found to be the most common substance of abuse. At minimum, the rate of problem gambling among people with substance use disorders is four to five times that found in the general population.
•It is important to recognize that even though pathological gambling often is viewed as an addictive disorder, clinicians cannot assume that their knowledge or experience in substance abuse treatment qualifies them automatically to treat people with a pathological gambling problem.
•With clients with substance use disorders who are pathological gamblers, it often is essential to identify specific triggers for each addiction. It is also helpful to identify ways in which use of addictive substances or addictive activities such as gambling act as mutual triggers.
In individuals with COD, it is particularly important to evaluate patterns of substance use and gambling. The following bullets provide several examples:
•Cocaine use and gambling may coexist as part of a broader antisocial lifestyle.
•Someone who is addicted to cocaine may see gambling as a way of getting money to support drug use.
•A pathological gambler may use cocaine to maintain energy levels and focus during gambling and sell drugs to obtain gambling money.
•Cocaine may artificially inflate a gambler’s sense of certainty of winning and gambling skill, contributing to taking greater gambling risks.
•The gambler may use drugs or alcohol as a way of celebrating a win or relieving depression.

•One of the more common patterns that has been seen clinically is that of a sequential addiction. A frequent pattern is that someone who has had a history of alcohol dependence—often with many years of recovery and AA attendance—develops a gambling problem.

During the evaluation, it became clear that treatment would have to address both his gambling as well as his alcohol dependence, since these were so intertwined. Education was provided on both disorders, using standard information at the substance abuse treatment agency as well as materials from Gamblers Anonymous (GA). Group and individual therapy repeatedly pointed out the interaction between the disorders and the triggers for each, emphasizing the development of coping skills and relapse prevention strategies for both disorders. Louis Q. also was referred to a local GA meeting and was fortunate to have another member of his addictions group to guide him there. The family was involved in treatment planning and money management, including efforts to organize, structure, and monitor debt repayment. Legal assistance was obtained to advise him on potential legal charges due to embezzlement at work. He began attending both AA and GA meetings, obtaining sponsors in both programs.

Substance-Induced Disorders

The toxic effects of substances can mimic mental illness in ways that can be difficult to distinguish from mental illness. This chapter focuses on symptoms of mental illness that are the result of substance abuse—a condition referred to as “substance-induced mental disorders.”


As defined in the Diagnostic and Statistical Manual of Mental
Disorders, 4th edition, Text Revision (American Psychiatric Association [APA] 2000) (DSM-IV-TR), substance-induced disorders include:

  1. Substance-induced delirium
  2. Substance-induced persisting dementia
  3. Substance-induced persisting amnestic disorder
  4. Substance-induced psychotic disorder
  5. Substance-induced mood disorder
  6. Substance-induced anxiety disorder
  7. Hallucinogen persisting perceptual disorder
  8. Substance-induced sexual dysfunction
  9. Substance-induced sleep disorder

Substance-induced disorders are distinct from independent co-occurring mental disorders in that all or most of the psychiatric symptoms are the direct result of substance use. This is not to state that substance-induced disorders preclude co-occurring mental disorders, only that the specific symptom cluster at a specific point in time is more likely the result of substance use, abuse, intoxication, or withdrawal than of underlying mental illness. A client might even have both independent and substance-induced mental disorders. For example, a client may present with well-established independent and controlled bipolar disorder and alcohol dependence in remission, but the same client could be experiencing amphetamine-induced auditory hallucinations and paranoia from an amphetamine abuse relapse over the last 3 weeks.

Symptoms of substance-induced disorders run the gamut from mild anxiety and depression (these are the most common across all substances) to full-blown manic and other psychotic reactions (much less common). The “teeter-totter principle”—i.e., what goes up must come down—is useful to predict what kind of syndrome or symptoms might be caused by what substances. For example, acute withdrawal symptoms from physiological depressants such as alcohol and benzodiazepines are hyperactivity, elevated blood pressure, agitation, and anxiety (i.e., the shakes). On the other hand, those who “crash” from stimulants are tired, withdrawn, and depressed. Virtually any substance taken in very large quantities over a long enough period can lead to a psychotic state.
Because clients vary greatly in how they respond to both intoxication and withdrawal given the same exposure to the same substance, and also because different substances may be taken at the same time, prediction of any particular substance-related syndrome has its limits. What is most important is to continue to evaluate psychiatric symptoms and their relationship to abstinence or ongoing substance abuse over time. Most substance-induced symptoms begin to improve within hours or days after substance use has stopped. Notable exceptions to this are psychotic symptoms caused by heavy and longterm amphetamine abuse and the dementia (problems with memory, concentration, and problemsolving) caused by using substances directly toxic to the brain, which most commonly include alcohol, inhalants like gasoline, and again amphetamines. Following is an overview of the most common classes of substances of abuse and the accompanying psychiatric symptoms seen in intoxication, withdrawal, or chronic use.


In most people, moderate to heavy consumption is associated with euphoria, mood lability, decreased impulse control, and increased social confidence (i.e., getting high). Such symptoms might even appear “hypomanic.” However these often are followed with nextday mild fatigue, nausea, and dysphoria (i.e., a hangover). In a person who has many life stresses, losses, and struggles, which is often the case as addiction to alcohol proceeds, the mood lability and lowered impulse control can lead to increased rates of violence toward others and self. Prolonged drinking increases the incidence of dysphoria, anxiety, and such violence potential. Symptoms of alcohol withdrawal include agitation, anxiety, tremor, malaise, hyperreflexia (exaggeration of reflexes), mild tachycardia (rapid heart beat), increasing blood pressure, sweating, insomnia, nausea or vomiting, and perceptual distortions.

Following acute withdrawal (a few days), some people will experience continued mood instability, fatigue, insomnia, reduced sexual interest, and hostility for weeks, so called “protracted withdrawal.” Differentiating protracted withdrawal from a major depression or anxiety disorder is often difficult. More severe withdrawal is characterized by severe instability in vital signs, agitation, hallucinations, delusions, and often seizures. The best predictor of whether this type of withdrawal may happen again is if it happened before. Alcohol-induced deliriums after high-dose drinking are characterized by fluctuating mental status, confusion, and disorientation and are reversible once both alcohol and its withdrawal symptoms are gone, while by definition, alcohol dementias are associated with brain damage and are not entirely reversible even with sobriety.


When consumed in large quantities, caffeine can cause mild to moderate anxiety, though the amount of caffeine that leads to anxiety varies. Caffeine is also associated with an increase in the number of panic attacks in individuals who are predisposed to them.

Cocaine and Amphetamines

Mild to moderate intoxication from cocaine, methamphetamine, or other stimulants is associated with euphoria, and a sense of internal well-being, and perceived increased powers of thought, strength, and accomplishment. In fact, low to moderate doses of amphetamines may actually increase certain test-taking skills temporarily in those with attention deficit disorders (see this in appendix D) and even in people who do not have attention deficit disorders. However, as more substance is used and intoxication increases, attention, ability to concentrate, and function decrease.

With street cocaine and methamphetamines, dosing is almost always beyond the functional window. As dosage increases, the chances of impulsive dangerous behaviors, which may involve violence, promiscuous sexual activity, and others, also increases. Many who become chronic heavy users go on to experience temporary paranoid delusional states. As mentioned above, with methamphetamines, these psychotic states may last for weeks, months, and even years. Unlike schizophrenic psychotic states, the client experiencing a paranoid state induced by cocaine more likely has intact abstract reasoning and linear thinking and the delusions are more likely paranoid and less bizarre (Mendoza and Miller 1992). After intoxication comes a crash in which the person is desperately fatigued, depressed, and often craves more stimulant to relieve these withdrawal symptoms. This dynamic is why it is thought that people who abuse stimulants often go on week- or month-long binges and have a hard time stopping. At some point the ability of stimulants to push the person back into a high is lost (probably through washing out of neurotransmitters), and then a serious crash ensues.

Even with several weeks of abstinence, many people who are addicted to stimulants report a dysphoric state that is marked by anhedonia (absence of pleasure) and/or anxiety, but which may not meet the symptom severity criteria to qualify as DSM-IV Major Depression (Rounsaville et al. 1991). These anhedonic states can persist for weeks. As mentioned above, heavy, long-term amphetamine use appears to cause long-term changes in the functional structure of the brain, and this is accompanied by long-term problems with concentration, memory, and, at times, psychotic symptoms. Month-long methamphetamine binges followed by week- or month-long alcohol binges, a not uncommon pattern, might appear to be “bipolar” disorder if the drug use is not discovered.


Hallucinogens produce visual distortions and frank hallucinations. Some people who use hallucinogens experience a marked distortion of their sense of time and feelings of depersonalization. Hallucinogens may also be associated with drug-induced panic, paranoia, and even delusional states in addition to the hallucinations. Hallucinogen hallucinations usually are more visual (e.g., enhanced colors and shapes) as compared to schizophrenictype hallucinations, which tend to be more auditory (e.g., voices). The existence of a marijuana-induced psychotic state has been debated (Gruber and Pope 1994), although a review of the research suggests that there is no such entity. A few people who use hallucinogens experience chronic reactions, involving prolonged psychotic reactions, depression, exacerbations of preexisting mental disorders, and flashbacks. The latter are symptoms that occur after one or more psychedelic “trips” and consist of flashes of light and after-image prolongation in the periphery. The DSM-IV defines flashbacks as a “hallucinogen persisting perception disorder.” A diagnosis requires that they be distressing or impairing to the client (APA 1994, p. 234).


Clients who are dependent on nicotine are more likely to experience depression than people who are not addicted to it; however, it is unclear how much this is cause or effect. In some cases, the client may use nicotine to regulate mood. Whether there is a causal relationship between nicotine use and the symptoms of depression remains to be seen. At present, it can be said that many persons who quit smoking do experience both craving and depressive symptoms to varying degrees, which are relieved by resumption of nicotine use (see chapter 8 for more information on nicotine dependence).

Opioids Opioid intoxication is characterized by intense euphoria and well-being. Withdrawal results in agitation, severe body aches, gastrointestinal symptoms, dysphoria, and craving to use more opioids. Symptoms during withdrawal vary—some will become acutely anxious and agitated, while others will experience depression and anhedonia. Even with abstinence, anxiety, depression, and sleep disturbance can persist for weeks as a protracted withdrawal syndrome. Again, differentiating this from major depression or anxiety is difficult and many clinicians may just treat the ongoing symptom cluster. For many people who become opioid dependent, and then try abstinence, these ongoing withdrawal symptoms are so powerful that relapse occurs even with the best of treatments and client motivation. For these clients, opioid replacement therapy (methadone, suboxone, etc.) becomes necessary and many times life saving. There are reports of an atypical opioid withdrawal syndrome characterized by delirium after abrupt cessation of methadone (Levinson et al. 1995). Such clients do not appear to have the autonomic symptoms typically seen in opioid withdrawal. Long-term use of opioids is commonly associated with moderate to severe depression.

Phencyclidine (PCP) causes dissociative and delusional symptoms, and may lead to violent behavior and amnesia of the intoxication. Zukin and Zukin (1992) report that people who use PCP and who exhibit an acute psychotic state with PCP are more likely to experience another with repeated use.


Acute intoxication with sedatives like diazepam is similar to what is experienced with alcohol. Withdrawal symptoms are also similar to alcohol and include mood instability with anxiety and/or depression, sleep disturbance, autonomic hyperactivity, tremor, nausea or vomiting, and, in more severe cases, transient hallucinations or illusions and grand mal seizures. There are reports of a protracted withdrawal syndrome characterized by anxiety, depression, paresthesias, perceptual distortions, muscle pain and twitching, tinnitus, dizziness, headache, derealization and depersonalization, and impaired concentration. Most symptoms resolve within weeks, though some symptoms, such as anxiety, depression, tinnitus (ringing in the ears), and paresthesias (sensations such as prickling, burning, etc.), have been reported to last a year or more after withdrawal in rare cases. No chronic dementia-type syndromes have been characterized with chronic use; however, many people who use sedatives chronically seem to experience difficulty with anxiety symptoms, which respond poorly to other anxiety treatments.

Diagnostic Considerations

Criteria for Diagnosis of Substance-Induced Mood Disorders

  1. A prominent and persistent disturbance in mood predominates, characterized by (a) a depressed mood or markedly diminished interest or pleasure in activities, or (b) an elevated, expansive, or irritable mood.
  2. There is evidence from the history, physical examination, or laboratory findings that the symptoms developed during or within a month after substance intoxication or withdrawal, or medication use, is etiologically related to the mood disturbance.
  3. The disturbance is not better explained by a mood disorder.
  4. The disturbance did not occur exclusively during a delirium.
  5. The symptoms cause clinically significant distress or impairment.

Some people who have what appear to be substance-induced disorders may turn out to have both a substance-induced disorder and an independent mental disorder. For most people who are addicted to substances, drugs eventually become more important than jobs, friends, family, and even children. These changes in priorities often look, sound, and feel like a personality disorder, but diagnostic clarity regarding personality disorders in general is difficult, and in clients with substancerelated disorders the true diagnostic picture might not emerge or reveal itself for weeks or months. Moreover, it is not unusual for the symptoms of a personality disorder to clear with abstinence—sometimes even fairly early in recovery. Preexisting mood state, personal expectations, drug dosage, and environmental surroundings all warrant consideration in developing an understanding of how a particular client might experience a substanceinduced disorder. Treatment of the substance use disorder and an abstinent period of weeks or months may be required for a definitive diagnosis of an independent, co-occurring mental disorder. As described in chapter 4 on assessment, substance abuse treatment programs and clinical staff can concentrate on screening for mental disorders and determining the severity and acuity of symptoms, along with an understanding of the client’s support network and overall life situation. The text box above provides an example of the diagnostic criteria for one substanceinduced disorder—substance-induced mood disorders.

Case Studies: Identifying Disorders

George M. is a 37-year-old divorced male who was brought into the emergency room intoxicated. His blood alcohol level was .152, and the toxicology screen was positive for cocaine. He was also suicidal (“I’m going to do it right this time!”). He has a history of three psychiatric hospitalizations and two inpatient substance abuse treatments. Each psychiatric admission was preceded by substance use. George M. has never followed through with mental health care. He has intermittently attended Alcoholics Anonymous, but not recently.
Teresa G. is a 37-year-old divorced female who was brought into a detoxification unit 4 days ago with a blood alcohol level of .150. She is observed to be depressed, withdrawn, with little energy, fleeting suicidal thoughts, and poor concentration, but states she is just fine, not depressed, and life was good last week before her relapse. She has never used drugs (other than alcohol), and began drinking alcohol only 3 years ago. However, she has had several alcohol-related problems since then. She has a history of three psychiatric hospitalizations for depression, at ages 19, 23, and 32. She reports a positive response to antidepressants. She is currently not receiving mental health services or substance abuse treatment. She is diagnosed with alcohol dependence (relapse) and substanceinduced mood disorder, with a likely history of, but not active, major depression.


Many factors must be examined when making initial diagnostic and treatment decisions. For example, if George M.’s psychiatric admissions were 2 or 3 days long, usually with discharges related to leaving against medical advice, decisions about diagnosis and treatment would be different (i.e., it is likely this is a substance-induced suicidal state and referral at discharge should be to a substance abuse treatment agency rather than a mental health center) than if two of his psychiatric admissions were 2 or 3 weeks long with clearly defined manic and psychotic symptoms continuing throughout the course, despite aggressive use of mental health care and medication (this is more likely a person with both bipolar disorder and alcohol dependence who requires integrated treatment for both his severe alcoholism and bipolar disorder).

Similarly, if Teresa G. had become increasingly depressed and withdrawn over the past 3 months, and had for a month experienced disordered sleep, poor concentration, and suicidal thoughts, she would be best diagnosed with major depression with an acute alcohol relapse rather than substanceinduced mood disorder secondary to her alcohol relapse.

What is comorbidity?

When two disorders or illnesses occur in the same person, simultaneously or sequentially, they are described as comorbid. Comorbidity also implies interactions between the illnesses that affect the course and prognosis of both.

Is drug addiction a mental illness?

Yes, because addiction changes the brain in fundamental ways, disturbing a person's normal hierarchy of needs and desires and substituting new priorities connected with procuring and using the drug. The resulting compulsive behaviors that override the ability to control impulses despite the consequences are similar to hallmarks of other mental illnesses.

Addiction changes the brain, disturbing the normal hierarchy of needs and desires.

In fact, the DSM, which is the definitive resource of diagnostic criteria for all mental disorders, includes criteria for drug use disorders, distinguishing between two types: drug abuse and drug dependence. Drug dependence is synonymous with addiction. By comparison, the criteria for drug abuse hinge on the harmful consequences of repeated use but do not include the compulsive use, tolerance (i.e., needing higher doses to achieve the same effect), or withdrawal (i.e., symptoms that occur when use is stopped) that can be signs of addiction.

How common are comorbid drug use and other mental disorders?

Many people who regularly abuse drugs are also diagnosed with mental disorders and vice versa. The high prevalence of this comorbidity has been documented in multiple national population surveys since the 1980s. Data show that persons diagnosed with mood or anxiety disorders are about twice as likely to suffer also from a drug use disorder (abuse or dependence) compared with respondents in general. The same is true for those diagnosed with an antisocial syndrome, such as antisocial personality or conduct disorder. Similarly, persons diagnosed with drug disorders are roughly twice as likely to suffer also from mood and anxiety disorders.

Gender is also a factor in the specific patterns of observed comorbidities. For example, the overall rates of abuse and dependence for most drugs tend to be higher among males than females. Further, males are more likely to suffer from antisocial personality disorder, while women have higher rates of mood and anxiety disorders, all of which are risk factors for substance abuse.

Numerous studies have documented an increased risk for drug use disorders in youth with untreated ADHD, although some suggest that only a subset of these individuals are vulnerable: those with comorbid conduct disorders. Given this linkage, it is important to determine whether effective treatment of ADHD could prevent subsequent drug abuse and associated behavioral problems. Treatment of childhood ADHD with stimulant medications such as methylphenidate or amphetamine reduces the impulsive behavior, fidgeting, and inability to concentrate that characterize ADHD. Yet, some physicians and parents have expressed concern that treating childhood ADHD with stimulants might increase a child's vulnerability to drug abuse later in life. Recent reviews of long-term studies of children with ADHD who were treated with stimulant medications (e.g., Adderal, Ritalin, Concerta) found no evidence for this increase. However, most of these studies have methodological limitations, including small sample sizes and nonrandomized study designs, indicating that more research is needed, particularly with adolescents.

Why do drug use disorders often co-occur with other mental illnesses?

The high prevalence of comorbidity between drug use disorders and other mental illnesses does not mean that one caused the other, even if one appeared first. In fact, establishing causality or directionality is difficult for several reasons. Diagnosis of a mental disorder may not occur until symptoms have progressed to a specified level (per DSM); however, subclinical symptoms may also prompt drug use, and imperfect recollections of when drug use or abuse started can create confusion as to which came first. Still, three scenarios deserve consideration:

  1. Drugs of abuse can cause abusers to experience one or more symptoms of another mental illness. The increased risk of psychosis in some marijuana abusers has been offered as evidence for this possibility.
  2. Mental illnesses can lead to drug abuse. Individuals with overt, mild, or even subclinical mental disorders may abuse drugs as a form of self-medication. For example, the use of tobacco products by patients with schizophrenia is believed to lessen the symptoms of the disease and improve cognition.
  3. Both drug use disorders and other mental illnesses are caused by overlapping factors such as underlying brain deficits, genetic vulnerabilities, and/or early exposure to stress or trauma.

All three scenarios probably contribute, in varying degrees, to how and whether specific comorbidities manifest themselves.

Common Factors

Overlapping Genetic Vulnerabilities. A particularly active area of comorbidity research involves the search for genes that might predispose individuals to develop both addiction and other mental illnesses, or to have a greater risk of a second disorder occurring after the first appears. It is estimated that 40-60 percent of an individual's vulnerability to addiction is attributable to genetics; most of this vulnerability arises from complex interactions among multiple genes and from genetic interactions with environmental influences. In some instances, a gene product may act directly, as when a protein influences how a person responds to a drug (e.g., whether the drug experience is pleasurable or not) or how long a drug remains in the body. But genes can also act indirectly by altering how an individual responds to stress or by increasing the likelihood of risk-taking and novelty-seeking behaviors, which could influence the development of drug use disorders and other mental illnesses. Several regions of the human genome have been linked to increased risk of both drug use disorders and mental illness, including associations with greater vulnerability to adolescent drug dependence and conduct disorders.

Involvement of Similar Brain Regions. Some areas of the brain are affected by both drug use disorders and other mental illnesses. For example, the circuits in the brain that use the neurotransmitter dopamine–a chemical that carries messages from one neuron to another– are typically affected by addictive substances and may also be involved in depression, schizophrenia, and other psychiatric disorders.

Indeed, some antidepressants and essentially all antipsychotic medications directly target the regulation of dopamine in this system, whereas others may have indirect effects. Importantly, dopamine pathways have also been implicated in the way in which stress can increase vulnerability to drug addiction. Stress is also a known risk factor for a range of mental disorders and therefore provides one likely common neurobiological link between the disease processes of addiction and those of other mental disorders.

The overlap of brain areas involved in both drug use disorders and other mental illnesses suggests that brain changes stemming from one may affect the other. For example, drug abuse that precedes the first symptoms of a mental illness may produce changes in brain structure and function that kindle an underlying propensity to develop that mental illness. If the mental disorder develops first, associated changes in brain activity may increase the vulnerability to abusing substances by enhancing their positive effects, reducing awareness of their negative effects, or alleviating the unpleasant effects associated with the mental disorder or the medication used to treat it.

The Influence of Developmental Stage

Adolescence–A Vulnerable Time. Although drug abuse and addiction can happen at any time during a person's life, drug use typically starts in adolescence, a period when the first signs of mental illness commonly appear. It is therefore not surprising that comorbid disorders can already be seen among youth. Significant changes in the brain occur during adolescence, which may enhance vulnerability to drug use and the development of addiction and other mental disorders. Drugs of abuse affect brain circuits involved in learning and memory, reward, decisionmaking, and behavioral control, all of which are still maturing into early adulthood. Thus, understanding the long-term impact of early drug exposure is a critical area of comorbidity research.

The brain continues to develop into adulthood and undergoes dramatic changes during adolescence.

One of the brain areas still maturing during adolescence is the prefrontal cortex– the part of the brain that enables us to assess situations, make sound decisions, and keep our emotions and desires under control. The fact that this critical part of an adolescent's brain is still a work in progress puts them at increased risk for poor decisions (such as trying drugs or continuing abuse). Thus, introducing drugs while the brain is still developing may have profound and long-lasting consequences.

The high rate of comorbidity between drug abuse and addiction and other mental disorders argues for a comprehensive approach to intervention that identifies and evaluates each disorder concurrently, providing treatment as needed.

Early Occurrence Increases Later Risk. Strong evidence has emerged showing early drug use to be a risk factor for later substance abuse problems; additional findings suggest that it may also be a risk factor for the later occurrence of other mental illnesses. However, this link is not necessarily a simple one and may hinge upon genetic vulnerability, psychosocial experiences, and/or general environmental influences. A 2005 study highlights this complexity, with the finding that frequent marijuana use during adolescence can increase the risk of psychosis in adulthood, but only in individuals who carry a particular gene variant.

It is also true that having a mental disorder in childhood or adolescence can increase the risk of later drug abuse problems, as frequently occurs with conduct disorder and untreated attention-deficit hyperactivity disorder (ADHD). This presents a challenge when treating children with ADHD, since effective treatment often involves prescribing stimulant medications with abuse potential. This issue has generated strong interest from the research community, and although the results are not yet conclusive, most studies suggest that ADHD medications do not increase the risk of drug abuse among children with ADHD.

Regardless of how comorbidity develops, it is common in youth as well as adults. Given the high prevalence of comorbid mental disorders and their likely adverse impact on substance abuse treatment outcomes, drug abuse programs for adolescents should include screening and, as needed, treatment for comorbid mental disorders.

The Influence of Adolescent Marijuana Use on Adult Psychosis Is Affected by Genetic Variables

The above figure shows that variations in a gene can affect the likelihood of developing psychosis in adulthood following exposure to cannabis in adolescence. The catechol-O-methyltransferase gene regulates an enzyme that breaks down dopamine, a brain chemical involved in schizophrenia. It comes in two forms: Met and Val. Individuals with one or two copies of the Val variant have a higher risk of developing schizophrenic-type disorders if they used cannabis during adolescence (dark bars). Those with only the Met variant were unaffected by cannabis use. These findings hint at the complexity of factors that contribute to comorbid conditions.

How can comorbidity be diagnosed?

The high rate of comorbidity between drug use disorders and other mental illnesses argues for a comprehensive approach to intervention that identifies and evaluates each disorder concurrently, providing treatment as needed. The needed approach calls for broad assessment tools that are less likely to result in a missed diagnosis. Accordingly, patients entering treatment for psychiatric illnesses should also be screened for substance use disorders and vice versa. Accurate diagnosis is complicated, however, by the similarities between drug-related symptoms such as withdrawal and those of potentially comorbid mental disorders. Thus, when people who abuse drugs enter treatment, it may be necessary to observe them after a period of abstinence in order to distinguish between the effects of substance intoxication or withdrawal and the symptoms of comorbid mental disorders. This practice would allow for a more accurate diagnosis and more targeted treatment.

Exposure to Traumatic Events Puts People at Higher Risk of Substance Use Disorders

Physically or emotionally traumatized people are at much higher risk of abusing licit, illicit, and prescription drugs. This linkage is of particular concern for returning veterans since nearly 1 in 5 military service members back from Iraq and Afghanistan have reported symptoms of post-traumatic stress disorder (PTSD) or major depression. Recent epidemiological studies suggest that as many as half of all veterans diagnosed with PTSD also have a co-occurring substance use disorder (SUD), which could pose an enormous challenge for our health care system. Many PTSD programs do not accept individuals with active SUDs, and traditional SUD clinics defer treatment of trauma-related issues. Nevertheless, there are treatments at different stages of clinical validation for comorbid PTSD and SUD; these include various combinations of psychosocial (e.g., exposure therapy) and pharmacologic (e.g., mood stabilizers, anxiolytics, and antidepressants) interventions. However, research is urgently needed to identify the best treatment strategies for addressing PTSD/SUD comorbidities, and to explore whether different treatments might be needed in response to civilian versus combat PTSD.

How should comorbid conditions be treated?

A fundamental principle emerging from scientific research is the need to treat comorbid conditions concurrently–which can be a difficult proposition. Patients who have both a drug use disorder and another mental illness often exhibit symptoms that are more persistent, severe, and resistant to treatment compared with patients who have either disorder alone. Nevertheless, steady progress is being made through research on new and existing treatment options for comorbidity and through health services research on implementation of appropriate screening and treatment within a variety of settings, including criminal justice systems.


Effective medications exist for treating opioid, alcohol, and nicotine addiction and for alleviating the symptoms of many other mental disorders, yet most have not been well studied in comorbid populations. Some medications may benefit multiple problems. For example, evidence suggests that bupropion (trade names: Wellbutrin, Zyban), approved for treating depression and nicotine dependence, might also help reduce craving and use of the drug methamphetamine. Clearly, more research is needed to fully understand and assess the actions of combined or dually effective medications.

Behavioral Therapies

Behavioral treatment (alone or in combination with medications) is the cornerstone to successful outcomes for many individuals with drug use disorders or other mental illnesses. And while behavior therapies continue to be evaluated for use in comorbid populations, several strategies have shown promise for treating specific comorbid conditions.

Most clinicians and researchers agree that broad spectrum diagnosis and concurrent therapy will lead to more positive outcomes for patients with comorbid conditions. Preliminary findings support this notion, but research is needed to identify the most effective therapies (especially studies focused on adolescents).Examples of Promising Behavioral Therapies for Patients with Comorbid Conditions

Adolescents Multisystemic Therapy (MST)

MST targets key factors (attitudes, family, peer pressure, school and neighborhood culture) associated with serious antisocial behavior in children and adolescents who abuse drugs.

Brief Strategic Family Therapy (BSFT)

BSFT targets family interactions that are thought to maintain or exacerbate adolescent drug abuse and other co-occurring problem behaviors. These problem behaviors include conduct problems at home and at school, oppositional behavior, delinquency, associating with antisocial peers, aggressive and violent behavior, and risky sexual behaviors.

Cognitive-Behavioral Therapy (CBT)

CBT is designed to modify harmful beliefs and maladaptive behaviors. CBT is the most effective psychotherapy for children and adolescents with anxiety and mood disorders, and also shows strong efficacy for substance abusers. (CBT is also effective for adult populations suffering from drug use disorders and a range of other psychiatric problems.)

Adults Therapeutic Communities (TCs)

TCs focus on the "resocialization" of the individual and use broad-based community programs as active components of treatment. TCs are particularly well suited to deal with criminal justice inmates, individuals with vocational deficits, women who need special protections from harsh social environments, vulnerable or neglected youth, and homeless individuals. In addition, some evidence suggests the utility of incorporating TCs for adolescents who have been in treatment for substance abuse and related problems.

Assertive Community Treatment (ACT)

ACT programs integrate the behavioral treatment of other severe mental disorders, such as schizophrenia, and co-occurring substance use disorders. ACT is differentiated from other forms of case management through factors such as a smaller caseload size, team management, outreach emphasis, a highly individualized approach, and an assertive approach to maintaining contact with patients.

Dialectical Behavior Therapy (DBT)

DBT is designed specifically to reduce self-harm behaviors (such as self-mutilation and suicidal attempts, thoughts, or urges) and drug abuse. It is one of the few treatments that is effective for individuals who meet the criteria for borderline personality disorder.

Exposure Therapy

Exposure therapy is a behavioral treatment for some anxiety disorders (phobias, PTSD) that involves repeated exposure to or confrontation with a feared situation, object, traumatic event, or memory. This exposure can be real, visualized, or simulated, and always is contained in a controlled therapeutic environment. The goal is to desensitize patients to the triggering stimuli and help them learn to cope, eventually reducing or even eliminating symptoms. Several studies suggest that exposure therapy may be helpful for individuals with comorbid PTSD and cocaine addiction, although retention in treatment is difficult.

Integrated Group Therapy (IGT)

IGT is a new treatment developed specifically for patients with bipolar disorder and drug addiction, designed to address both problems simultaneously.

Barriers to Comprehensive Treatment of Comorbidity

Although research supports the need for comprehensive treatment to address comorbidity, provision of such treatment can be problematic for a number of reasons:


Webster’s Third New International Dictionary (1981, p. 2260) defined stress as “a physical, chemical, or emotional factor (as trauma, histamine, or fear) to which an individual fails to make a satisfactory adaptation, and which causes physiologic tensions that may be a contributing cause of disease.” Although this term now is widely used in the common vernacular, it is interesting to note that the scientific conceptualization of this phenomenon dates back only about 150 years.

Most stress research historians agree that the French physiologist, Claude Bernard (1865), was the first to recognize a key element in the stress response—the phenomenon now known as feedback regulation. Bernard noticed that the internal environment of cells (“milieu intérieur”) is tightly regulated and largely dependent on feedback it receives from the periphery or “external environment” (Goldstein and Kopin 2007). Some 65 years later, Sir Walter Cannon coined the term “homeostasis” to capture the “coordinated physiological processes that maintain most of the steady states of the organism” (Cannon 1929 as cited by Goldstein and McEwen 2002, p. 55). From Cannon’s perspective, which derived from his study of the sympathetic nervous system (he also coined the phrase “fight-or-flight responses”), all organisms adjusted to challenges to their internal environments by making compensatory responses intended to restore homeostasis. By accomplishing such, the organism’s chances for survival improved because the homeostatic or steady state was viewed as optimal and fixed at some preordained, stable level (Goldstein and Kopin 2007; Neylan 1998).

The Hungarian scientist, Hans Selye, who was influenced by Cannon’s work, developed the concept of the General Adaptation Syndrome in 1936. Selye’s theories, which dominated thinking on the nature of the stress response for more than 50 years, hypothesized that a classical syndrome developed in all organisms “the symptoms of which are independent of the damaging agent or the pharmacological type of the drug employed” (Selye 1936, p. 32). He further hypothesized that this stress response had three stages: an initial alarm reaction (akin to Cannon’s fight-or-flight response) that involved the release of anterior pituitary hormones; a second, adaptation phase, wherein an attempt is made to resist the stressor; and a third, exhaustion phase, which, at its extreme, could lead to death of the organism (Goldstein and Kopin 2007; Selye 1936).

Over time, scientists began challenging two key concepts in this definition of stress as any real or imagined threat to homeostasis (McEwen and Stellar 1993). First, Selye’s assertion that stress responses were uniform and generalized regardless of stressor type was modified in recognition that certain types of stressors (e.g., physical versus emotional, see below) evoked activation of specific effector systems. For example, exposure to extreme cold produces a marked activation of the sympathetic noradrenergic system in an effort to regulate core body temperature, yet it has minimal effects on the endocrine or hormonal stress response (Goldstein and Kopin 2007). Thus, Selye’s doctrine of a unitary, nonspecific stress response gave way to a more refined view that individuals activate stress systems more selectively depending on the characteristics of the stressor.

Second, scientists began recognizing that physiological regulatory systems spanned multiple domains, were dynamic and not static, and fluctuated constantly based on the animal’s biological rhythms and physiological demands. Moreover, the notion that there existed some static, ideal, homeostatic set point gave way to thinking that, instead, these set points vary across a dynamic operating range which change over time. Thus, Sterling and Eyer ([1988] as cited in McEwen and Stellar 1993) coined the term allostasis to describe this operating range and the organism’s ability to increase or decrease body functions to a new steady state when challenged.

McEwen and Stellar (1993) embellished on the principle of allostasis by defining a new concept that these authors labeled allostatic load. This term connotes the toll placed on individuals when they have to constantly or repeatedly adjust the operating range to maintain fluctuating set points. This “wear and tear” can predispose the individual to disease, especially in the context of chronic stress.

It is interesting to note that in this seminal paper, the authors cite “the reciprocal relationship between stress and alcohol consumption” as an example of allostatic load:

In short, whereas drinking may help the person cope with stress in the short-term, there is a longer-term cost. As the person tries to balance the reciprocal effects of stress and alcohol consumption in this manner, the upward spiral of both stress and drinking increases this overall cost (allostatic load) both behaviorally and biologically (McEwen and Stellar 1993, p. 2096).

In summary, although the use of the term stress has become commonplace, the scientific conceptualization of this state is a relatively recent phenomenon and is still evolving. Stress has been broadly defined “as a threat, real or implied, to the psychological or physical integrity of an individual” (McEwen 2000, p. 108). Other terms, however, such as allostasis (“maintaining stability, or homeostasis, through change” [Sterling and Eyer 1988 as cited in McEwen 2000, p. 108]) and allostatic load (“the price the body pays for being forced to adapt to adverse psychosocial or physical situations” [McEwen 2000, p. 110]) are newly emerged and are helping to better define the relationships between stress and disease risk, including the risk for AUDs, as described below.

Stress and Addiction to Alcohol and Other Drugs

Koob and Le Moal (1997, 2001) began formally linking the brain’s stress and reward systems in an allostatic model of alcohol and other drug addiction that still holds sway over the field today. As described in detail elsewhere (Koob and Le Moal 1997, 2001) and alluded to in Koob and colleagues’ contribution in this edition (see pp. 516–521), these scientists hypothesized that alcohol and other drug addiction represents an allostatic state whereby an individual’s hedonic set point has drifted downward and been recalibrated at a new point below the normal, homeostatic range. The fluctuating hysteresis of this proposed downward sloping “mood” curve reflects the operating range of the brain’s reward and stress systems, which engage in a struggle to adjust and readjust in the setting of repetitive alcohol (or other drug) use. Thus, in this allostatic model, alcohol drinking can be viewed as both a reward and a stressor—an interpretation which is consistent with observations that acute doses of alcohol simultaneously increase brain concentrations of mesolimbic dopamine and other reinforcing neurotransmitters as well as brain levels of corticotropin-releasing factor (CRF) and blood levels of adrenocorticotropin hormone (ACTH) and cortisol, the major stress hormones in the brain and body (Rivier and Lee 1996).

At first glance, this notion of alcohol and other drugs of abuse working as stressors (i.e., taxing to the individual) flies in the face of the more commonly held belief that ethanol has stress-response–dampening effects. However, several characteristics of the drug may explain this paradox. First, alcohol’s rewarding properties may counterbalance or mask its stress-provoking effects. This happens on a number of different levels: (1) the drug produces brain depressant effects by acutely enhancing GABAergic tone, while inhibiting excitatory glutamatergic signaling; (2) ethanol acutely enhances the release of reinforcing neurotransmitters (e.g., dopamine and endogenous opiates) and neuromodulators (e.g., endocannabinoids); and (3) alcohol’s effects on the release of the stress hormone, cortisol, in the periphery triggers further rewarding properties in the brain.

Second, consistent with the second phase in Selye’s general adaptation syndrome, and the opponent-process model (Solomon and Corbit 1973) evoked in Koob and Le Moal’s allostatic model of addiction, the brain resists or adapts to repeated, alcohol-induced stress hormone elevations. This neuroadaptation underlies the allostatic change associated with chronic heavy drinking and manifests as a blunted stress response in recently abstinent alcoholics (see Stephens and Wand, pp. 468–483).

In summary, although low doses of alcohol in non–alcohol-dependent individuals produce rewarding effects that are perceived to attenuate stress, in actuality, the drug stimulates the release of CRF and stress hormones. Chronic, heavy use of ethanol produces an allostatic state wherein reinforcing and stress-provoking effects of the drug battle and oppose each other but generally contribute to an altered set point below that associated with normal mood states. When repeated over many months to years, this struggle exerts its toll (i.e., produces allostatic load) on the brain and body, as there is a cost associated with the chronic efforts to adapt to these stressors. Thus, drinking to relieve stress proves to be a double-edged sword.

Factors Influencing Stress Reactivity

Casual readers of the alcohol and stress literature can become frustrated by the apparent lack of uniformity of findings. For example, when analyzing studies attempting to determine whether stress leads to relapse to alcoholism (see the article by Thomas and colleagues in this edition, pp. 459–467), readers will observe that sometimes blunted hormonal responses are associated with increased relapse risk; whereas, in other instances, exaggerated hormonal responses predict the return to drinking. However, when one considers that stress responsivity is governed by a host of factors related to (1) the characteristics of the stressor and (2) the characteristics of the individual, some of this heterogeneity in findings can be explained.

Painstakingly detailed neuroanatomical studies in experimental animals were among the first to demonstrate that organisms have evolved different stress circuits to adapt to life’s variety of stressors (Goldstein and Kopin 2007; Pacak et al. 1998). This stressor-specific strategy certainly makes sense from an evolutionary standpoint: it would be extremely inefficient to mobilize the same effector systems to keep an animal’s core temperature up when exposed to cold weather as it would to respond to hemorrhagic hypotension. However, there also is an advantage to having some redundancy across these effector systems. For example, the hypothalamic– pituitary–adrenal (HPA) axis, which mediates the endocrine or hormonal response to certain stressors, interconnects with the adrenomedullary hormonal system and the sympathetic noradrenergic system (SNS). This does not mean, however, that specific stressors activate all three effector systems to the same extent. Thus, when researchers measure the outputs of these effector systems (i.e., ACTH and cortisol in the bloodstream of humans to monitor HPA axis reactivity versus heart rate and blood pressure which reflect SNS activity) in response to various stress paradigms they may not necessarily find unanimity of responses.

Scientists have conceptualized different categories of stressors to better capture this phenomenon. Thus, distinctions such as “psychogenic versus neurogenic,” “processive versus systemic” (see the article by Herman, pp. 441–447), and “physical versus psychological versus pharmacologic” stress have been used to describe the various stress induction paradigms used in experimental animals and humans (for a partial list, see table 1). The stress-response patterns generated by these different types of stressors are not uniform, however, which is a point frequently lost among casual observers.

Other Stressor Characteristics

In addition to the types of stressors influencing stress reactivity, there are other features associated with the stressful experience that affect an individual’s responsiveness (see table 1). For example, the degree of controllability of the stressor influences response, with uncontrollable stress creating a greater level of response compared with events considered to be under an individual’s control (Anisman and Matheson 2005). It is interesting to note that even this seemingly behavioral, subjective phenomenon seems to be governed by stressor-specific neural circuits. For instance, experiments in rodents have demonstrated that the brain’s serotonin system seems to be of primary importance in modulating uncontrollable versus controllable stress (Hammack 2002). Whether a stressor is predictable or unpredictable influences the magnitude of the stress response, as does its duration (i.e., chronicity) (Anisman and Matheson 2005).

Exposure to stress often is psychologically distressing. The impact of stress on alcohol use and the risk of alcohol use disorders (AUDs) depends on the type, timing during the life course, duration, and severity of the stress experienced. Four important categories of stressors that can influence alcohol consumption are general life stress, catastrophic/fateful stress, childhood maltreatment, and minority stress. General life stressors, including divorce and job loss, increase the risk for AUDs. Exposure to terrorism or other disasters causes population-level increases in overall alcohol consumption but little increase in the incidence of AUDs. However, individuals with a history of AUDs are more likely to drink to cope with the traumatic event. Early onset of drinking in adolescence, as well as adult AUDs, are more common among people who experience childhood maltreatment. Finally, both perceptions and objective indicators of discrimination are associated with alcohol use and AUDs among racial/ethnic and sexual minorities. These observations demonstrate that exposure to stress in many forms is related to subsequent alcohol consumption and AUDs. However, many areas of this research remain to be studied, including greater attention to the role of various stressors in the course of AUDs and potential risk moderators when individuals are exposed to stressors.

Exposure to varying forms of stress is an integral life experience that can provoke a variety of reactions. In research on alcohol, drug, and psychiatric disorders, the term “stress” often is understood to indicate any experience denoting adversity (Dohrenwend 2000). Stress exposures consist of external stimuli that are threatening or harmful; elicit fear, anxiety, anger, excitement, and/or sadness; and are negative in impact and outcome (Sinha 2001, 2008). Mild to moderate levels of stress can present challenges that are within a person’s capability to overcome, producing a sense of mastery and accomplishment that eventually result in a positive outcome. However, adverse experiences that exceed the coping abilities of the individual increase the risk for psychopathology (Lazarus 1999; Levine 2005; McEwen 2007; Selye 1976; Sinha 2008).

Just as people vary in their capabilities, stress exposures can be viewed as varying across several dimensions (see figure 1). One dimension is severity, which can range from mild (e.g., the daily hassles of family and job among healthy individuals whose basic needs are met) to severe (e.g., extreme adversity that threatens the life, physical integrity, health and home of oneself and one’s loved ones). Other dimensions, not necessarily orthogonal to each other, include whether the stressor occurred during childhood or maturity, the degree to which the stressor is acute or chronic and expected or unexpected, whether the threat is emotional or physical, and the difficulty of discerning whether the stressor was the cause or consequence of the health outcome under consideration.

This article presents evidence for the effect of four categories of stressors, including general life stress, catastrophic/ fateful stress, childhood maltreatment, and minority stress, each of which encompasses a range of specific kinds of stressors (see figure 2). Each category of stressors is evaluated according to the dimensions shown in figure 1, and the extant epidemiologic evidence for the effect of each on both alcohol use and alcohol use disorders (AUDs) is reviewed.

Various studies in smaller adult community samples also have found that the number of general life stressors is associated with alcohol consumption and problem alcohol use (which may not necessarily meet the criteria of an AUD) (Cole et al. 1990; King et al. 2003). However, one population-based longitudinal study of older adults (mean age 61 years) did not demonstrate long-term effects (i.e., at 1 year or more after the event) of acute stressful life events on patterns of alcohol consumption (Skaff et al. 1999). A national prospective study of 3,006 women found an increased risk of alcohol abuse after being an assault victim, with no evidence of reverse causation (i.e., that alcohol consumption alone contributed to the risk for assault) (Kilpatrick et al. 1997). However, other studies have indicated that excessive alcohol use also increases the risk for sexual assault (Abbey et al. 1994; Corbin et al. 2001); therefore, the relationship between assault and alcohol use likely is bidirectional. Finally, several general population studies have found an increase in the incidence of AUDs following job loss, particularly among men (Catalano et al. 1993; Crawford et al. 1987). It is noteworthy, however, that the context of a job loss likely is important for its impact on the risk of AUDs. For example, the meaning of the lost job may be different for a worker whose plant is shut down after he or she has worked for 30 years in the same position compared with an artist or a musician accustomed to temporary work. Nevertheless, these studies indicate that any type of job loss is associated with increased risk of AUDs.

Fateful/Catastrophic Events and AUDs

With respect to the various correlated dimensions of stress in human populations described earlier, fateful/catastrophic events, such as direct exposure to a disaster or terrorism attack, typically lie on the more extreme end of the severity continuum. These stressors usually are acute and unexpected, and exposure is very unlikely to result from an individual’s alcohol consumption. However, the “fatefulness” of the event may depend on the specific circumstances of the event. For example, studies of people exposed to nightclub disasters (e.g., from fires and terrorist attacks) (Kennedy et al. 2005; Mahoney et al. 2005) involve individuals who are younger and more likely to consume alcohol than the general population. The study of such events still may provide important information, but the type of individuals involved and the appropriate control group must be considered carefully. Fateful/catastrophic events can involve both physical threat to one’s life and emotional threat (e.g., knowing someone lost or killed in the fateful/catastrophic incident, fear of additional exposures) and generally can occur at any point in the life course.

Both in the United States and internationally, many studies have addressed the relationship between different types of natural and man-made disasters and alcohol consumption, including studies of exposure to natural disasters, such as flooding (North et al. 2004), volcano eruptions (Adams and Adams 1984), earthquakes (Shimizu et al. 2000), and hurricanes (Cerda et al. 2011; Kohn et al. 2005). Studies also have investigated the consequences of exposure to man-made disasters, such as mass shootings (North et al. 1994; Smith et al. 1999), fire or grotesque death (Green et al. 1985; Reijneveld et al. 2003; Sims and Sims 1998), ferry disasters (Joseph et al. 1993), and nuclear accidents (Kasl et al. 1981). Studies covering a timeframe of a year or less after the disaster consistently have indicated postdisaster increases in alcohol consumption (Joseph et al. 1993; Kasl et al. 1981; Kohn et al. 2005; Reijneveld et al. 2003; Sims and Sims 1998; Smith et al. 1999). Studies with multiple and/or longer followups generally have found attenuation of this relationship over time (Joseph et al. 1993).

Several studies also have addressed alcohol consumption in response to exposure to terrorism. Substantial research on mental health in general and alcohol consumption specifically has been conducted after the terrorist attacks on the World Trade Center in New York City and the Pentagon in Washington, DC, on September 11, 2001 (9/11). These studies have indicated that alcohol consumption generally increased in both New York City and elsewhere in the short term following the attacks. Thus, increased alcohol use was found among the following groups:

Few studies have examined alcohol use and terrorism exposure outside the United States, but two studies of adolescents in different cities in Israel found that geographic proximity to terrorist attacks was associated with greater quantity and frequency of drinking as well as with binge drinking (Schiff et al. 2006, 2007).

Several studies have been able to control for predisaster drinking levels, the lack of which had been a limitation of most of the aforementioned epidemiologic research. These studies have documented an increase in alcohol consumption following exposure to disaster independent of the consumption levels measured prior to the exposure (Cerda et al. 2011; Hasin et al. 2007a; Richman et al. 2004). A recent meta-analysis of 27 studies assessing substance use in response to terrorism that included studies with follow-up times ranging from 1 week to more than 2 years found a pooled effect indicating that the population level of alcohol consumption is increased following a terrorist attack (DiMaggio et al. 2009).

The research described above focuses on any alcohol consumption after disaster. Studies of AUDs and problem drinking following major disasters have been less consistent. Following the Oklahoma City bombings in 1995, North and colleagues reported no increase in incident AUDs, either in survivors of the attack (North et al. 1999) or in rescue workers (North et al. 2002). Survivors of other disasters, such as Hurricane Andrew (David et al. 1996), flooding (Green et al. 1992; North et al. 2004), and jet crashes (Smith et al. 1990), as well as a combined sample of survivors from the Oklahoma City terrorist bombing and the bombing of the U.S. embassy in Nairobi, Kenya (North et al. 2005) also showed no evidence of increases in incident AUDs. Studies assessing the impact of 9/11 found that neither living near the attack site nor knowing someone lost or killed was associated with incident alcohol problems 6 months following the attack (Vlahov et al. 2006); moreover, exposure to 9/11 was not associated with the trajectory of alcohol use and binge drinking in the 3 years following the attack (Cerda et al. 2008). In a recent pooled analysis of data from 10 different disasters, including exposure to flooding, shootings, and plane crashes, North and colleagues (2010) again reported no evidence of increased risk for incident AUDs after these events, although people with pre-existing AUDs were more likely to report increased drinking after these events.

Several studies contradict the above evidence, however, as follows:

Thus, the literature is inconsistent on the role of fateful traumatic events in the development of AUDs. It is noteworthy, however, that studies of incident AUDs after major disasters were conducted in adult populations in which the incidence of such disorders generally is low (Hasin et al. 2007b). Studies of incident AUD risk following exposure to disaster in adolescent and young adult populations are necessary to comprehensively understand the relation between disaster and incident AUDs.

A substantial literature also has documented increased alcohol consumption and risk for AUDs among war veterans, especially those exposed to active combat (Hoge et al. 2006; Jacobson et al. 2008; Milliken et al. 2007; Shipherd et al. 2005). Causal inference from this literature is complicated, however, because people who perform military duty most often are young men at high baseline risk for AUDs. In addition, exposure to combat is not randomly assigned, and people who have sensation- seeking personality characteristics are more likely to both be assigned to combat and, independently, develop AUDs.

Child Maltreatment and AUDs

Childhood maltreatment includes many adverse exposures (e.g., sexual, emotional, and/or physical abuse and emotional and/or physical neglect) during the first 18 years of life. With respect to the various correlated dimensions of stress in human populations described earlier, childhood maltreatment experiences range from mild (e.g., occasionally saying hurtful things) to severe (e.g., chronic physical and/or sexual abuse). Although these stressors can be acute, they often are chronic throughout childhood; furthermore, they are very unlikely to be a consequence of alcohol consumption as they typically occur before drinking initiation. Childhood maltreatment can involve both physical threat (e.g., physical and sexual abuse or physical neglect of needs) and emotional threat (e.g., emotional abuse and neglect). These experiences are common and may account for a significant proportion of all adult psychopathology (Afifi et al. 2008; Green et al. 2010). Further, events frequently co-occur (Dong et al. 2004; Dube et al. 2002; Edwards et al. 2003; Finkelhor et al. 2007)—in other words, exposure to one type of childhood maltreatment increases the risk of exposure to others.

Epidemiologic studies addressing the impact of adverse childhood events on alcohol consumption and AUDs have employed several types of designs, including cross-sectional studies of adults with retrospective assessment of adverse childhood events, prospective cohort studies, and studies of twin and other genetically informative samples. Studies generally have shown that most forms of child maltreatment are related to higher risk of adolescent alcohol consumption (Bensley et al. 1999; Hussey et al. 2006; Sartor et al. 2007; Thornberry et al. 2001) and adult alcohol consumption and AUDs (Anda et al. 2002; MacMillan et al. 2001; Molnar et al. 2001; Nelson et al. 2006). One review documented that childhood maltreatment and other childhood stressors were associated with earlier onset of adolescent alcohol consumption and with AUDs in adulthood (Enoch 2010).

Childhood maltreatment is more likely to occur among children of alcoholics (Gilbert et al. 2009); in these cases, the parents may not only engage in harmful parenting practices (Kettinger et al. 2000; Stanger et al. 2004; Suchman et al. 2007, 2008) but also may pass along genes increasing the risk of AUDs to their offspring. Thus, the specificity of the relationship between maltreatment and alcohol use in the context of these other risk factors remains an open debate. Furthermore, psychiatric comorbidity also may confound the relationship between early maltreatment and AUDs because maltreatment affects the risk for multiple psychiatric disorders (Green et al. 2010; Kendler et al. 2000; Kessler et al. 1997; Widom et al. 2007a), and AUDs are highly comorbid with other forms of psychopathology (Hasin et al. 2007b). Studies using animal models, which can control for environmental factors and comorbidity, have suggested that extended stress in early life leads to later self-administration of alcohol (Cruz et al. 2008; Miczek et al. 2008). However, some epidemiologic studies suggest that the relationship between maltreatment and AUDs may be at least partially confounded by family history of alcohol problems. For example, a prospective cohort study that compared court-recorded cases of abuse and neglect with matched community controls in the Midwest found no remaining association between early abuse and adult AUDs1 after controlling for family history of alcohol problems among men (Widom et al. 1995, 2007b); only among women physical neglect remained associated with AUDs.

However, several studies that controlled for family history of alcoholism have indicated a persistent relationship between childhood adverse events, including parental divorce (Pilowsky et al. 2009; Thompson et al. 2008) and death of a parent or foster home placement (Kendler et al. 1996; Pilowsky et al. 2009), and adult risk for AUDs. Another study documented strong and significantly increased odds of AUDs based on retrospective assessment of childhood sexual abuse among same-sex twins in Australia (Nelson et al. 2002), even after controlling for family background variables such as parental alcohol problems. Finally, recent data from a population-based study of twins in Virginia reported that participants who reported any maltreatment were 1.74 times as likely to experience an AUD in adulthood as were people who did not report maltreatment, and although controlling for family-level risk factors substantially attenuated the observed association, a direct effect remained after control (Young-Wolff et al. 2011).

Research now is examining specific genetic variations (i.e., polymorphisms) as moderators of the relationship between child maltreatment and AUDs. The finding that functional polymorphisms in the gene encoding the monoamine oxidase A enzyme (MAOA) (Caspi et al. 2002) interact with childhood maltreatment to predict antisocial behavior in adulthood stimulated research on whether this effect generalizes to substance use disorders; however, thus far, the findings could not be replicated (Young et al. 2006). Other studies have focused on the previously mentioned serotonin transporter promoter variant, 5-HTTLPR, and its interaction with stressful experiences in a wide variety of psychiatric outcomes after researchers detected such an interaction for major depression (Caspi et al. 2003). This DNA sequences exists in two alleles, l and s alleles; thus, a person can carry either two l or two s alleles (i.e., be homozygous for l or s) or one l and one s allele (i.e., be heterozygous). One study found that youth with court-documented maltreatment were at higher risk for early-onset alcohol use if they had the heterozygous (s/l) genotype compared with the l/l genotype (Kaufman et al. 2007). In another youth study, the effect of the same heterozygous genotype on increased risk for substance use was attenuated in families providing involved-supportive parenting (Brody et al. 2009a). In an innovative approach involving random assignment of the environment, the investigators then randomized at-risk families to an intervention designed to increase involved-supportive parenting or a control condition (Brody et al. 2009b). Among those with the heterozygous 5-HTTLPR genotype, children in treated families had less substance use at followup compared with children of the control families (Brody et al. 2009b). Taken together, these studies suggest that the risk for later alcohol outcomes is affected by an interaction of stressful early home environments and genetic vulnerability.

Minority Stress and AUDs

Minority stress is defined as exposure to specific stressors that result from a person’s minority status, especially prejudice and discrimination events (Meyer 2003b; Williams et al. 2003). These events range from mild (e.g., daily hassles, such as being followed in a store) to more severe (e.g., being a victim of a violent crime) and include both emotional (e.g., workplace harassment [Waldo 1999]) and physical (e.g., hate crimes [Herek 2009]) threats to self. Minority status cannot be attributed to having an AUD, making one aspect of interpretation straightforward in studies in this area. Although minority stress can involve acute events, it most frequently is viewed as a chronic exposure that occurs across the entire life course (Williams et al. 2003). Finally, minority stressors vary with respect to whether they are expected. Research has indicated that although many stressors that members of minority groups confront are unanticipated, one consequence of repeated exposure to discrimination is that people begin to expect rejection based on their stigmatized identity (Mendoza-Denton et al. 2002).

Racial/Ethnic Minorities

According to minority stress models, the stress resulting from prejudice and discrimination should lead to elevations in alcohol use among minority group members. Patterns of alcohol use among racial/ethnic minorities, however, fail to correspond to these predictions. Although Native Americans have higher rates of alcohol consumption and AUDs compared with non-Hispanic Whites (Hasin et al. 2007b), several large surveys have indicated lower rates of alcohol consumption and AUDs among non-Hispanic Blacks, Asians, and Hispanics compared with Whites (Breslau et al. 2006; Hasin et al. 2007b; Kessler et al. 1994). These minority groups also have lower rates of other psychiatric disorders (e.g., major depression), leading to what has been called the “minority paradox” (Williams 2001) in mental health research—that is, minority groups such as Blacks and Hispanics have lower rates of psychiatric and substance disorders despite greater exposure to institutional and interpersonal discrimination that has been shown to engender substantial stress via biological (Lewis et al. 2006) and psychological (Hatzenbuehler 2009) mechanisms. In contrast to these findings from between-group studies, within-group studies consistently show that perceived discrimination is associated with alcohol outcomes. This association has been found in Blacks (McLaughlin et al. 2010b; Taylor and Jackson 1990; Yen et al. 1999), Filipino Americans (Gee et al. 2007) and Asian-American adolescents (Yoo et al. 2010).

In contrast to racial/ethnic minorities, lesbian, gay, and bisexual (LGB) individuals have higher rates of substance use and substance use disorders than their heterosexual peers (Garofalo et al. 1998; Russell et al. 2002; Ziyadeh et al. 2007); this difference applies to both adolescents (Eisenberg and Wechsler 2003; Hatzenbuehler et al. 2008) and adults (Burgard et al. 2005; Cochran et al. 2000; Drabble et al. 2005). Although research has tended to primarily examine perceived discrimination as a risk factor for internalizing psychopathology, such as depression and anxiety, recent studies also have shown higher levels of alcohol use (Hatzenbuehler et al. 2011) and AUDs (McCabe et al. 2010) among LGBs who perceive that they have experienced higher levels of discrimination.

Because of their design, these studies cannot rule out reverse causality—that is, that individuals with alcohol problems may perceive and report greater discrimination. In order to address some of these methodological limitations of subjective measures of discrimination, recent studies have developed novel measures for operationalizing objective stressors that LGB individuals confront, including institutional forms of discrimination (e.g., anti-marriage laws or employment discrimination policies). Because these institutional stressors occur outside the control of LGB individuals, they are not confounded with mental health status and therefore provide a stronger test of the effect of discrimination on mental health than measures of subjective stress. Studies are beginning to document the relationship between these objective stressors and LGB health, including alcohol use. For example, a recent study examined the impact of State-level ballot initiatives banning gay marriage on the prevalence of psychiatric and substance use disorders in LGB populations (Hatzenbuehler et al. 2010). The results indicated that LGB respondents living in States that passed such bans in 2004 had significantly greater increases in psychiatric disorders and AUDs than did LGB respondents in States that did not pass such bans (Hatzenbuehler et al. 2010). This research demonstrates the potential importance of incorporating more objectively-defined indices of social stress into research on alcohol use among minority populations. Indeed, an examination of how and why such social stressors contribute to the development and maintenance of AUDs within LGB populations represents a crucial avenue for future inquiry.

Childhood Trauma, Posttraumatic Stress Disorder, and Alcohol Dependence

Early-childhood trauma is strongly associated with developing mental health problems, including alcohol dependence, later in life. People with early-life trauma may use alcohol to help cope with trauma-related symptoms. This article reviews the prevalence of early-childhood trauma and its robust association with the development of alcohol use disorders and posttraumatic stress disorder. It also examines the potential biological mechanisms by which early adverse experiences can result in long-lasting changes in neurobiology underlying this vulnerability, as well as pharmacological and behavioral interventions. Recent investigations highlight the importance of assessing trauma among patients with alcohol use disorders and the positive benefits associated with the application of integrative psychosocial interventions that target both trauma-related symptoms and alcohol dependence.

Key words: Alcohol dependence; alcohol use disorders; childhood; childhood trauma; trauma-related symptoms; posttraumatic stress disorder; coping with stress or anxiety; neurobiology; biological mechanisms; treatment; pharmacological intervention; behavioral intervention; integrative psychosocial intervention; adverse child-rearing environment

Children exposed to severe adversity early in life are at increased risk of subsequently developing mental health problems, including alcohol dependence. In general, the onset of trauma precedes the onset of alcohol dependence. Although it is impossible to establish a direct causal relationship, this temporal relationship suggests a robust and positive relationship between exposure to early-life trauma and alcohol-related problems later in life. People with trauma-related symptoms and other negative consequences of early-life trauma may use alcohol to help mitigate such symptoms. People with both a positive history of early childhood trauma and co-occurring alcohol dependence have a more severe clinical profile, as well as worse treatment outcomes when compared with those with either early trauma or alcohol dependence alone. Recent investigations highlight the importance of assessing trauma among patients with alcohol use disorders and the positive benefits associated with the application of integrative psychosocial interventions that target both trauma-related symptoms and alcohol dependence. This article reviews the prevalence of early-childhood trauma and its robust association with the development of alcohol use disorders and posttraumatic stress disorder (PTSD). It also examines the potential biological mechanisms by which early adverse experiences can result in long-lasting changes in neurobiology underlying this vulnerability, as well as pharmacologic and behavioral interventions.


There is little doubt that severe childhood adversity may place an individual at life-long risk for a variety of problems, including those related to mental health, physical health, employment, and legal difficulties (Putnam 2006). In a study conducted by the Centers for Disease Control and Prevention and Kaiser Permanente (Adverse Childhood Experiences [ACE] study; Felitti et al. 1998), a sample of 17,337 adults recruited from a large health maintenance organization were surveyed concerning a range of adverse events that might occur during childhood (e.g., physical or sexual abuse, incarcerated household member, emotional neglect) and adult risk behaviors, health status, and disease. The investigators found a graded relationship between the number of adverse childhood experiences (i.e., ACE score), risk behaviors during adulthood, and leading causes of morbidity and mortality in the United States, including heart disease, diabetes, liver disease, and emphysema. It is possible that these increased rates of medical conditions are not a direct result of childhood adversity but rather the result of dysfunctional and unhealthy behaviors in which many victims of childhood abuse engage.

A number of studies also report that victims of child maltreatment are more likely to have emotional difficulties and psychiatric disorders. One of the most consistent results across these studies is the finding that childhood maltreatment is associated with an increased risk for alcohol and drug use disorders (Enoch 2011). In a population-based sample of 1,411 female adult twins, self-reported childhood sexual abuse was positively associated with a number of psychiatric disorders, but the strongest associations were with alcohol and drug dependence (Kendler et al. 2000). In the ACE study, the risk of alcohol dependence increased 7.2-fold, and illicit drug use increased 4.5-fold for people with four or more ACEs (Anda et al. 2006). People with a history of childhood abuse or neglect are vulnerable to using alcohol in order to cope with stressful situations, which in turn may lead to excessive alcohol use (Schuck and Widom 2001). An investigation by Widom and colleagues (2007) demonstrates that the increased risk of excessive alcohol use among victims of childhood abuse or neglect is consistent and stable into middle adulthood (e.g., age 40). Furthermore, research has shown that alcohol-dependent patients with a history of sexual abuse are more likely than nonabused patients to relapse to alcohol use (87.5 vs. 63.3 percent) and to relapse more quickly (median time to first drink = 60 vs. 115 days) in the first year following inpatient treatment for alcohol dependence (Greenfield et al. 2002).

In addition to alcohol use disorders, childhood adversity is associated with an increased risk of PTSD (Widom 1999). Data from a number of studies over the last 20 years have emphasized the high co-occurrence of PTSD and alcohol disorders. For example, among 3,768 female twins participating in the longitudinal Missouri Adolescent Female Twin Study (MOAFTS), Sartor and colleagues (2010) found that women exposed to trauma were nearly twice as likely to develop alcohol dependence (hazard ratio 1.85), and women exposed to trauma who also had PTSD were even more likely to develop alcohol dependence (hazard ratio 3.54; significantly higher than women with trauma exposure alone) when compared with women who had not experienced trauma. Studies of samples of individuals seeking treatment for alcohol use disorders also find a high prevalence of reported childhood adversity and PTSD. In a study of men and women in treatment for addictions, 62 percent reported having been victims of childhood physical or sexual abuse (Grice et al. 1995). A review of studies of individuals seeking treatment for addictions reveals rates of PTSD as high as 50 percent or greater (Dansky et al. 1994). In the majority of cases, the development of PTSD precedes the development of the substance use disorder.

These high rates of childhood victimization in individuals with PTSD and alcohol and other substance-related problems suggests that there is a link between childhood adversity and the development of these disorders, although it is impossible to establish a direct causal relationship. However, even when studies control for demographic differences, family discord, and parental pathology, the specific relationship between childhood abuse and the development of substance use disorders holds true. Several theoretical connections have been postulated (Miller et al. 1993). Childhood victimization may lead to low self-esteem and the subsequent use of alcohol to deal with negative cognitions. It also is possible that victims of childhood abuse feel that their experiences make them “different” from other children and lead them to withdraw from healthier social circles toward fringe groups, where alcohol use is more accepted. In any case, given that victims of child abuse are more likely to develop alcohol use disorders as adults, early intervention, prevention, and training for parents are all important in interrupting this cycle of violence and alcohol problems.


Recognizing the pervasive and detrimental effects of adverse childhood experiences on quality of life and health outcomes has led to the exploration of potential biological mechanisms by which early experiences can produce long-lasting changes. Evidence from both animal and human research suggests that early stressors can lead to neurobiological changes in systems known to be involved in the pathophysiology of depression, anxiety, and substance use disorders (De Bellis et al. 1999; Heim and Nemeroff 2001). The hypothalamic–pituitary–adrenal (HPA) axis plays a critical role in the stress response and is involved in the pathophysiology of addictive disorders. Early stressors cause long-term increases in the stress response of the hormone cortisol (Plotsky and Meaney 1993) as well as decreased genetic expression of cortisol receptors and increased expression of corticotropin-releasing factor in the hypothalamus, both of which may contribute to dysregulation of the HPA axis (Ladd et al. 1996). The noradrenergic system also plays a key role in stress (Bremner 2003), and early stressors can lead to long-term decreases in a-2 noradrenergic receptors in the locus coeruleus, which may lead to loss of feedback inhibition of noradrenergic activity with associated increases in the noradrenergic stress responses (Caldji et al. 1998; Sanchez et al. 2001).

In addition to the long-lasting effects of early trauma on the stress response, a number of studies indicate that early trauma has specific effects on the neurotransmitter systems involved in the positive reinforcing effects of alcohol and drugs, particularly the brain pathway for dopamine (i.e., the mesocorticolimbic dopamine system) (Meaney et al. 2002). Higley and colleagues (1991) found that adult rhesus monkeys raised in peer groups without maternal care showed increased HPA response to stress and increased alcohol consumption during periods of stress (Higley et al. 1991). In a series of studies, Meaney and colleagues (2002) demonstrated that repeated periods of maternal separation in the early life of rats decreased dopamine transporter expression and increased dopamine responses to stress and behavioral responses to stress, cocaine, and amphetamine. These findings suggest that early-life experiences can affect the development of the mesocorticolimbic dopamine system and lead to a vulnerability to addiction in later life. Thus, in addition to effects on stress reactivity, early-life events might predispose individuals to the development of alcohol use disorders by directly influencing the reinforcing effects of alcohol. Other neurotransmitter systems involved in the pathophysiology of alcohol dependence, such as brain-derived neurotrophic factor (BDNF), serotonin, and γ-aminobutyric acid (GABA) systems also are affected by early-life trauma in ways that may influence vulnerability to the development of alcohol dependence, but the mechanistic connections in these systems are under active investigation and are not as well understood (Enoch 2011).

Not all children exposed to early-life trauma develop alcohol dependence or other significant pathology, clearly suggesting that resilience and mediating factors play a role (Enoch 2011). The genetic risk for alcohol and drug dependence involves multiple genes. Emerging evidence suggests that variation in some stress-related genes may determine the risk for psychopathology or resilience in people exposed to early-life trauma. In particular, it seems that there are important variations in the genes encoding the CRF system that can influence the development of alcohol dependence following an early-life trauma in a gene-by-environment interaction. One study of at-risk children found an interaction between a particular genetic variant coding for the CRF receptor (i.e., CRHR1) and sexual trauma in adolescents that predicted an earlier age of onset of drinking and heavy alcohol consumption (Blomeyer et al. 2008). This finding is supported by animal studies demonstrating that the CRHR1 genotype and expression interact with environmental stress to reinstate alcohol-seeking in rodents (Hansson et al. 2006), and a functional CRF promoter variant in monkeys conferred increased stress reactivity and was associated with increased alcohol consumption in animals reared under stressful conditions (Barr et al. 2009). These findings suggest that the interaction of genetic susceptibility and environmental exposure can lead to a pathologically activated CRF system, which increases the risk for the development of alcohol dependence in some people.


Both behavioral and pharmacological interventions are important to consider in the treatment of alcohol dependence and trauma/PTSD (Davis et al. 2006; Weiss and Kueppenbender 2006). To date, most empirical studies of behavioral or pharmacological agents have investigated the treatment of either alcohol dependence or PTSD alone.

Psychosocial Interventions

With regard to psychosocial interventions, cognitive–behavioral therapies (CBTs) are the most widely studied and empirically valid treatments for both PTSD and alcohol use disorders. The CBTs used to treat PTSD fall into three main categories: (1) exposure-based therapies, (2) cognition-focused therapy, and (3) anxiety/stress-management therapy. Exposure-based therapies are considered the gold standard treatment for PTSD (Institute of Medicine 2008) and involve having patients confront safe, but anxiety-provoking situations (i.e., physical location where childhood abuse occurred), known as in vivo exposure; and the memory of the traumatic experience, known as imaginal exposure (Foa et al. 2006). With prolonged, repeated in vivo and imaginal exposure, the trauma-related anxiety is extinguished. Cognition-focused therapy includes cognitive therapy, which addresses the meaning that people assign to early-life trauma; and cognitive- processing therapy, which combines a narrative element of exposure therapy with efforts to identify and modify unhelpful cognitions related to the themes of safety, trust, power, esteem, and intimacy (Resick and Schnicke 1992). Finally, stress inoculation training (Meichenbaum and Novaco 1985), one of the most widely used and empirically investigated forms of anxiety management therapies, aims to provide a sense of mastery over PTSD symptoms by teaching patients a variety of coping skills. Stress inoculation training also has been incorporated into CBTs for substance use disorders and includes relaxation training, breathing retraining, thought stopping, self-instruction training, assertiveness training, cognitive restructuring, anger management, and problem solving.

Recently, integrative psychosocial interventions have been developed to address both trauma/PTSD and substance use disorders simultaneously (Back 2010). Clinicians previously believed that trauma interventions were inappropriate until after a patient had been abstinent from alcohol or drugs for a sustained period of time (e.g., 3 months). This model, known as the “sequential” model, posits that continued alcohol use impedes therapeutic efforts to address and process the trauma, and that trauma interventions commenced before sustained abstinence would result in increased risk of relapse. Contrary to these beliefs, however, recent data reported by several different investigators in the United States and Australia show that treatment outcomes of substance dependent patients who engage in integrative CBT interventions typically experience significant improvements in both conditions and that rates of relapse are not increased by the introduction of therapy for trauma (Brady et al. 2001; Hien et al. 2004; McGovern et al. 2009; Najavits 2002; Triffleman et al. 1999). Proponents of integrative treatments posit that unprocessed trauma-related memories and PTSD symptoms may, at least in part, drive alcohol use. Thus, attending to and treating the trauma-related symptoms early in the process of therapy may improve the chances of long-term recovery from alcohol (Back et al. 2006; Hien et al. 2010). Although more randomized controlled trials of integrative treatments are needed, the studies to date clearly demonstrate that for the majority of alcohol-dependent patients with trauma/PTSD, the inclusion of trauma interventions confers substantial therapeutic benefits.

Pharmacological Interventions

There are several general issues to consider when treating co-occurring alcohol dependence and trauma/PTSD. When pharmacological agents are used, treatment should generally follow routine clinical practice for the treatment of PTSD. Regardless, relapse is common, and it is critical to consider the potential toxic interactions that may occur between the prescribed medication and alcohol. Given the high co-occurrence of alcohol and illicit drug use, potential toxic interactions between the prescribed medication and other substances of abuse must also be addressed. The pharmacological agent with the least abuse liability potential should be chosen for this population. Although benzodiazepines are effective in providing immediate relief of anxiety symptoms, they are generally not considered a first-line treatment for patients with alcohol dependence given the abuse potential of benzodiazepines. During the initial phase of treatment, when latency of onset of antidepressants is an issue, benzodiazepines may be considered as adjunctive medication. The amount of benzodiazepines prescribed to the patient should be limited, and the patient should be closely monitored for relapse or nonmedical use of benzodiazepines or other medications.

The use of pharmacological agents to specifically target alcohol dependence and PTSD is underexplored. Most studies to date, however, show promise and suggest that patients with co-occurring alcohol dependence and trauma/PTSD respond well to standard PTSD pharmacotherapies. Sertraline, a serotonin-specific reuptake inhibitor, has been investigated in patients with comorbid alcohol dependence and PTSD. The first study was a small (n = 9) open-label, 12-week trial, which demonstrated significant pre–post decreases in alcohol use severity (e.g., number of drinking days, number of drinks per day), as well as PTSD symptoms of re-experiencing the trauma, avoidance, and hyperarousal (Brady et al. 1995). A second study examined the efficacy of 12 weeks of sertraline compared with placebo in 94 patients with alcohol dependence and PTSD (Brady et al. 2005). The primary outcome analysis indicated no significant effect of sertraline on alcohol-related outcomes and only trend-level findings for the PTSD outcomes. The sertraline- treated group showed statistical trends for greater improvement in the experience of sudden flashbacks of the traumatic event and hyperarousal symptoms (e.g., insomnia, inability to concentrate). Follow-up cluster analyses suggested that individuals with primary PTSD, compared with primary alcohol dependence, derived more benefit from sertraline treatment as evidenced by significantly less severe alcohol use. The results suggested that patients with early- onset alcohol dependence actually had worse alcohol-related outcomes with sertraline treatment compared with placebo (Brady et al. 2005).

In another study of 254 veterans with alcohol dependence and a variety of co-occurring mood and anxiety disorders (Petrakis et al. 2005), naltrexone, disulfiram, or a combination of both was added to treatment as usual. A high percentage (42.9 percent) of the study participants had PTSD, although data analysis for specific disorders was not conducted. Alcohol-related outcomes improved significantly in patients treated with either medication alone or with combination therapy, compared with placebo, but there was no added improvement with combination therapy when compared with monotherapy. This study strongly suggests that alcohol-dependent patients with co-occurring PTSD should receive medications targeting alcohol consumption.

There is good rationale for the exploration of a number of other compounds in the treatment of co-occurring PTSD and alcohol dependence. Prazosin blocks a specific a1-adrenergic receptor and has shown promise in several well-controlled trials for the treatment of PTSD, particularly in decreasing PTSD- related sleep disturbance and nightmares (Raskin et al. 2007). In a preliminary study, prazosin decreased alcohol consumption in an alcohol-dependent population (Simpson et al. 2009). This inexpensive and relatively safe drug warrants investigation in the treatment of co-occurring PTSD and alcohol dependence. In addition, several anticonvulsant agents, such as topirimate, have shown promise in the treatment of alcohol dependence (Johnson et al. 2003). It is hypothesized that actions on the glutamatergic systems might be responsible for these agents’ therapeutic actions. PTSD also has been associated with glutamatergic dysregulation, and anticonvulsant agents have shown promise in small-number, open-label studies in the treatment of PTSD. This is another area in which additional investigation is warranted. More research clearly is needed to help advance the behavioral and pharmacological treatment of co-occurring trauma/PTSD and substance use disorders.

Anxiety and Alcohol Use Disorders: Comorbidity and Treatment Considerations

The co-occurrence of anxiety disorders and alcohol use disorders (AUDs) is relatively common and is associated with a complex clinical presentation. Sound diagnosis and treatment planning requires that clinicians have an integrated understanding of the developmental pathways and course of this comorbidity. Moreover, standard interventions for anxiety disorders or AUDs may need to be modified and combined in targeted ways to accommodate the unique needs of people who have both disorders. Optimal combination of evidence-based treatments should be based on a comparative balance that considers the advantages and disadvantages of sequential, parallel, and integrated approaches.

Key words: Alcohol use disorders; stress; anxiety disorders; comorbidity; developmental pathway; treatment; treatment method; sequential approach; parallel approach; integrated approach

Co-occurring anxiety disorders and alcohol use disorders (AUDs) are of great interest to researchers and clinicians. Cumulative evidence from epidemiological and clinical studies over the past few decades has highlighted both the frequency and clinical impact of this comorbidity. Investigations into the unique connections between specific anxiety disorders and AUDs have shown that this association is multifaceted and complex, underscoring the importance of careful diagnostic scrutiny. Of clinical relevance, treatment for people with comorbid anxiety and AUDs can be complicated, and both the methods used and the timing of the interventions are relevant factors in treatment planning and delivery. This article explores the relationship between anxiety disorders and AUDs, focusing on the prevalence, clinical impact, developmental and maintenance characteristics, and treatment considerations associated with this fairly common comorbidity. The distinctive nature of the relationship between posttraumatic stress disorder (PTSD) and AUDs is discussed separately, in the article by Brady and Back, p. 408 in this journal issue.

Prevalence and Clinical Impact of Comorbid Anxiety and AUDs

Accuracy in prevalence estimates of comorbid anxiety and AUDs is essential for gauging the magnitude of the clinical and social impact of this comorbidity; therefore, data should be carefully selected with attention to sampling methods. Information derived from clinical samples, although enlightening in its own right, produces inflated approximations of the prevalence of comorbidity (Kushner et al. 2008; Regier et al. 1990; Ross 1995). The most frequently offered explanation for the biased estimates from clinic-based samples suggests that individuals with multiple disorders are more likely to be referred for treatment than individuals with a single disorder (Galbaud Du Fort et al. 1993; Kushner et al. 2008). To avoid this bias, epidemiological data drawn from large-scale community samples can provide the most informative figures.

Over the past three decades, multiple population-based studies have surveyed the prevalence of addictive and mental disorders in the United States and abroad, including the following:

The respective prevalences of comorbid anxiety disorders and AUDs from each of these epidemiological studies are summarized in table 1. These data show that, across different large-scale studies, at different times, and both in the United States and abroad, anxiety and AUDs co-occur at rates greater than would be expected by chance alone. The odds ratios (ORs) characterizing the comorbidity between an AUD and any anxiety disorder in these studies ranged between 2.1 and 3.3—in other words, the two conditions co-occurred about two to three times as often as would be expected by chance alone.

Three additional trends emerging from community-based samples are noteworthy. First, anxiety disorders are more strongly associated with alcohol dependence than with alcohol abuse (e.g., Hasin et al. 2007; Kessler et al. 1996; Kushner et al. 2008). Analysis of the NESARC data demonstrated that this finding generally was consistent across racial/ethnic groups (Smith et al. 2006). Alternative explanations for these results suggest that either people with anxiety disorders are more likely to become psychologically dependent on alcohol because they use it to self-medicate (e.g., Tran and Smith 2008) or anxiety disorders in these individuals largely are an artifact of alcohol withdrawal (e.g., Schuckit and Hesselbrock 1994).

Second, the magnitude of the relationship between specific anxiety disorders and AUDs varies across the specific combinations. For example, panic disorder typically has a relatively large association with AUDs (odds ratio [OR] = 1.7–4.1 in table 1), whereas obsessive-compulsive disorder has the least consistent and typically weakest relationship with alcohol problems (e.g., Gentil et al. 2009; Kessler et al. 1997; Schuckit et al. 1997; Torres et al. 2006). A classic review in this field (Kushner et al. 1990) indicated even more pronounced differences in the comorbidity rates of specific anxiety disorders among clinic-based samples of patients with alcohol problems. These ranged from rates near community-based rate estimates (e.g., for simple phobia) to rates nine times greater than community estimates (e.g., for social phobia). It is important to note, however, that the influence of treatment seeking and related variables confounds interpretation of these clinic-based estimates.

Third, different comorbidity patterns exist among patient subgroups with different demographic characteristics such as race/ethnicity and gender. For example, in the NESARC, Native Americans had elevated rates both of anxiety disorders and of AUDs over the past 12 months but lower rates of co-occurrence between these disorders compared with other ethnic groups (Smith et al. 2006). Gender differences in anxiety–alcohol comorbidity have been reported across a variety of samples (e.g., Hesselbrock et al. 1985; Kessler et al. 1997; Mangrum et al. 2006; Merikangas et al. 1998), and research in this area also has identified notable clinical differences between men and women. These gender differences are discussed in more detail in the sidebar.

The importance of these prevalence data is underscored by the clinical impact of comorbid anxiety and AUDs. Both types of disorder are associated with substantial societal costs that have been estimated in monetary terms at $184.6 billion per year for AUDs (Harwood 2000) and between $42 and $47 billion for anxiety disorders (DuPont et al. 1996; Greenberg et al. 1999). Kessler and Greenberg (2002) suggested that the costs for anxiety disorders were grossly underestimated and actually exceeded $100 billion per year in the total U.S. population. Furthermore, clinical studies have shown that both anxiety and AUDs can negatively impact the course and treatment outcome for the other condition. For example, anxiety problems have been associated with increased severity and persistence of AUDs, increased risk for relapse following treatment, and increased lifetime service utilization in the context of substance use disorders more generally (Driessen et al. 2001; Falk et al. 2008; Kushner et al. 2005; Johnston et al. 1991; Perkonigg et al. 2006; Sannibale and Hall 2001). Conversely, concurrent AUDs have been associated with greater severity and chronicity of anxiety disorders, and substance use problems can decrease the likelihood of recovery from anxiety disorders (Bruce et al. 2005; Hornig and McNally 1995; Schade et al. 2004). Studies also have demonstrated that alcohol use can increase anxiety (see Kushner et al. 2000), which can result in a positive feedback loop leading to exacerbation of both disorders.

Taken together, the epidemiological and clinical literature describing the relationship between anxiety and AUDs shows that this comorbidity is both prevalent and clinically relevant. Therefore, it is important to enhance understanding of this comorbidity. The following sections will review fundamental concepts related to how these disorders co-occur and describe approaches to diagnosing and treating comorbid anxiety and AUDs.

Development of Comorbid Anxiety and AUDs

The question of how anxiety and AUDs coalesce has intrigued investigators and clinicians for decades and still is a subject of debate. Three primary pathways have been proposed:

The Common-Factor Model

The common-factor model of comorbid anxiety and AUDs presumes that no direct causal relationship exists between the two disorders. Instead, so-called third variables are posited to account for their joint presence. The potential relevance of such factors was demonstrated in a 21-year longitudinal study of young people (Goodwin et al. 2004), in which early presence of anxiety disorders seemed to predict the later development of alcohol dependence. However, when the investigators controlled for other variables, such as prior other drug dependence and depression, the presence of anxiety disorders no longer was a significant predictor. The results of this study suggest that the link between anxiety and AUDs was not direct but instead may have been a consequence of those other variables studied. The potential range of common factors can be difficult to estimate, but a review of the literature shows that the most consistently proposed third variables are genetic factors and personality traits such as anxiety sensitivity. Support for the role of genetic factors as a cause for the co-presence of these disorders indirectly has been provided by family and twin studies (e.g., Merikangas et al. 1994, 1996; Tambs et al. 1997). Anxiety sensitivity also has been linked to the incidence of both anxiety and substance use disorders (DeHaas et al. 2001; DeMartini and Carey 2011; Schmidt et al. 2007). Based on findings demonstrating a genetic contribution to anxiety sensitivity (Stein et al. 1999), Stewart and Conrod (2008) proposed a causal sequence wherein genetic factors and anxiety sensitivity operate together to create a genetically based personality that is vulnerable to comorbid anxiety and alcohol use problems. To date, rigorous empirical evaluation of the common-factor model has been limited, and publications directly addressing this topic are sparse. Additional research and exploration of additional third variables therefore is necessary to more clearly appraise their unique and interactive influence on the relationship between these disorders.

The Self-Medication Model

The self-medication explanation for the comorbidity of anxiety and AUDs has received the most attention in the clinical and research literature. This model proposes that people with anxiety disorders attempt to alleviate negative consequences of these conditions (i.e., are negatively reinforced) by drinking alcohol to cope with their symptoms, eventually leading to the later onset of AUDs. This concept, in fact, is shared by several models of alcoholism, including the self-medication (Khantzian 1985; Quitkin et al. 1972), tension reduction (Conger et al. 1999), and stress-response dampening models (Sher 1987; Sher and Levenson 1982). Several lines of evidence provide support for this pathway. When people with comorbid anxiety and AUDs are queried about their drinking, they typically endorse purposeful and targeted drinking to cope with their anxiety. The reported rates of self-medication in clinical samples of people with both types of disorders have ranged from 50 to 97 percent, with the highest rates among people with phobias (Bibb and Chambless 1986; Smail et al. 1984; Thomas et al. 2003; Turner et al. 1986).

It is interesting to note that participants with anxiety disorders in community samples show significantly less robust rates of self-medication than typically found in clinical samples, highlighting the potential selection bias in treatment settings (e.g., Bolton et al. 2006; Menary et al. 2011; Robinson et al. 2009). For example, in the NCS (Bolton et al. 2006) only 21.9 percent of individuals with anxiety disorders in the community endorsed self-medicating with either alcohol or drugs, with the highest rates found among those with generalized anxiety disorder (35.6 percent), panic disorder (23 percent), or social phobia–complex subtype (21.2 percent). In the NESARC, Robinson and colleagues (2009) separately analyzed rates of self-medication with alcohol, drugs, or both among respondents with anxiety disorders. The investigators found that these individuals were most likely to endorse self-medication with alcohol alone and that the highest rates of alcohol-based self-medication were found among respondents with generalized anxiety disorder (18.3 percent), social phobia (16.9 percent), and panic disorder with agoraphobia (15.0 percent). More recently published longitudinal analyses of alcohol-using NESARC participants showed nearly identical rates of self-medication with alcohol among those with anxiety disorders at both Wave 1 (20.3 percent) and Wave 2 (20.8 percent) (Menary et al. 2011). Interestingly, this report also showed that although only 1 in 5 individuals with anxiety disorders reported using alcohol to cope with anxiety, the rate of alcohol dependence in this subgroup (34.5 percent) was almost four times higher than the comparison rates found among respondents with anxiety who did not report self-medication (9.3 percent) and almost seven times higher than among respondents with no anxiety diagnosis (5.1 percent). Moreover, endorsement of alcohol-based self-medication at Wave 1 increased the risk of developing new alcohol dependence at Wave 2 nearly four-fold (OR = 3.77). These epidemiological findings reveal that although only a minority of people with anxiety disorders uses alcohol to self-medicate, the risk for co-occurring alcohol dependence is concentrated among this subgroup.

Additional epidemiological support for this causal pathway comes from analyses of order of onset as well as from analyses of whether the anxiety disorders are considered independent or substance induced. Data showing that anxiety disorders predate AUDs and that anxiety disorders are independent (i.e., not merely a consequence) of AUDs are essential prerequisites for the self-medication model. Consistent with this causal explanation of comorbidity, timelines gathered in community surveys show that anxiety disorders often predate the development of alcohol dependence. For example, Kushner and colleagues (2008) reviewed findings from several large-scale studies and calculated that three of four individuals with comorbid disorders developed the anxiety disorders first. The classification of anxiety disorders as independent versus substance-induced requires that one of two conditions is met: (1) the anxiety disorder must precede the AUD and (2) the anxiety disorder persists outside the direct influence of alcohol use. Because alcohol withdrawal can mimic and/or exacerbate anxiety problems, an extended period of abstinence (e.g., 4 weeks) from alcohol is necessary for a disorder to be considered a stand-alone, independent diagnosis. Using these criteria with the NESARC sample, which strictly followed DSM–IV rules for differential diagnosis, only 0.2 percent of anxiety disorders were not classified as independent (Grant et al. 2004). Likewise, low rates of substance-induced anxiety disorders (0.3 percent) were found in a community sample of 1,095 Australian women (Williams et al. 2010), based on DSM–IV–TR criteria (APA 2000).

Taken together, all of these findings provide compelling support for the self-medication explanation for co-occurring anxiety and AUDs. However, these lines of evidence are associated with several limitations. For example, the analyses often rely on retrospective self-reported data. Findings derived from clinical samples also can inflate prevalence estimates of self-medication, especially if alcohol-dependent individuals are evaluated during acute alcohol withdrawal. Finally, it is notable that laboratory studies examining alcohol’s anxiety-reducing (i.e., anxiolytic) effects have produced mixed findings (see Tran and Smith 2008). One possible explanation for the incongruence between laboratory and self-report survey data is that a person’s expectations about alcohol’s effects can motivate drinking independent of alcohol’s actual physiological effects (e.g., Abrams and Kushner 2004). Never­theless, laboratory-based investigations of whether (and how) alcohol actually reduces anxiety are essential to critically evaluate the self-medication hypothesis. The current state of the science on this point is inconclusive, and additional research is necessary before any firm conclusions regarding this pathway can be drawn.

The Substance-Induced Anxiety Model

The third causal explanation for comorbid anxiety and AUDs asserts that anxiety largely is a consequence of heavy, prolonged alcohol consumption. Alcoholism leads to a range of biopsychosocial problems, and anxiety can result from alcohol-related disturbances in each of these domains. The course of alcohol dependence is fraught with repeated intermittent episodes of excessive and frequent consumption and withdrawal, which can result in changes in the nervous systems that produce and/or worsen anxiety. For example, whereas acute alcohol intake has anxiolytic effect by increasing the activity of the brain chemical (i.e., neurotransmitter) γ-aminobutyric acid (GABA), chronic alcohol dependence results in an overall GABA deficiency that offsets the effects of acute consumption and may induce anxiety. Withdrawal periods also can induce changes in the brain, which can include excessive activity (i.e., hyperexcitability) of certain brain systems (i.e., the limbic system and the norepinephrine system) (Kushner et al. 2000; Marshall 1997), both of which are involved in the production of panic attacks (Graeff and Del-Ben 2008; Marshall 1997). Across time, repeated withdrawal episodes can result in a progressive neural adaptation (i.e., a process known as kindling) that makes the drinker more susceptible to anxiety and exacerbates stress-induced negative affect when alcohol intake stops (Breese et al. 2005). Not surprisingly, clinical studies show that people with alcoholism who are recently abstinent characteristically report increased feelings of anxiety, panic, and phobic-like behaviors in the short term, and symptoms of autonomic activity (i.e., sympathetic activation, such as increased heart rate and faster/shallower breathing) and persistent anxiety across protracted withdrawal (see Schuckit and Hesselbrock 1994).

The psychosocial impact of alcoholism also has been implicated in the genesis of anxiety. Social consequences of habitual excessive drinking are common and include pervasive and cumulative problems in vital areas of life, such as employment, interpersonal relationships, and finances (Klingemann 2001; Klingemann and Gmel 2001). In fact, such difficulties in everyday living are so intertwined with heavy use that they are reflected in the DSM–IV criteria for AUDs (APA 2000). The interaction between pathologic alcohol use and enhanced life stress can lead to anxiety in at least two ways. First, the consistent presence of social disturbances may activate and intensify anxiety symptoms among these already vulnerable individuals. Second, alcohol use in the presence of stress stimuli may interfere with extinction-based learning necessary for normal adaptation to stressors. Thus, hazardous drinking can lead to anxiety through a noxious combination of greater levels of life stress coupled with relatively poor coping skills.

Evidence for the substance-induced hypothesis comes from multiple sources. A central prediction of this causal model is that abstinence from alcohol should be followed closely by a conspicuous decrement in anxiety symptoms. Data from a study of 53 patients who participated in alcohol treatment at a residential substance abuse program were consistent with this prediction (Kushner et al. 2005). Thus, among those 23 patients who had an anxiety disorder at baseline and remained abstinent after approximately 120 days, 61 percent no longer met criteria for an anxiety disorder at follow-up. Another study with 171 male veterans demonstrated that self-reported measures of temporary anxiety (i.e., state anxiety) decreased rapidly during inpatient alcohol treatment (Brown et al. 1991). It was furthermore noteworthy that scores on a measure of the participants’ overall anxiety levels (i.e., trait anxiety) also changed significantly at 3-month follow-up. This latter finding suggests that state anxiety that occurs during early abstinence can lead respondents to consider their increased anxiety levels as more chronic than they actually are. Therefore, retrospective self-reports collected at baseline should be interpreted with caution.

Additional evidence for the substance-induced pathway comes from prospective studies demonstrating that the presence of alcohol dependence predicts the later development of anxiety disorders. For example, in a sample of college students followed for 7 years, anxiety disorders increased fourfold among those diagnosed as alcohol dependent at either year 1 or year 4 of the study period (Kushner et al. 1999). A final line of support is found in differential comorbidity rates among samples of anxiety and alcohol patients. In a seminal review, Schuckit and Hesselbrock (1994) noted that the frequency of alcoholism among anxiety patients was not markedly higher than in the general population, contrary to what would be predicted by the self-medication hypothesis. In contrast, some studies have found greatly elevated rates of anxiety disorders in samples of individuals with alcohol problems (e.g., Kushner et al. 1990).

Similar to the common-factor and self-medication hypotheses, the literature underpinning the substance-induced pathway to comorbid anxiety and AUDs is convincing but cannot account for the findings consistent with the other causal models. It also is important to note that reliance on timeframes, although useful, could mask an independent course of anxiety symptoms among individuals who also have an AUD. For example, it is possible that an anxiety disorder which appears at a time when the person is experiencing alcohol-related problems may have an etiology separate from alcohol use. Likewise, a reduction in anxiety symptoms following alcohol treatment, which often is interpreted as an indication that the anxiety symptoms were a consequence of alcohol use, could also be explained by anxiolytic therapy and/or the natural course of anxiety independent of any effects related to abstinence.

Compared side by side, these proposed causal models provide competing explanations for the joint development of anxiety disorders and AUDs. It is apparent that the collective findings in this area do not unequivocally point to one pathway or exclude another. It is unclear whether this is a result of a failure of the aforementioned theoretical models or of the methods used to test the pathways or if it simply reflects the complexity inherent within this comorbidity. In fact, the support for multiple causal models may reflect that etiological differences exist among individuals who share this comorbidity, based on which disorder or predisposing variable was initially present. The continued viability of all these competing hypotheses suggests that further and more advanced research attention is essential to disentangle the predisposing factors, primary variables, sequencing, and early course involved with these co-occurring disorders.

Mutual Maintenance of Anxiety and AUDs

Once comorbidity between anxiety disorders and AUDs has been established, the two disorders may influence and maintain each other in ways that are independent of the developmental pathway. In other words, the processes involved in the initiation and the maintenance of comorbidity may differ in meaningful ways. One hypothesis emerging from the comorbidity literature is that anxiety and AUDs become intertwined in a reciprocal, perpetuating cycle. This positive feedback loop often is characterized as a feed-forward or mutual-maintenance pattern. Stewart and Conrod (2008) dubbed this progressive sequence the “vicious cycle of comorbidity” in which biopsycho­social outcomes of one disorder (e.g., anxiety) serve to maintain or even worsen the other disorder (e.g., alcoholism), whose respective outcomes, in turn, further maintain or exacerbate the first disorder, and so on. For example, a person who copes with anxiety by self-medicating with increasing amounts of alcohol likely will experience greater alcohol-related consequences (e.g., poor job performance, interpersonal problems, and anxiety induction from alcohol withdrawal), thus exacerbating the initial anxiety and leading to further drinking, which in turn sustains and/or amplifies the cycle.

Empirical support for this mutual-maintenance model comes from various sources, which in many ways reflects a synthesis of data supporting the three developmental pathways. Taken together, the sets of supportive findings suggest that (1) anxiety disorders can increase the severity, persistence, and poor treatment response of comorbid AUDs and (2) AUDs can increase the severity, persistence, and poor treatment response of comorbid anxiety disorders. Evidence that comorbid anxiety disorders can worsen and perpetuate AUDs and impair alcohol treatment response includes the following findings:

Similarly, other studies reported a negative impact of comorbid AUDs on the course of anxiety disorders, consistent with the mutual maintenance hypothesis, as follows:

Collectively, these independent findings are consistent with the mutual-maintenance model of comorbid anxiety and AUDs. However, although it may be reasonable to infer that the pattern of results demonstrates the heuristic utility of this model as a way to synthesize outcomes from various studies in this research area, the conclusion that a discontinuity between developmental and maintenance phases of this comorbidity exists remains speculative. Furthermore, to date no studies have empirically tested these dynamic and interactive factors in a longitudinal model. Thus, the status of the science underpinning the mutual maintenance hypothesis at this time only yields indirect agreement.

Diagnostic and Treatment Considerations for Comorbid Anxiety and AUDs

The developmental and maintenance factors associated with comorbid anxiety and AUDs show that the pairing of these two types of disorders is heterogeneous, interactive, and potentially progressive. Treatment approaches for comorbid patients correspondingly require comprehensive assessment and thoughtful planning. One paramount concern is the establishment of the correct diagnosis and exclusion of other diagnoses, especially because of the inherent difficulty in discerning whether anxiety present at the initial assessment is substance-induced or the sign of an independent anxiety disorder. As indicated earlier, reliance on self-report data can impair the accuracy of diagnoses, especially in the presence of recall bias that can be expected when a person is acutely anxious (e.g., Brown et al. 1991). Careful assessment therefore entails gathering a thorough and detailed retrospective timeline, interviewing collateral informants, reviewing the patient’s medical record and any available laboratory data, and observing symptoms over a sustained period of abstinence (Anthenelli 1997; Watkins et al. 2005). The exact duration of abstinence necessary to establish an independent anxiety disorder varies across disorders. For example, anxiety disorders whose cardinal symptoms are consistent with anxiety induced by alcohol withdrawal (e.g., panic disorder and generalized anxiety disorder) require longer periods of abstinence for a diagnosis than anxiety disorders with less symptom overlap (e.g., obsessive-compulsive disorder). Thus, a prudent diagnostician will wait several weeks to determine the likely source of symptoms that also frequently occur during withdrawal, such as panic or free-floating worry. Conversely, certain types of anxiety (e.g., social anxiety) typically predate alcohol use problems, and the presence of these symptoms therefore is less likely to be an artifact of alcohol withdrawal. A more comprehensive diagnostic algorithm for differential diagnosis is provided by Anthenelli (1997). A realistic limitation of the diagnostic process is that some individuals may not be able to sustain abstinence for a period long enough to clarify whether the constellation of anxiety symptoms represents a substance-induced syndrome or an independent anxiety disorder. In such cases, a prospective functional analysis may be used to identify the antecedents and consequences of both anxiety and alcohol use (Wyman and Castle 2006).

Perhaps most importantly, once the complete assessment data have been gathered through all the available strategies, the full spectrum of information should be integrated and considered as a whole to yield the most accurate diagnosis. To select an appropriate treatment approach using these differential diagnosis methods it also is crucial to consider that substance-induced mood and anxiety disorders can negatively impact treatment and increase overall clinical severity (Grant et al. 2004). Consequently, when it has been determined that an anxiety disorder likely is substance induced it may not be the best approach to simply treat the AUD alone and wait for the subsequent remission of the anxiety disorder.

When a diagnosis has been established, the treatment provider also needs to take into consideration the unique factors associated with this comorbidity when selecting the appropriate treatment protocol. As discussed below, a variety of pharmacotherapy and psychotherapy approaches are available to address anxiety and AUDs. Each modality has proven to be efficacious for these problems in isolation, and several evidence-based treatment alternatives for each disorder are available (see table 2). However, it sometimes may be necessary to modify these treatment approaches for comorbid individuals because even strategies considered the gold standard for one disorder potentially can have a negative impact on individuals with the other disorder (e.g., Jenson et al. 1990; Larson et al. 1992; Randall et al. 2001; Thevos et al. 2000; Tonigan et al. 2010).

Pharmacotherapy for Anxiety Disorders

Medication-based treatments for anxiety include an assortment of agents from several classes of medication, including benzodiazepines, tricyclic antidepressant drugs (TCAs), monoamine oxidase inhibitors (MAO-Is), and serotonergic-based medications (e.g., selective serotonin reuptake inhibitors [SSRIs], serotonin-norepinephrine reuptake inhibitors [SNRIs], and the 5-HT1a partial agonist buspirone). The efficacy of these drugs for anxiety treatment has been established firmly in well-controlled, randomized clinical trials. However, it is important to note that these studies typically exclude people with AUDs—a requisite standard practice to enhance the internal validity of efficacy studies. This exclusion means, however, that treatment providers must use clinical judgment when prescribing these medications to comorbid patients.

Benzodiazepines. Benzodiazepines can be very safe and effective agents for the short-term management of anxiety disorders. These medications are well-tolerated and have few medical scenarios in which they must not be used (i.e., few contraindications), although patients with pulmonary disorders may be sensitive to the depressant effects of these agents on the central nervous system. Because these medi­cations are absorbed into the body fairly rapidly, patients can experience relatively fast-acting anxiolytic effects from a single oral dose. When multiple doses of benzodiazepines are used to manage anxiety, the duration of action will vary based on the medication’s accumulation in the body, which is determined by pharmacokinetic characteristics such as elimination half-life and clearance. According to their elimination half-life, benzodiazepines can be classified into three groups (Greenblatt et al. 1981):

Because benzodiazepines are effective in managing anxiety in the short-term by producing a relatively fast-acting anxiolytic effect, their use as a front-line choice for individuals with comorbid anxiety and AUDs has been controversial (e.g., Brady and Verduin 2005; Ciraulo and Nace 2000; Posternak and Mueller 2001; Sattar and Bhatia 2003). For example, when discussing the relative benefits and risks associated with these medications, Longo and Johnson (2000) elegantly stated that, “Their greatest asset is also their greatest liability: drugs that work immediately tend to be addictive.” (p. 2127). Perhaps not surprisingly, the addiction potential of benzodiazepines is highest for the shorter-acting compounds as well as for those agents (e.g., alprazolam) that quickly cross the blood–brain barrier (Longo 1998; Martinez-Cano et al. 1996; Roache and Meisch 1995). People who have a history of AUDs seem to be more sensitive to the rewarding properties of these agents, and benzodiazepines have a positive effect on mood in alcoholics that is not seen in nonalcoholics (Ciraulo et al. 1988, 1997). Additional findings from clinical samples alternately have shown that abuse of sedatives (mostly benzodiazepines) among patients with anxiety was associated with concurrent alcoholism (Van Valkenberg 1999) and that alcohol- dependent patients (who also engaged in other drug abuse) were more likely to abuse benzodiazepines if they also reported panic attacks (Jenson et al. 1990). These factors together suggest an enhanced risk of benzodiazepine misuse among people with co-occurring anxiety and AUDs. Because effective and safe alternatives to manage anxiety are available (e.g., SSRIs and buspirone), it has been suggested that because of these risks, benzodiazepines generally should be avoided when treating patients with alcoholism, especially those with severe alcohol dependence or polydrug abuse (e.g., Longo and Bohn 2001; Sellers et al. 1993).

Some clinical scholars have questioned this viewpoint, however, and proposed that withholding access to potentially beneficial medications is unethical, especially when some studies suggest that a history of substance abuse is not a major risk factor for benzodiazepine abuse (e.g., Posternak and Mueller 2001; Sattar and Bhatia 2003). For example, in prospective studies Mueller and colleagues (1996, 2005) found little evidence that these anxiolytics were associated with poor outcomes among those with both anxiety and AUDs.1 Specifically, they found that (1) a history of AUDs was not a strong predictor of benzodiazepine use among participants with anxiety disorders, (2) use of these anxiolytics did not increase across time among comorbid participants, and (3) benzodiazepine use was not associated with the later occurrence of any new AUDs. These findings suggest that although the risk for benzodiazepine abuse should be an important consideration when prescribing within this patient subpopulation, these agents safely may be used in cases where they are clinically indicated (e.g., when other treatments are ineffective or potentially harmful). When benzodiazepines are used, patients should be monitored closely and only limited amounts of the agents should be prescribed. A useful algorithm to guide treatment decisions for people with co-occurring anxiety and AUDs was provided by Sattar and Bhatia (2003).

MAO-Is and TCAs. Caution also is suggested with the use of MAO-Is and TCAs for comorbid individuals. Although MAO-Is are quite effective in reducing anxiety, patients taking these agents may suffer a sudden severe increase in blood pressure (i.e., hypertensive crisis) after consuming certain foods and beverages that contain the amino acid tyramine (McCabe-Sellers et al. 2006), resulting in dietary restrictions for MAO-I users. These beverages include certain beers (e.g., imported beers, beer on tap, and nonalcoholic or reduced-alcohol beers), red wines, sherry, liqueurs, and vermouth, which is critical to know when treating people who also have alcohol problems. TCAs also should be used with caution among people with co-occurring AUDs and be prescribed only after other treatments have been ruled out because these medications can have an enhanced adverse-effect profile in this population. Moreover, the impaired judgment and impulsivity among persons with co-occurring alcohol use problems may increase the risks of taking an overdose of the medications that can result in toxicity and, potentially, suicidality. Finally, TCAs may react with alcohol in the brain to cause respiratory depression (Bakker et al. 2002).

Serotonergic-Based Medications. Medications that target a brain signaling system which uses the neuro­transmitter serotonin and its receptors perhaps are the safest and most widely used agents to treat anxiety disorders. These agents include the SSRIs, SNRIs, and the serotonin partial agonist buspirone. At present, SSRIs (e.g., fluoxetine, paroxetine, and sertraline) and SNRIs (e.g., venlafaxine and duloxetine) generally are used as first-line treatment in this area because they consistently demonstrate anxiolytic efficacy, including in patients with comorbid AUDs. For example, a direct examination of the efficacy of paroxetine in this population showed that it reduced social anxiety relative to placebo (Book et al. 2008), providing an empirical foundation for its use in these patients. Moreover, serotonergic agents have favorable properties, such as being well-tolerated and having virtually no abuse potential. Another welcome characteristic of SSRIs in patients with comorbid AUDs is that, in contrast to TCAs, they do not interact with alcohol to increase the risk of respiratory depression (Bakker et al. 2002). With both SSRIs and SNRIs it is advisable to inform patients that it may take about 1 to 2 weeks before these medications show full effectiveness. In addition, there is a risk of an electrolyte imbalance involving decreased sodium concentrations in the blood (i.e., hyponatremia), which can reduce the seizure threshold. This may be especially relevant during alcohol withdrawal, and clinicians therefore should monitor fluid intake and sodium levels during these periods.

Buspirone specifically is approved by the U.S. Food and Drug Adminstration (FDA) for the management of generalized anxiety disorder. Similar to other serotonergic-based medications, buspirone has a desirable safety profile but a relatively delayed onset of anxiolytic effects. Previous trials have evaluated buspirone among patients with comorbid generalized anxiety disorder (or anxiety symptoms) and AUDs. The majority of these studies have found reductions in both anxiety and alcohol outcome measures, including cravings (Bruno 1989; Tollefson et al. 1991) and drinking measures (Kranzler et al. 1994). However, one study found no effect of buspirone on either anxiety or alcohol use (Malcolm et al. 1992).

Psychotherapy for Anxiety Disorders

The psychosocial treatment of choice for anxiety disorders is established more clearly, with a family of strategies known collectively as cognitive–behavioral therapies (CBTs) considered the practice standard for people with anxiety problems. Meta-analyses of CBTs for anxiety disorders have shown strong evidence for their efficacy (Hofmann and Smits 2008; Olatunji et al. 2010). The CBT approaches to anxiety consist of two overarching strategies (Gerardi et al. 2009):

Exposure to feared stimuli is a powerful and active treatment ingredient that is recommended across the spectrum of anxiety disorders. Although the specific cues differ, application of exposure for each disorder generally involves repeated presentation of feared stimuli until the patient has become used to them (i.e., habituation is reached), resulting in extinction of the fear response. The technique largely is effective because when clients who typically avoid and/or escape from situations that lead to anxiety are exposed to these situations for prolonged periods, they encounter corrective information that previously was unavailable.

It nevertheless is appropriate to recognize that anxious clients who also have comorbid AUDs may be vulnerable to negative outcomes from this treatment method. For many of these individuals, drinking itself is a means of limiting exposure to feared situations and thus can be conceptualized as an avoidance strategy that has prevented the development of alternative ways of coping. To borrow terminology from the respective CBT approaches for anxiety and AUDs, the link between anxiety and drinking for comorbid clients may mean that in effect an exposure exercise also becomes a high-risk situation for alcohol relapse. Relapse to avoidance strategies (e.g., reliance on checking behaviors in obsessive-compulsive disorder or avoidance of social gatherings in social anxiety disorder) in the process of exposure is undesirable even for people suffering only from an anxiety disorder. For people who use alcohol as an avoidance strategy, however, a relapse can be especially costly. Moreover, use of alcohol to avoid anxiety during an exposure exercise also can interfere with the corrective learning process required for extinction of the anxiety response. Indeed, research findings suggest that exposure-based methods can lead to worse alcohol outcomes for comorbid individuals and that alcohol use during exposure may hinder extinction (e.g., Randall et al. 2001). Therefore, as a matter of course clinicians carefully should appraise this risk when weighing the potential costs and benefits of this CBT component for people with comorbid anxiety and AUDs. To address this issue, treatment providers may try to enhance the clients’ preparedness by focusing on relapse prevention skills prior to engaging in exposure exercises, especially those activities requiring the direct confrontation of feared stimuli (e.g., during prolonged in vivo exposure therapy). Also, therapists can manage the intensity of exposure therapy by introducing clients to feared stimuli using intermediate or purposefully protracted techniques, such as imaginal exposure (e.g., retelling traumatic memories or imagining feared situations or objects) and graded exposure (e.g., step-by-step exposure to stimuli based on a fear hierarchy). Such alterations can allow therapists to calibrate the dose of exposure that optimizes efficacy for extinction of the target fear response while minimizing the risk for relapse to drinking.

Pharmacotherapy for AUDs

There currently are three medications that have received FDA approval for the maintenance treatment of alcoholism:

Another drug receiving strong empirical support for the treatment of alcohol dependence is the anticonvulsant topiramate (Shinn and Greenfield 2010), although its use has not yet been approved by the FDA. Topiramate reduces the release of the neurotransmitter dopamine in the midbrain, which may reduce the rewarding experiences associated with alcohol intake. However, it is unclear at this time whether adverse effects may hinder its utility as an adjunctive alcoholism treatment, because a recent review of 26 published studies found that its use was associated with high rates of numbness of tingling on the skin (i.e., paresthesia) and cognitive symptoms (Shinn and Greenfield 2010). Additional research in randomized trials evaluating topiramate alongside more established medications, such as disulfiram and naltrexone, may shed light on its relative efficacy and tolerability.

Administration of medications for AUDs may require some adjustment for individuals who also have anxiety disorders compared with the regimen for alcoholics without this comorbidity. As with other conditions, randomized, controlled trials of pharmacotherapies to determine efficacy for alcoholism treatment often exclude individuals with comorbid conditions. Therefore, the impact of these agents on co-occurring psychiatric symptoms has not been explored fully. Some early clinical reports have suggested that disulfiram may precipitate psychiatric problems such as anxiety (e.g., Larson et al. 1992; Snyder and Keeler 1981). However, more thorough analyses suggest that these reports may not reflect current conceptualizations of psychiatric symptoms and dosing schedules (see Petrakis et al. 2002). Another concern is that people with a comorbid anxiety disorder may be taking additional medications to treat their concurrent condition and clinicians therefore must remain vigilant of potential interactions and dosage scheduling associated with multiple drugs. In one study in this underexamined area, data from 254 individuals treated for alcohol dependence on an outpatient basis and with other comorbid psychiatric disorders (including generalized anxiety disorder and panic disorder) showed that both naltrexone and disulfiram were effective and well-tolerated in this population (Petrakis et al. 2005). And in a secondary analysis of a randomized, double-blind trial Krystal and colleagues (2008) reported that among patients receiving antidepressants for mood/anxiety disorders, those receiving naltrexone showed greater reductions in drinking than did those receiving a placebo. Nevertheless, at least in the case of disulfiram, the combination of some historical clinical reports of anxiety induction and overall limited data suggests that clinicians administering this medication should closely monitor comorbid patients for any signs of increased anxiety.

Psychotherapy for AUDs

Psychosocial approaches to treating AUDs have evolved markedly over the past few decades. The historical roots of this treatment modality largely can be traced back to the development of Alcoholics Anonymous (AA) in Akron, Ohio, in the 1930s and 1940s. It has been estimated that nearly 1 in every 10 Americans has attended at least one AA meeting, and it is “the most frequently consulted source of help for drinking problems” (McCrady and Miller 1993, p. 3). Anecdotal and research evidence suggests that AA participation can promote positive alcohol-related outcomes (e.g., Project MATCH Research Group 1997, 1998; McKellar et al. 2003; Tonigan 2009), lending some credence to the oft-quoted adage, “It works if you work it.” Several alternative treatments have been developed since and have received favorable empirical support. In a systematic analysis of 10 published reviews of evidence-based psychosocial therapies for AUDs, a majority of the reviews found support for CBTs, the community reinforcement approach (CRA), motivational interviewing (MI), relapse prevention therapy (RPT), social skills training (SST), behavioral marital (couples) therapy (BCT), and brief intervention (BI) (Miller et al. 2005).

Similar to the other modalities described here, administration of these psychosocial treatment strategies for alcohol problems can be less straightforward with individuals who have comorbid anxiety and AUDs. Clients with social anxiety disorder, for example, may have difficulties with several elements of standard psychosocial approaches for alcoholism. Many treatment programs, as well as AA, heavily rely on the mutual help in group settings. Individuals with social anxiety, however, may be reluctant to attend group therapy or AA meetings or may avoid meaningful participation should they make the effort to attend. Other activities that are integral to participation in AA, such as sharing one’s story (i.e., public speaking), obtaining a sponsor, and becoming a sponsor (i.e., initiating social contact) also can be impaired among socially anxious alcoholics. Consistent with these hypotheses, research has shown that at least among women with social phobia, participation in AA may be less appealing and less effective than other approaches (Thevos et al. 2000; Tonigan et al. 2010). Two critical elements of CBT skills training also may be especially difficult for patients with comorbid social anxiety disorder, including drink-refusal skills and enhancing one’s social support network. In essence, clients need to show assertiveness to engage in the parallel process of ending relationships and habits that are high risk for relapse while also proactively initiating contacts and improving relationships with others who will support recovery efforts. Therefore, clients in CBT who also have social anxiety may particularly benefit from additional practice with assertiveness, perhaps including adjunctive social-skills training.

Standard delivery of RPT also may require a pivotal adaptation when applied to clients with comorbid anxiety disorders. RPT emphasizes the importance of identifying an individual’s unique risk factors (e.g., high-risk situations) for relapse and incorporates skill-development techniques to help reduce the likelihood of lapses and to manage them should they occur. It is widely understood in the RPT literature that negative emotional states are particularly perilous to recovery efforts. A classic analysis of over 300 relapse episodes implicated negative emotional states, conflict with others, and social pressure to use in nearly 75 percent of the relapses studied (Cummings et al. 1980). To prevent relapse resulting from negative emotional states such as anxiety, RPT recommends stimulus control (i.e., avoidance of high-risk situations, with escape as the next best option) as a first-order strategy (Parks et al. 2004). Relaxation training also is recommended because it “can help clients reduce their anxiety and tension when facing stressful situations and minimize their typical levels of motor and psychological tension” (Parks et al. 2004, p. 78). For clients with both alcohol use and anxiety disorders, however, a potential limitation of RPT is that avoidance of anxiety-inducing situations can preclude any potential anxiety reduction via exposure therapy, which in contrast requires clients to directly confront such situations. In short, for comorbid individuals, the avoidance and escape-oriented coping strategies taught within RPT could perpetuate anxiety problems. Skillful use of RPT with this subgroup of alcoholics therefore may require adjustments to complement the goals of exposure therapy for anxiety (e.g., allowing prolonged in vivo exposure within carefully planned high-risk situations designed to elicit anxiety) while also reducing the chances of drinking as much as feasible. This can be achieved, for example, by using abstinence-focused social support during in vivo exposure to situations eliciting anxiety or by conducting in vivo exposure only in environments without access to alcohol. A structured plan using imaginal and/or graded exposure to cues that elicit anxiety also may offer a practical balance of therapeutic risk and reward.

It also is notable that comorbid individuals seem to be especially ambivalent about changing their alcohol use (e.g., Grothues et al. 2005; Velasquez et al. 1999). For example, Grothues and colleagues (2005) found that people with problematic drinking and a comorbid anxiety disorder were more likely to be in the contemplation stage of change compared with problematic drinkers with or without depression, that comorbid participants rated both the positive and negative aspects of drinking higher than comparison groups, and that they had lower self-efficacy to quit drinking. Also, both Grothues and colleagues (2005) and Velasquez and colleagues (1999) found that comorbid individuals reported greater temptation to drink than did individuals without comorbidity. People who are highly ambivalent regarding their desire to stop drinking characteristically experience two opposing alcohol-related motivations—the desire to experience the pleasure associated with drinking (i.e., an appetitive- approach motivation) and the desire to avoid alcohol and its negative consequences (i.e., negative-avoidance motivation). This ambivalence can be a negative prognostic indicator.

For example, profiles of approach–avoidance drinkers have discriminated between “high lapsers” and abstainers among alcohol-dependent patients (Stritzke et al. 2007). These findings jointly suggest that ambivalence about changing alcohol use may be particularly salient among people with comorbid anxiety and AUDs, such that decisional balance likely is a principal treatment target.

The resolution of such ambivalence is a key concept of MI and is considered essential for a meaningful change to occur (Miller and Rollnick 1991, 2002). Accordingly, this counseling style seeks to help clients resolve their ambivalence by eliciting a specific class of verbal expressions (i.e., change talk) within sessions that most strongly are associated with actual behavior changes, especially phrases that signify a desire, ability, reasons, need, commitment, or steps taken to reach specified goals (Rollnick et al. 2007). An MI approach therefore may be particularly well-suited for clients with high ambivalence. In fact, meta-analyses have provided support for MI as a BI for problem drinking (Vasilaki et al. 2006). However, brief MI may not be optimal for drinkers with comorbid anxiety disorders because previous studies reported no additive benefit of BIs on either drinking outcomes or further help-seeking in this dually diagnosed population (Grothues et al. 2008a, b).

Application of Treatment Methods

In addition to adjusting standard pharmacotherapy and psychotherapy protocols for anxiety and AUDs when treating comorbid clients, it also is crucial to apply these methods in a way that produces the best outcomes for both disorders. Case conceptualizations that implicate one disorder as primary (e.g., because the patient histories are consistent with either the self-medication or the substance-induced models of comorbidity development) may tempt clinicians to focus treatment solely on that primary disorder. However, it generally is accepted in the comorbidity literature that this approach is not advisable (e.g., Kushner et al. 2007; Lingford-Hughes et al. 2002; Stewart and Conrod 2008). As reviewed earlier, one implication of the mutual-maintenance model of comorbidity is that neglecting to treat the second disorder would place individuals at high risk of relapse to the disorder that was treated, and published studies have supported this notion (e.g., Bruce et al. 2005; Driessen et al. 2001; Kushner et al. 2005). Recommendations to treat both anxiety and AUDs therefore appear warranted on both theoretical and empirical grounds. The literature for treating dual problem specifies three primary approaches, including the sequential, parallel, and integrated models (for a comparison, see table 3).

The Sequential Approach. In the sequential approach to treating comorbid anxiety and AUDs one disorder is treated prior to addressing the other disorder. Advocates of this approach point out that it may be prudent to begin, for example, by treating a client’s alcohol problem and waiting to see whether abstinence leads to remission of the psychiatric problem (e.g., Allan et al. 2002; Schuckit and Monteiro 1988). This model also allows clinicians to engage clients who may be more ready to address one disorder than the other, and this may be a pragmatic early treatment strategy for comorbid clients who may only have interest in changing one of their problems (Stewart and Conrod 2008). This hypothesis is supported by recent findings from a double-blind, randomized controlled trial of paroxetine for comorbid social anxiety and AUDs, which demonstrated that although this medication did not modify drinking overall, it did reduce drinking prior to social situations and appeared to uncouple social anxiety and alcohol use (Thomas et al. 2008). The results of this study suggest that paroxetine may be useful in this subgroup of alcoholics by alleviating social anxiety as a reason for drinking, and that once social anxiety symptoms are reduced, the stage may be set for the introduction of an alcohol intervention. Examination of this sequential treatment strategy is underway.

The Parallel Approach. The parallel-treatment approach requires that specific treatments for both disorders are delivered simultaneously, although not necessarily by the same provider or even in the same facility. However, coordination among providers and between facilities becomes a critical issue with parallel treatments when they are not colocated. There are noteworthy advantages of this approach relative to sequenced treatment, such as, at least theoretically, reducing the chances of relapse by attending to both disorders. In light of the mutual-maintenance patterns mentioned earlier this may be a quite significant benefit. Also, parallel treatment may be sensible from a practical standpoint, given that in the current treatment culture addiction and mental health settings generally are separated and efforts to unify and integrate treatment services for comorbid clients have lagged well beyond expert recommendations (Substance Abuse and Mental Health Administration [SAMHSA] 2002). However, several limitations of the parallel approach also exist beyond inherent difficulties with case coordination (Stewart and Conrod 2008). For example, clients may become overburdened with the time and effort involved with participation in two treatments with potentially two providers in separate locations. Thus, previous research has suggested that parallel psychosocial treatments for anxiety and AUDs may be too demanding for clients, which can negatively influence treatment outcomes (Randall et al. 2001). In addition, the parallel approach may convey an implicit (and erroneous) suggestion that the two disorders are separate, and the approach generally may be inefficient.

The Integrated Approach. Integrated treatment strategies are akin to parallel methods of combining treatments, but with two additional features: both disorders are treated by a single provider and treatment explicitly addresses the functional interrelationship of the comorbid disorders. This intuitively appealing approach theoretically is matched to the mutual maintenance model, is efficient, and communicates to clients that their dual problems are in fact intertwined and equally require management. Based on the range of potential advantages associated with integrated therapy, expert opinion strongly suggests adopting this approach to treating anxiety and AUDs (e.g., Castle 2008; Stewart and Conrod 2008; Watkins et al. 2005). Research has provided some support for such an integrated approach in the case of co-occurring panic disorder and AUDs (Kushner et al. 2006, 2009). To date, however, unfortunately only few data exist on integrated treatment, and the incongruence between the strength of expert opinion and paucity of supportive data has been noted in several reviews (Baillie et al. 2010; Hesse 2009; Smith and Book 2008; Stewart and Conrod 2008; Watkins et al. 2005). In addition, the practical obstacles to achieving integrated treatments also are considerable, including the need for specialty training in an underdeveloped area, conceptual incongruence between elements of standard anxiety and AUD treatments, and relative lack of funding opportunities from granting agencies for these niche treatments.

Because of the overall lack of empirical data to guide clinical decisions on how to best sequence and combine therapies for anxiety disorders and AUDs, it is recommended that clinicians consider and weigh the relative advantages and disadvantages of each approach when planning treatment for their patients. The sequential, parallel, and integrated models each are beneficial in certain respects, and each method should be considered a valuable option in the practitioner’s toolkit.

How Does Stress Lead to Risk of Alcohol Relapse?

Empirical findings from human laboratory and brain-imaging studies are consistent with clinical observations and indicate that chronic alcohol-related dysfunction in emotional and stress responses plays a role in motivation to consume alcohol in people with alcohol use disorders. Recent findings on differences in stress responsivity in alcohol-dependent versus nondependent social drinkers demonstrate alterations in stress pathways that partially may explain the significant contribution of stress-related mechanisms on craving and relapse susceptibility. These findings have significant implications for clinical practice, including (1) the development of novel brain and stress biology–related measures of relapse risk that could serve as biomarkers to identify those most at risk of alcohol relapse during early recovery from alcoholism; and (2) the development of novel interventions that target stress-related effects on the motivation to drink alcohol and on relapse outcomes

It has long been known that stress increases the risk of alcohol relapse (Sinha 2001). Clinical observations, surveys, and epidemiological studies document an association between self-reports of stressors and subsequent return to drinking. Studies assessing alcohol relapse after treatment completion and discharge also indicate the contribution of highly stressful events independent of alcohol use history that increase the risk of subsequent relapse (Brown et al. 1990). Furthermore, negative mood and stress are associated with increased craving, and high levels of urges to use alcohol predict relapse (Cooney et al. 2007). However, the mechanisms by which stress exposure increases alcohol relapse risk have been elusive, until recently. The last two decades have seen a dramatic increase in preclinical and clinical research to understand psychobiological and neural evidence linking stress and alcohol consumption. Evidence suggests that the neural circuits involved in stress and emotions overlap substantially with the brain systems involved in drug reward. Chronic alcohol use can result in neuroadaptive changes in stress and reward pathways. Such changes may alter an alcohol-dependent person’s response to stress, particularly with respect to stress and emotion regulation and motivation for alcohol, which in turn may increase the risk of relapse (Sinha 2001, 2005).

To put the stress and alcohol relapse linkage in the clinical context, the sidebar presents sample descriptions of an acute stressful life event and an acute alcohol-related situation that led to subsequent alcohol use in a person with alcohol dependence. The patient vignettes are descriptions provided by patients currently in treatment and refer to previous experiences and episodes of alcohol use and relapse.

Converging lines of evidence indicate that regular and chronic alcohol use is associated with changes in emotion, stress, and motivational pathways. These changes may in turn influence alcohol craving and relapse risk. Chronic alcohol use increases stress-related symptoms and is associated with increased anxiety and negative emotions; changes in sleep and appetite; aggressive behaviors; changes in attention, concentration, and memory; and desire/craving for alcohol (Sinha 2001, 2007, 2009). Stress-related symptoms are most prominent during early abstinence from chronic alcohol use, but some of these changes also have been documented during active use of specific drugs. Chronic alcohol abuse and acute alcohol withdrawal states are associated with heightened activity in the brain stress systems, such as increased secretion of the stress hormones corticotropin-releasing factor (CRF), norepinephrine, and cortisol in a number of the brain’s stress and emotion centers, such as the hypothalamus1, amygdala, hippocampus, and prefrontal regions (Koob and Kreek 2007). Chronic alcohol abuse also alters dopaminergic signaling in the ventral striatum (VS) and the ventral tegmental area (VTA). And such changes are associated with increased alcohol seeking (craving) and alcohol self-administration in laboratory animals (Cleck and Blendy 2008; Koob and Kreek 2007; Koob et al. 2004; Rasmussen et al. 2006). Further corroboration from human neuroimaging studies indicates that chronic alcohol abuse reduces dopamine receptors (i.e., D2 receptors) in striatal regions and dopamine transmission in the frontal lobe in alcoholics during acute withdrawal and protracted withdrawal (up to 3–4 months) (see Volkow 2004 for review). Functional imaging studies indicate increased VS activity in response to alcohol cues and altered brain response in the amygdala to emotional stimuli with chronic alcohol use (Gilman and Hommer 2008; Heinz et al. 2004, 2005; Martinez et al. 2007).

The biological stress response is most commonly detected in humans by activation of the hypothalamic– pituitary–adrenal (HPA) axis involving CRF-stimulated release of adrenocorticotropin (ACTH) from the anterior pituitary, which in turn stimulates the adrenal glands to release the stress hormone cortisol, which is involved in mobilizing and regulating the body’s stress response. The second pathway involved in the biological stress response is the autonomic nervous system, comprising the sympathetic and the parasympathetic components. The sympathetic component mobilizes arousal by increasing heart rate and blood pressure; the parasympathetic component enforces the “brakes” for sympathetic arousal and functions to decrease and regulate autonomic function. Alcohol use stimulates the HPA axis and initially stimulates the autonomic systems by provoking sympathetic arousal, followed by depressing such activation (Ehrenreich et al. 1997; Lee and Rivier 1997). Reductions in this alcohol-related HPA axis response (similar to tolerance) has been demonstrated with regular and chronic alcohol abuse in animals (Lee and Rivier 1997; Richardson et al. 2008; Zhou et al. 2000) and in humans (Adinoff et al. 1998, 2005; Wand and Dobs 1991).

Likewise, chronic alcohol abuse increases physiological arousal as measured by heart rate but also decreases heart rate variability, which serves as a measure of parasympathetic function (Ingjaldsson et al. 2003; Rechlin et al. 1996; Shively et al. 2007; Thayer and Sternberg 2006). These data represent alcohol-induced changes in peripheral stress pathways, which parallel basic science findings of alcohol-related adaptations in central stress systems, namely the extrahypothalamic CRF and the noradrenergic pathways that are indicative of hyperresponsive brain stress pathways noted in the previous paragraph (Cleck and Blendy 2008; Koob and Kreek 2007; Koob 2009; Rasmussen et al. 2006). These neurochemical changes indicate specific dysregulation in the neurochemical systems that play a role in emotion, stress, and motivation functions in alcoholics. Such changes raise the question of whether these measures contribute to the high levels of emotional distress, alcohol craving, and compulsive alcohol seeking that may lead to increased relapse susceptibility.

Drug craving or “wanting” for drug is a hallmark feature of addiction. It is an important component in maintaining addictive behaviors (Dackis and Gold 1985; O’Brien et al. 1998; Robinson and Berridge 1993, 2000; Tiffany 1990). Chronic alcohol use leads to changes in the brain reward and motivation pathways that can increase alcohol craving in the context of alcohol and alcohol-related stimuli, but also in the context of stress. In support of these ideas, a growing literature indicates that people with alcohol abuse show greater alcohol craving than social drinkers (Glautier et al. 1992; Greeley et al. 1993; Kaplan et al. 1985; Pomerleau et al. 1983; Willner et al. 1998). Further­more, severity of alcohol use has been shown to affect the magnitude of cue-related physiological arousal, compulsive alcohol seeking, and stress-related changes, including alcohol-related morbidity (Fox et al. 2005; Grusser et al. 2006, 2007; Rosenberg and Mazzola 2007; Sinha 2008; Yoon et al. 2006). These data are consistent with large population-based studies indicating that the risk of alcohol-related problems, addiction, and chronic diseases increases with greater weekly or daily alcohol and drug use (Dawson et al. 2005; Rehm et al. 2009; Room et al. 2005). Given these responses, the author’s research examined whether increases in craving are associated with altered stress responses that occur with chronic alcohol use.

In the clinical context, alcoholic patients entering outpatient substance abuse treatment report high levels of stress and an inability to manage distress adaptively, thereby increasing the risk of succumbing to high levels of drug craving and relapse to drug use (Sinha 2007). Although patients often are successful in learning cognitive– behavioral strategies in treatment, relapse rates remain high (Brandon et al. 2007; Sinha 2011). These data suggest possible difficulties in applying and accessing cognitive–behavioral strategies in real-world relapse situations. Thus, to understand the biobehavioral mechanisms underlying the high stress and craving state during early recovery, the author began to study this phenomenon in the laboratory, using an ecologically relevant method that models such relapse risk. This research used two of the most common relapse situations—emotionally stressful situations and alcohol-/drug-related situations—in order to develop a comparable method of provoking stress and the drug-related craving state, and these are compared to a relaxing situation that serves as an experimental control condition to account for the nonspecific aspects of the experimental procedures (Sinha 2009).

To assess relapse risk in laboratory studies, Sinha and O’Malley (1999) targeted alcohol and drug craving as a primary outcome measure that is both a common feature of alcoholism and substance abuse and also is known to relate to the disease state (i.e., high amounts of alcohol use and abuse). The researchers initially compared a commonly used standard social stress task (i.e., giving a speech in front of a video camera with the potential for a monetary reward) with 5-minute individualized guided imagery exposure of each participants’ own recent stressful scenarios. In addicted individuals, stress imagery elicited multiple emotions of fear, sadness, and anger when compared with the stress of public speaking, which elicited increased fear, but no anger and sadness. In addition, individualized stress imagery resulted in significant increases in drug craving, whereas public speaking did not (Sinha and O’Malley 1999).

Another study examined stress-induced and drug-related craving and physiological responses using individualized scripts of comparable length and style for stress, drug- related, and neutral- related situations. Among cocaine-dependent individuals, the imagery exposure to stress and nonstress drug cues resulted in significant increases in heart rate, salivary cortisol levels, drug craving, and subjective anxiety, compared with neutral-relaxing cues (Sinha et al. 2000). Using these methods, researchers have been able to reliably induce alcohol and drug craving in multiple groups of treatment-engaged cocaine-, alcohol-, and opiate-dependent individuals and also increase the desire for the drug in healthy social drinkers (Chaplin et al. 2008; Fox et al. 2007; Hyman et al. 2007; Sinha et al., 2003; see Sinha 2009 for review). In addition, mild to moderate levels of physiological arousal and subjective levels of distress were found to accompany the alcohol/drug craving state (Sinha 2009).

As discussed in the previous section, alcohol-dependent individuals in early recovery show increased stress and alcohol cue induced craving responses. In a study comparing 4-week abstinent alcoholics with matched social drinkers (drinking less than 25 drinks per month), Sinha and colleagues (2009) found that the recovering alcoholics showed greater levels of basal heart rate and salivary cortisol levels compared with the control drinkers. Upon stress and alcohol cue exposure, they showed greater subjective distress, alcohol craving, and blood pressure responses but blunted stress-induced heart rate and cortisol responses compared with control subjects (Sinha et al. 2009). Furthermore, after exposure to stress imagery, alcoholic patients showed a persistent increase in alcohol craving, subjective distress, and blood pressure responses across multiple time points compared with social drinkers, suggesting an inability to regulate this high alcohol craving and emotional stress state. These data indicate greater allostatic load in abstinent alcoholics, which is accompanied by dysregulated stress responses and high levels of craving or compulsive seeking for the preferred drug.

Together, these data indicate altered stress responses in alcoholics, and these alterations also include an enhanced susceptibility to stress and cue-induced alcohol seeking, which is not seen in healthy nonaddicted individuals. In addition, there are basal alterations in peripheral markers of stress (i.e., stress hormones, such as ACTH and cortisol and in heart rate), indicative of stress-related dysregulation in the CRF–HPA axis and in autonomic responses as measured by basal salivary cortisol and heart rate responses. These high basal responses are associated with lower or blunted stress-related arousal (Sinha et al. 2009). It is important to note that these alterations cannot be accounted for by smoking status or lifetime history of anxiety or mood disorders and therefore seem to be related to history of chronic alcohol abuse. The persistence of emotional distress and alcohol craving induced by stress and alcohol cue exposure suggests a dysfunction in emotion regulatory mechanisms. As HPA axis responses and autonomic– parasympathetic responses contribute to regulating and normalizing stress responses and regaining homeostasis, dysfunction in these pathways and their related central mechanisms may be involved in perpetuating alcohol craving and relapse susceptibility.

An important aspect of modeling hallmark addictive symptoms, such as alcohol craving, in the laboratory is to understand the related mechanisms. Furthermore, researchers should test the predictive validity of the laboratory model by examining whether laboratory responses predict future drug-use behaviors and/or real-world clinical outcomes. Because the laboratory studies described earlier were conducted with treatment-engaged alcoholics who were inpatients at a treatment research unit, it was possible to assess relapse rates after discharge. Then researchers could examine specific markers of the stress and craving states that are predictive of relapse outcomes. They followed the alcohol-dependent individuals (who had been in inpatient treatment for 5 weeks) after discharge for 90 days to assess relapse outcomes. Face-to-face follow-up assessments were conducted at 14, 30, 90, and 180 days after discharge from the inpatient unit. The follow-up rates for these assessments were 96, 89, 92, and 86 percent, respectively.

Initial evidence suggested that laboratory responses to stress- and alcohol-related stimuli exposure were predictive of alcohol treatment outcomes. Stress-induced alcohol craving in the laboratory during inpatient treatment was predictive of number of days of alcohol used and total number of drinks consumed during the 90-day follow-up period (Breese et al. 2005). These data corroborate findings in cocaine abusers, showing that stress-induced cocaine craving and HPA arousal are associated with earlier relapse and more cocaine use at follow-up (Sinha et al. 2006). In a more comprehensive analysis of stress dysregulation, anxiety, alcohol craving, and subsequent return to drinking, researchers found clear evidence of stress dysregulation and alcohol craving relating to relapse risk (Sinha et al. 2011a). Alcohol-dependent patients, compared with the control group, were more likely to have significant HPA axis dysregulation, marked by higher basal ACTH and higher basal salivary cortisol, lack of stress- and cue-induced ACTH and cortisol responses, higher anxiety after exposure to neutral relaxed and to alcohol cues, and greater stress- and cue-induced alcohol craving (Sinha et al. 2009, 2011a). Stress- and cue-induced anxiety and stress-induced alcohol craving were associated with fewer days in aftercare alcohol treatment. High alcohol craving to both stress and to alcohol cue provocation and greater neutral-relaxed state cortisol/ACTH ratio (adrenal sensitivity) were each predictive of shorter time to alcohol relapse. Although a greater cortisol-to-ACTH ratio in the stress and alcohol cue conditions also predicted relapse, the strongest predictor of relapse was the neutral relaxed state adrenal sensitivity (Sinha et al. 2011a). These results identify a significant effect of high adrenal sensitivity, anxiety, and increased stress- and cue-induced alcohol craving on subsequent alcohol relapse and treatment outcomes. They also are consistent with earlier reports of stress system involvement in relapse outcomes in alcoholics. Negative mood and stress-induced alcohol craving and blunted stress and cue-induced cortisol responses have been associated with alcohol relapse outcomes (Breese et al. 2005; Cooney et al. 1997; Junghanns et al. 2003).

In summary, these findings support the involvement of stress-related pathophysiology in the alcohol relapse process. Among alcoholics in early recovery, the alcohol-craving state is marked by anxiety and compulsive motivation for drugs, along with poor stress regulatory responses (i.e., high basal HPA axis responses but blunted stress HPA responses), resulting in an enhanced susceptibility to addiction relapse.

Several studies have used brain-imaging techniques to assess chronic alcohol-related brain changes and whether such changes are associated with alcohol craving and alcohol use. Neuro­anatomically, the cortico–striatal–limbic brain regions have been most studied in the context of stress, emotion, and motivation for alcohol reward. These regions include the frontal and insular cortices, the ventral and dorsal striatum, the amygdala, hippocampus, and thalamic nuclei, and midbrain regions, such as the VTA and the substantia nigra. An early study to measure blood flow with single-photon emission computed tomography found a change in the caudate nucleus during induction of craving in alcoholics (Modell and Mountz 1995). Subsequently, George and colleagues (2001) found a greater increase in brain response to alcohol cues in alcoholics compared with controls in the anterior thalamus and left dorsal lateral prefrontal cortex using functional magnetic resonance imaging (fMRI). Using a memory task during fMRI, Tapert and colleagues (2001) found dysfunctional cortical responses in alcoholics distinct from those of control subjects. Subsequently, other imaging studies with alcoholic patients have shown an increased association between dorsal striatum regions and alcohol craving in response to the presentation of alcohol-related stimuli (Grusser et al. 2004; Wrase et al. 2002). Myrick and colleagues (2004) reported that alcohol cues produced changes in the left orbital frontal cortex, anterior cingulate cortex, and nucleus accumbens in alcoholics but not in other study participants (Myrick et al. 2004).

Using fMRI, Sinha and colleagues (2007) compared alcohol-dependent individuals abstinent from alcohol for 4 weeks with social drinkers to assess brain structural changes and also functional responses to stress, alcohol cues, and neutral relaxing guided imagery. Alcoholic patients showed greater activity in the ventromedial prefrontal cortex, the ventral striatum, insula, and specific regions of the thalamus and cerebellum during the neutral-relaxing condition (Sinha 2007; Sinha and Li 2007). These findings indicate that abstinent alcoholics show overall hyper­responsivity of the medial prefrontal and striatal-limbic regions, with no differences in brain responses to the neutral relaxed and stressful cues (Sinha and Li 2007; Sinha et al. 2007a). Hyperresponsivity of prefrontal and striatal-limbic regions is consistent with an overall kindling2 process, which blunts the neural informational processing responses to stressful stimuli, resulting in a dysregulated response to stress in alcoholics (see also review by Breese et al. 2011).

Using positron emission tomography (PET) techniques, researchers have documented reduced glucose metabolism, especially in frontal regions during both acute and protracted alcohol withdrawal (up to 3 to 4 months) (see Volkow and Fowler 2000 for review). Alcoholics also show significant reductions in dopamine D2 receptors compared with nonalcoholics, particularly in frontal-striatal regions (Volkow and Fowler 2000). Researchers have reported significant associations between dopamine D2 receptor binding in the ventral striatum and alcohol craving (Heinz et al. 2004, 2005) as well as motivation for alcohol self-administration in alcoholics (Martinez et al. 2005, 2007). To emphasize the importance of this approach, recent PET studies have shown significant positive correlations between selected dorsal striatum brain regions and drug cue–induced cocaine craving (Volkow et al. 2006; Wong et al. 2006). These data point to alterations in frontal and striatal regions of the dopaminergic and noradrenergic pathways that exist past acute withdrawal and may be associated with difficulties in regulating emotions, stress, and problems selecting goal-directed adaptive responses as opposed to the selection of habitual maladaptive responses such as alcohol consumption.

In addition, the research literature has documented chronic alcohol-related structural brain changes, particularly in frontal, parietal, and temporal cortical regions associated with stress, emotion, and cognitive functioning (Cardenas et al. 2007; Fein et al. 2002; Pfefferbaum et al. 1995, 1998). More severe gray matter deficits have been reported in alcohol relapsers than those who maintained abstinence (Pfefferbaum et al. 1998). In a whole-brain analysis, Rando and colleagues (2011) found significantly smaller gray-matter volume in recently abstinent alcohol-dependent patients relative to healthy study participants in three regions: the medial frontal cortex, right lateral prefrontal cortex, and a posterior region surrounding the parietal-occipital sulcus. Smaller medial frontal and parietal-occipital gray-matter volume were each predictive of shorter time to subsequent any alcohol use (first lapse) and to heavy-drinking relapse (Rando et al. 2011). These data suggest that smaller gray-matter volume in specific medial frontal and posterior parietal-occipital brain regions are predictive of an earlier return to alcohol drinking and relapse risk, suggesting a significant role for gray matter atrophy in poor clinical outcomes in alcoholism. Thus, the extent of gray-matter volume deficits in these regions involved in impulse control, emotion regulation, and abstraction abilities could serve as useful neural markers of relapse risk and alcoholism treatment outcome.

The risk for alcohol dependence throughout development is determined by both genetic and environmental factors. Genetic factors that are thought to modulate this risk act on neurobiological pathways regulating reward, impulsivity, and stress responses. For example, genetic variations in pathways using the brain signaling molecule (i.e., neurotransmitter) dopamine, which likely mediate alcohol’s rewarding effects, and in two hormonal systems involved in the stress response (i.e., the hypothalamic–pituitary–adrenal axis and the corticotropin-releasing factor system) affect alcoholism risk. This liability is modified further by exposure to environmental risk factors, such as environmental stress and alcohol use itself, and the effects of these factors may be enhanced in genetically vulnerable individuals. The transition from alcohol use to dependence is the result of complex interactions of genes, environment, and neurobiology, which fluctuate throughout development. Therefore, the relevant genetic and environmental risk factors may differ during the different stages of alcohol initiation, abuse, and dependence. The complex interaction of these factors is yet to be fully elucidated, and translational studies, ranging from animal studies to research in humans, and well-characterized longitudinal studies are necessary to further understand the development of alcohol dependence.

Key words: Alcohol dependence; alcoholism; alcohol use and abuse; alcohol and other drug use initiation; risk factors; genetic factors; environmental factors; stress; stress response; neurobiology; biological development; brain; hypothalamic– pituitary–adrenal axis; corticotropin-releasing factor system; animal studies; human studies; literature review

The development of alcohol dependence is a complex process influenced by both genetic and environmental risk factors (Prescott and Kendler 1999). The relative contributions of genetic and environmental influences fluctuate across development. During adolescence the initiation of alcohol use is strongly influenced by environmental factors (Dick et al. 2007; Heath et al. 1997; Karvonen 1995; Latendresse et al. 2008; McGue et al. 2000), whereas the genetic contribution to alcohol use at this stage is nonspecific and increases the risk for general externalizing behavior (Moffitt 1993; Moffitt et al. 2002). Specific genetic factors increasingly become relevant, however, as patterns of alcohol use are established (Hopfer et al. 2003; Pagan et al. 2006), particularly in mid-adulthood when dependence tends to emerge (Kendler et al. 2010; Schuckit et al. 1995). Gene–environment interactions also play a role because the influence of certain genetic factors seems to increase when a person is exposed to relevant environmental risk factors (Uhart and Wand 2009). Therefore, the development of dependence can be conceptualized within a temporal framework of genes, environment, and behavior.

The purpose of this review is to explore, within this framework, the contribution of some of the neurobiological systems that are important for the development of alcohol dependence. One of these is the mesolimbic dopaminergic system, which is involved in inducing the rewarding effects of alcohol and plays a central role in early alcohol use. Another pathway that also has been implicated in alcohol abuse, and particularly in the transition to alcohol dependence, involves two stress-response systems, the hypothalamic–pituitary– adrenal (HPA) axis and the extra-hypothalamic corticotropin-releasing factor (CRF) stress response system, which mediate the interaction of psychosocial stress and early alcohol use. Both of these systems exemplify how the effects of genes and environment may be augmented during critical periods of alcohol use and dependence across the lifespan. For example, the dopaminergic system undergoes developmental transformations during adolescence that are associated with increased reward sensitivity and risk taking (Spear 2000), which presents a window of vulnerability for exposure to alcohol and stress. Then, as alcohol use continues through life, chronic exposure to alcohol can enhance the activity of (i.e., upregulate) the HPA and CRF systems. This dysregulation of the stress response systems becomes a pathological feature of alcohol dependence, perpetuating chronic alcohol drinking based on an allostatic shift1 of the CRF system (Koob 2010). Moreover, the HPA, CRF, and dopaminergic systems can influence early alcohol drinking as a result of gene–environment interactions. This article will summarize the literature that has explored how genetic variation within the dopaminergic and stress response systems can influence the risk of alcohol dependence and how the exposure to relevant environmental risk factors and their interaction with genetic variants may influence alcoholism pathology. The effects of genes and environment on alcohol dependence will be discussed in a developmental framework from early childhood to adolescence as well as in the context of the development of dependence, when drinking behavior shifts from recreational use to dependence.

1 The term allostasis refers to the process through which various biological processes attempt to restore the body’s internal balance (i.e., homeostasis) when an organism is threatened by various types of stress in the internal or external environment. Allostatic responses can involve alterations in HPA axis function, the nervous system, various signaling molecules in the body, or other systems.

Several environmental factors have been shown to influence the initiation of alcohol consumption and its use during adolescence, including the level and quality of parental monitoring, peer-group influences, alcohol availability, and socioregional effects (Dick et al. 2007; Heath et al. 1997; Karvonen 1995; Latendresse et al. 2008; McGue et al. 2000). Thus, maternal and paternal alcohol use has been positively correlated with adolescent alcohol use at ages 14 and 17 (Latendresse et al. 2008). Moreover, the level of urbanization was found to correlate with alcohol use in Finnish adolescents at ages 16 and 18 (Karvonen 1995), and peer-group drinking behavior was one of the strongest predictors of problematic drinking in a cohort of Spanish adolescents (Ariza Cardenal and Nebot Adell 2000).

Once alcohol use has been initiated, neuronal networks are activated that engage the brain circuits mediating the rewarding effects of alcohol use (i.e., the reward neurocircuitry). This activation attributes salience to alcohol and serves as an incentive for alcohol use to continue (Robinson and Berridge 1993). Neuronal networks that are known to mediate these effects include those using the signaling molecules (i.e., neurotransmitters) glutamate and γ-aminobutyric acid (GABA) as well as the endogenous opioids (Gass and Olive 2008; Malcolm 2003; Oswald and Wand 2004). In addition, signal transmission involving the neurotransmitter dopamine in the mesolimbic system (Di Chiara and Imperato 1988) is particularly important for the establishment of regular alcohol consumption because alcohol-induced dopamine release is believed to contribute to the rewarding effects of alcohol (for reviews see, Soderpalm et al. 2009; Tupala and Tiihonen 2004). The mesolimbic system is a set of interconnected brain structures including the ventral tegmental area (VTA), nucleus accumbens (NAc), and components of the limbic system (e.g., the amygdala). Studies in rats found that alcohol consumption can increase dopamine signaling in the NAc (Weiss et al. 1996). Conversely, dopaminergic neurotransmission is decreased during withdrawal in the NAc and VTA of rats treated chronically with ethanol (Diana et al. 1993).

Environmental risk factors during early life and adolescence may interact with the dopaminergic system to influence alcohol intake. Two such factors are exposure to environmental stress and alcohol consumption itself. The developing adolescent brain undergoes substantial changes in the strength with which signals are transmitted between neurons (i.e., in synaptic plasticity) (Bava and Tapert 2010; Giedd 2003). These changes include increased dopaminergic inputs to the prefrontal cortex that peak during adolescence and decrease later in life (Kalsbeek et al. 1988; Rosenberg and Lewis 1994). Furthermore, dopamine levels in the NAc also peak during adolescence, before decreasing during subsequent brain maturation (Philpot and Kirstein 2004). These neuronal alterations are believed to promote sensation-seeking and risk-taking behavior during adolescence, which in turn increase the propensity for alcohol initiation and alcohol use (Spear 2000). Exposure to alcohol and/or stress during early life (i.e., from the prenatal period through adolescence) has been shown to have lasting consequences on the dopamine system that have a significant impact on the risk for alcohol abuse.

Studies in rats found that exposure to alcohol during the prenatal period decreases the levels of two important enzymes involved in regulating dopamine activity—the dopamine transporter and the dopamine hydroxylase enzyme— in the VTA (Szot et al. 1999). More­over, rats chronically treated with ethanol during adolescence displayed persistently elevated baseline dopamine levels in the NAc during adulthood, even after a period of 15 days abstinence (Badanich et al. 2007). Finally, repeated ethanol injections in preadolescent and adolescent rats increased subsequent dopamine activity in the NAc, with the largest increases observed in preadolescence. Early ethanol exposure in these rats decreased the ability of subsequent ethanol injections to elicit dopamine release from the NAc (Philpot and Kirstein 2004). These findings suggest that ethanol exposure in early life may influence the response to alcohol in later life. Indeed, additional studies have confirmed that both pre- and postnatal exposure to alcohol increase the sensitivity of rats to the locomotor effects of alcohol and to an agent that mimics dopamine’s effects (i.e., a dopamine agonist), apomorphine (Barbier et al. 2009). Therefore, at least in rodents, early alcohol exposure seems to confer lasting effects on neuronal dopamine activity that can alter behavioral responses to subsequent alcohol exposure. Indeed, rats chronically treated with ethanol both prenatally and during adolescence also show an increased preference for alcohol and increased alcohol intake as adults (Barbier et al. 2009; Pascual et al. 2009). Further­more, stress-induced alcohol consumption was associated with an earlier age of drinking onset in Wistar rats (Fullgrabe et al. 2007; Siegmund et al. 2005).

Studies in humans have confirmed the potential long-lasting impact of early alcohol exposure, demonstrating that an early initiation of alcohol use is associated with an increased risk of later problems with alcohol. For example, Hawkins and colleagues (1997) noted that the earlier drinking is initiated in adolescence, the greater the levels of alcohol misuse at ages 17 to 18. Furthermore, people who begin drinking at age 14 or younger are more likely to become alcohol dependent later in life (Grant and Dawson 1997). Few studies have been conducted to determine the precise mechanism by which early alcohol exposure affects the risk for subsequent alcohol abuse and dependence. However, Pascual and colleagues (2009) demonstrated that in adolescent rats chronically treated with ethanol, two neurotransmitter receptors—dopamine receptor 2 (DRD2) and glutamate receptor (NMDAR2B)— show lower levels of a chemical modification (i.e., phosphorylation) in the prefrontal cortex compared with adults chronically treated with ethanol. This finding suggests that alcohol use during adolescence causes neurobiological changes to the dopamine system that are not observed in adult animals.

Environmental stress is one of the most pertinent risk factors for alcohol dependence. The exposure to early-life stress sensitizes animals to drugs of abuse (Fahlke et al. 1994; Piazza et al. 1991; Shaham and Stewart 1994) and also increases alcohol consumption in later life (Fahlke et al. 2000). Alterations in the dopaminergic mesolimbic system that persist into adulthood are believed to explain, at least in part, these behavioral adaptations (for review, see Rodrigues et al. 2011). For example, studies in rats found that chronic exposure to cold stress in adolescence altered both basal and stress-evoked release of dopamine and another neurotransmitter, norepinephrine,2 in the medial prefrontal cortex, NAc, and striatum compared with stress-naïve rats (Gresch et al. 1994). Other studies in Sprague-Dawley rats demonstrated that stress caused by separation from the mother during the first 2 weeks of life blunted the animals’ dopamine response to restraint stress in adulthood (Jahng et al. 2010). Although no human studies analyzing the effect of early-life stress and alcohol sensitization exist, imaging studies using functional magnetic resonance imaging (fMRI) to analyze reward anticipation have found that childhood adversity is associated with blunted subjective responses to reward-predicting cues as well as with impaired reward-related learning and motivation (Dillon et al. 2009). Such findings demonstrate that early environmental experiences can alter the impact of a reward and that similar effects can be observed across species.

Other studies have evaluated the effects of early-life stress on alcohol consumption or alcohol dependence. Such studies found that even exposure to prenatal stress can have an impact on later alcohol-related behaviors because the offspring of mice that repeatedly were restrained during the last 7 days of gestation subsequently demonstrated enhanced alcohol consumption—an effect that has been linked to persistently elevated dopaminergic and glutamatergic neurotransmission in the forebrain (Campbell et al. 2009). In humans, retrospective studies examining early-life experiences and alcohol consumption found that childhood stressors were associated with alcohol dependence during adulthood (Ducci et al. 2009; Pilowsky et al. 2009). In a study of the adult American population (i.e., the National Epidemiologic Survey on Alcohol and Related Conditions [NESARC]), two or more stressful life events in childhood significantly increased the risk for alcohol dependence in adult­hood (Pilowsky et al. 2009). Further­more, early initiation of alcohol use in human adolescents is associated with exposure to traumatic life events and symptoms of posttraumatic stress disorder (Wu et al. 2010).

Thus, exposure to stress and/or alcohol consumption during early life may influence dopaminergic neurotransmission, with lasting adaptations into adulthood and notable consequences for subsequent alcohol use. However, the impact on different individuals varies, and a portion of this variability can be attributed to genetic factors. Indeed, studies of rats have shown that exposure to chronic unpredictable stress increases the levels of a dopamine-metabolizing enzyme, tyrosine hydroxylase (TH), in the VTA but that the extent of this increase differs drastically between different rat strains (Ortiz et al. 1996). Additional research in Rhesus macaques identified a variation (i.e., polymorphism) in the gene encoding dopamine receptor 1 (DRD1)3 that was associated with increased alcohol consumption in animals exposed to peer-rearing conditions compared with maternally reared animals that carried the same polymorphism (Newman et al. 2009).

Studies in humans also have shown that genetic factors mediate the effects of stress and alcohol on the risk for alcohol dependence. Schmid and colleagues (2009) analyzed 291 young adults in the Mannheim Study of Children at Risk for two polymorphisms in the gene encoding the dopamine transporter. The investigators found that the age of first alcohol use and of intensive alcohol consumption mediated the association between these polymorphisms and early alcohol abuse and dependence. Genetic variation in another gene, KCNJ6, which is expressed in the brain, mediates the effects of early-life stress on alcohol abuse in adolescence. It induces inhibition of neuronal signaling at the level of the signal-receiving (i.e., postsynaptic) dopaminergic neurons (Kuzhikandathil et al. 1998). Furthermore, the protein encoded by the KCNJ6 gene, the membrane potasium channel GIRK2, is co-expressed in TH-positive cells of mice (Schein et al. 1998). Individuals who carry a certain KCNJ6 variant and are exposed to high levels of psychosocial stress in early life display increased risky drinking behavior in adolescence; moreover, the same polymorphism is associated with alcohol dependence in adults (Clarke et al. 2011).

Genes in other neurobiological systems also mediate the effects of early-life stress on alcohol consumption, including genes encoding the serotonin receptor (Laucht et al. 2009) and the GABA receptor subunit α-2 (GABRA2) (Enoch et al. 2010). Another important gene is that encoding the μ-opioid receptor (OPRM1). It also moderates the effects of stress and alcohol with implications not only for alcohol use but also for recovery from alcohol dependence. Alcohol activates the μ-opioid receptor in the VTA, which causes inhibition of GABAergic neurons; this in turn results in disinhibition of dopaminergic neurons and, thus, increased dopamine release in the ventral striatum (Spanagel 2009). In macaques, a certain polymorphism in the OPRM1 gene (i.e., the C77G polymorphism) predicts the degree of distress upon exposure to maternal separation (Barr et al. 2008). In humans, the equivalent polymorphism (i.e., the A118G polymorphism) is associated with the quality of parent–child interactions under conditions of poor parenting (Copeland et al. 2011). Finally, in both macaques and humans the same polymorphisms are associated with subjective/behavioral responses to alcohol (Barr et al. 2007, 2008; Ramchandani et al. 2010). The role of this polymorphism further has been demonstrated in studies using a μ-opioid receptor antagonist, naltrexone, that commonly is used to treat alcohol dependence. In heavy drinkers, the A118G polymorphism mediates the effects of naltrexone on positive mood, craving, and enjoyment from alcohol (Ray and Hutchison 2004). Furthermore, the presence or absence of the A118G polymorphism can help predict which individuals will benefit from naltrexone treatment for alcohol dependence (Oslin et al. 2003).

Taken together, the findings described here indicate that early exposure to alcohol and stress can increase the subsequent risk for alcohol dependence, at least in part because they induce changes in the dopamine system. However, these effects are moderated by genetic factors in the dopamine pathways and other neurobiological systems.

As indicated by the observations discussed in the preceding section, the dopamine system is an important neuro­biological system mediating early alcohol use. In addition, stress response systems in the brain have been implicated in alcohol initiation and in the escalation of alcohol use from episodic use to abuse and, ultimately, dependence. Stress responses are crucial for survival by allowing the organism to coordinate appropriate behavioral adaptations to adverse stimuli and are essential homeostatic processes. Central components of the stress response include activation of the HPA axis, increases in norepinephrine turnover in a brain region, the locus coeruleus, and activation of CRF systems (Habib et al. 2001). CRF acts through two pathways. First, it acts as a signaling hormone inside the HPA axis, where it is released from the paraventricular nucleus of the hypothalamus. It then is transported to the anterior pituitary, where it binds to CRF receptors (CRF1 and CRF2), thereby eliciting the release of adrenocorticotrophic hormone (ACTH). ACTH production ultimately results in the release of stress hormones (i.e., glucocorticoids) from the adrenal glands. The main glucocorticoid in humans is cortisol. Second, CRF acts outside of the hypothalamus (i.e., extrahypothalamically) because immunological tests have detected its presence in the extended amygdala and the brainstem (Swanson et al. 1983).

Studies have demonstrated that exaggerated HPA axis responses to stress can precede the onset of alcoholism. Nondependent sons of alcoholic fathers (who are at increased risk of alcoholism) displayed increased cortisol and ACTH responses to psychosocial stress compared with people with no family history of alcoholism (Uhart et al. 2006; Zimmermann et al. 2004a, b). Furthermore, alcohol had a greater attenuating effect on ACTH and a related hormone (i.e., arginine vasopressin [AVP]) in people with alcoholic fathers, suggesting that alcohol may be more rewarding for such individuals (Zimmermann et al. 2004b). These findings also indicate that interindividual differences in HPA axis activity may underlie some of the variation observed in the vulnerability to alcohol dependence.

As alcohol dependence develops, the stress response systems are upregulated, and this hyperactivity may in fact be a pathological component of dependence (Koob 2008). It has been hypothesized that as dependence develops, the motivation for alcohol use shifts from positive reinforcement, whereby alcohol is consumed for its pleasurable effects, to negative reinforcement—that is, the drinker consumes alcohol to alleviate the negative emotional effects encountered during withdrawal and into protracted abstinence (Koob and Le Moal 2008). The development of negative emotional states has been proposed to include the recruitment and subsequent deregulation of various brain stress system, including the HPA axis, extrahypothalamic CRF, and various others4 (George et al. 2008; Koob 2008). Genetic variation in genes encoding components of these stress response systems therefore may be relevant for the risk for alcohol dependence.

The variability between individuals in stress responding results at least partially from inherited factors (Armbruster et al. 2009; Linkowski et al. 1993; Meikle et al. 1988) that also may influence the risk of alcohol dependence. For example, polymorphisms that affect only a single DNA building block (i.e., single nucleotide polymorphisms [SNPs]) in the gene encoding CRF1 were associated with alcohol consumption and a lifetime prevalence of drunkenness in two independent samples (Treutlein et al. 2006). One of those polymorphisms, known as rs1876831, was found to moderate the effects of stress on drinking. Thus, adolescents at age 15 who had experienced negative life events in the past 3 years and who carried the variant (i.e., allele) of rs1876831 that was associated with increased risk of drinking displayed increased alcohol consumption per drinking occasion and greater lifetime rates of heavy drinking (Blomeyer et al. 2008). A similar effect also was observed at age 19, when the risk allele was associated with earlier age of onset of alcohol use and higher alcohol consumption in individuals exposed to stressful life events (Schmid et al. 2010). Further­more, a gene–environment interaction was detected with a combination of several gene variants (i.e., a haplotype) in the CRF1 gene (which also contains rs1876831) and childhood sexual abuse in a large cohort of Australians recruited for the Nicotine Genetics Project (Saccone et al. 2007). Individuals who had experienced childhood abuse but carried a protective polymorphism of the CRF1 gene had lower lifetime alcohol consumption scores and rates of alcohol dependence (Nelson et al. 2009).

Further genetic factors mediating the association between the stress response and alcohol consumption are found in genes encoding the receptors to which cortisol binds after it is released from the adrenal gland when the HPA becomes activated (Bjorntorp 2001). Cortisol binds to glucocorticoid receptors (GRs) that are made up of two identical subunits (i.e., form homodi­mers). These receptors interact with certain DNA sequences, glucocorticoid response elements (GREs), in the target genes, thereby activating those genes as part of the stress response (Gower 1993; Simons et al. 1992). The GRs are encoded by a family of genes known as nuclear member subfamily 3 (NR3C) genes.

Researchers have identified functional polymorphisms in the genes encoding two receptors, NR3C1 and NR3C2, which are associated with differential responses to stress (Wust et al. 2004). For example, a SNP, N363S that results in an altered receptor, protein (i.e., a non-synonymous SNP) in NR3C1 is associated with increased glucocorticoid sensitivity (Huizenga et al. 1998) as well as elevated levels of cortisol in the saliva of healthy people in response to psychosocial stress (Wust et al. 2004). Moreover, a haplotype that includes three SNPs and is located in a noncoding region of the NR3C1 gene also is associated with enhanced sensitivity to glucocorticoids (Stevens et al. 2004). Because chronic alcohol consumption can increase HPA axis activity in animals and humans (Rivier 1996; Rivier and Lee 1996; Waltman et al. 1994), polymorphisms in genes encoding components of the HPA axis may increase the risk for alcohol abuse. Indeed, a recent study of 26 SNPs across the NR3C1 gene in 4,534 adolescents identified several variants that were associated with onset of drinking and drunkenness by age 14, suggesting that genetic variation in NR3C1 can influence the risk of alcohol abuse in adolescence (Desrivieres 2010). Likewise, variants in the gene encoding the ACTH precursor, promelanocortin (POMC), have been associated with substance abuse, including alcohol abuse (Zhang et al. 2009).

Genes encoding components of the norepinephrine stress response system also have been linked to variability in the response to stress. Thus, polymorphisms in the ADRA2A gene, which encodes adrenergic receptors that inhibit norepinephrine release from the neuron, are associated with certain aspects of the stress response as determined by measuring blood pressure and heart rate (Finley et al. 2004). In addition, variants in the ADRA2A gene are associated with alcohol abuse phenotypes in humans. For example, in a study analyzing 23 SNPs in ADRA2A as well as in a gene SLC6A2 (which encodes the norepinephrine transporter, NET1) in association with adult alcohol dependence identified two SNPs in ADRA2A associated with a positive family history of alcoholism and four SNPs in SLC6A2 associated with adult alcohol dependence (Clarke et al. 2010).

All of these studies demonstrate that genes that regulate stress responding also influence the risk for alcohol depen­dence. Thus, people who display increased sensitivity to stress may consume alcohol to dampen the exaggerated stress responses and therefore may find alcohol more rewarding. These people also may more readily experience the negative emotional states associated with withdrawal after chronic alcohol exposure, which may accelerate the transition to dependence. However, the precise relationship between genes, stress, and alcohol use is complex, and gene–environment interactions are notoriously difficult to elucidate (Flint and Munafo 2008). Therefore, translational studies analyzing the effects of genetic factors and stress and their interactions under tightly controlled experimental conditions using animal models are warranted (Barr and Goldman 2006). Indeed, the study of the extrahypothalamic CRF system in animals has helped to clearly delineate the role of brain stress systems in the pathology of alcoholism, and this system is now a plausible target for future alcoholism pharmacotherapies. (For more information on these studies, see the sidebar “The Extrahypothalamic CRF System and the Transition to Alcohol Dependence.”)

Another confounding issue for the study of gene–environment interactions is that many studies are conducted retrospectively, and the participants’ recall of environmental risk factors may not be accurate. Therefore, prospective longitudinal studies are of great importance to advance the field of gene– environment interactions in alcohol dependence. One study that illustrates how such methodological issues can be addressed is the IMAGEN study, a longitudinal initiative funded by the Framework 6 program of the European Commission and the Medical Research Council that tracks the interplay between genetic polymorphisms and environmental stressors from early adolescence onward. The study collects neuropsychological, behavioral, and functional/structural neuroimaging data and also conducts genetic analyses on a sample of 2,000 adolescents from age 14 onward. (For more information on this study, see the sidebar “The IMAGEN Study.”)

Addition Reading: Screening and Assessment of Co-Occurring Disorders


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