Post-traumatic Stress Disorder and Substance Abuse

Post-traumatic stress disorder (PTSD) is a major anxiety disorder with a community-based prevalence of 8% of adults in the Unites States. It is common among survivors of rape, military combat and captivity, and ethnically or politically motivated internment and genocide (DSM-IV-TR, p 466).

Though such figures imply no causality, 35% percent of men with PTSD demonstrate substance abuse/dependency compared to 15% of men without PTSD, and 28% of women with PTSD demonstrate substance abuse/dependency compared to 14% without PTSD (Kessler, 1995). There is a certainly a correlation between PTSD and substance abuse that is significant and worth investigating.

There is a significant statistical association between substance-related and other psychiatric disorders in the general, and 16 clinical populations (indicated by odds ratio greater than one) suggest that these disorders may be casually related to one another (Hubbard and Martin, 2001, p. 5; DSM-IV-TR # 309.81). Substance abuse has an odds ratio of approximately three (Hasin and Nunes, 1998, p. 1-30; DSM-IV-TR p. 465).

Two major survey studies indicate that PTSD is frequently co-morbid with substance abuse and dependency. The National Vietnam Veteran Readjustment Study (NVVRS) showed that veterans with PTSD also met the criteria for substance abuse (20%) and dependency (75%), which is considerably higher than the typical population or even the typical Vietnam veteran population (Kulka et al., 1990). Furthermore, the NVVRS showed that veterans exposed to high war zone stress had twice the rate of PTSD (Jordan et al., 1991). The Center for Disease Control also conducted a study that showed 39% of Vietnam veterans with PTSD were also substance abusers/dependent (Heath Status of Vietnam Veterans, 1989).

PTSD is not just “combat fatigue” or “shell-shock.” It is observed in different types of people, all of which have been exposed to trauma, but its manifestations are significantly different in children, who will not be considered further in this discussion. It is found with great frequency among women, usually victims of sexual assault (Breslau et al., 1991). These women also frequently demonstrate co-morbid substance abuse/dependency.

Clearly the relationship between substance abuse/dependency and PTSD is important and impacts a broad community, making it a highly relevant topic for development. Furthermore, because of PTSD’s symptoms, conventional substance abuse/dependency programs my not work as well as they would on a person without PTSD. Therefore treatment strategies are greatly impacted, and the entire approach of treatment is positioned differently. Unlike a typical co-morbid situation, where both problems can be treated independently, co-morbid PTSD and substance/abuse must be approached uniquely.

It is important to realize that there is no drug preference for those who meet PTSD criteria. One investigator hypothesized that a special relationship existed between narcotic use and PTSD since the dominant theory of the relationship between PTSD and substance abuse/dependency is the self-medication hypothesis. In testing his narcotic preference hypothesis, the investigator found that there was no particular drug preference for PTSD substance abusers. In fact there was marked variability, some preferring marijuana, others alcohol and others still preferring narcotics, hallucinogens and other drugs (Robins, 1975). This suggests that the self-medication hypothesis may not be as useful as thought since drugs that would assuage anxiety and other unpleasant PTSD symptoms (narcotics) should be preferred over drugs which wont be as useful.

Indeed, the relationship between PSTD and substance/abuse dependency is unclear. As mentioned earlier, the dominant hypothesis is the self-medication hypothesis. Essentially, this hypothesis states that PTSD is a primary disorder and that drugs are taken to assuage the uncomfortable anxiety-related symptoms of the psychiatric disorder (Khantzian, 1985) (Lehman et al., 1989). Substance abuse among trauma survivors may represent attempts at avoidance of negative memories and affective responses (Follette, 1998). Sometimes this is called “tension-reduction.” A particular investigator emphasized the importance of the euphoria produced by many drugs such as cocaine, opiates, marijuana, and, to a lesser degree, alcohol. Since a distinguishing (and sometimes anguishing) feature of PSTD is flat affect, these drugs may play a role in helping the PTSD afflicted individual restore feeling and fight numbness (Kosten and Krystal, 1988). One investigator said, “PTSD patients with pronounced avoidance/numbing symptoms may rely more on drug abuse to induce sensations that are otherwise blunted” (McFall et al., 1992, p 361). There is clearly some evidence for the self-medication model, and it is the most common understanding among contemporary psychiatrists.

Other investigators demonstrate that drug use prior to the development of PTSD predict drug abuse/dependency following the development of PTSD more readily than the self-medication hypothesis, which stipulates that PTSD must be primary (Helzer, 1984). This realization seriously undermines the self-medication hypothesis. Also, it has been found that to have significant success in treating PTSD and co-morbid substance abuse/dependency; both PTSD and the substance abuse must be individually treated (Volpiceli, 1987). This may seem obvious, but if PTSD is truly a primary disorder, and is successfully treated, the substance abuse/dependency should clear up. Though it is possible that those with PTSD are simply developing an addiction to the drug. This could explain why they continue to abuse despite successful PTSD treatment. The primary/secondary relationship between PTSD and substance abuse/dependency is unclear (Minkoff, 1989), but successful treatment approaches always tackle both problems together.

There are several treatment approaches for those with co-morbid PTSD and substance abuse/dependency. The most successful ones often take a broad approach targeting both PTSD and substance abuse/dependency by utilizing cognitive-behavior therapies, group therapies and self-help programs.

There tends to be a general recommendation against the use of drugs when treating co-morbid PTSD and substance abuse/dependency (Schnitt 1984), though there are several drugs that can be effectively prescribed for treating PTSD. This is because there is addiction potential with many drugs used to treat PTSD, and substance abusing PTSD patients are more likely to abuse a drug than a typical PTSD patient. Preferred drugs for treatment have minimal addiction potential. The most recommend drugs are the SSRIs: fluoxetine and sertraline (Hubbard and Martin, 2001, p26) (Asnis et al., 2004) because of lack of addiction potential (it is actually difficult to keep people on these drugs), good effectiveness and ease of administration (Taylor and Gorman, 1992). Also they are preferred because of lack of toxicity in case of overdose (Hubbard and Martin, 2001, p. 27). Higher does doses of these drugs may be required in alcohol abusing/dependency individuals due to hepatic injury resulting in elevated hepatic enzymes (Mason, 1996).

Neuroleptics like chlorpromazine and olanzepine are also used to treat anxiety associated with PTSD (Hubbard and Martin, 2001, p 28), but less frequently. Chlorpromazine has anxiety-inducing withdrawal symptoms and other negative side effects, and olanzepine has sedative effects, which lends the drug to possible abuse. For opioid dependence: methadone, buprenorphine, and l-alpha-acetylmethodol (LAAM) are used (Hubbary and Martin, 2001, p. 28) and may be helpful in PTSD patients with narcotics dependence. The new MDMA experimental therapy (Mithoefer, 2006) is vigorously not recommended due to addiction potential in PTSD patients with existing substance use problems.

There are drawbacks to drug therapies in general. To begin with, they all approach the PTSD as primary and drug abuse/dependency as secondary, as suggested by the self-medication model while it has been demonstrated that the primary/secondary relationship is unclear. They also completely overlook the entire substance use problem, which is best approached first (Follette, 1998, p. 231). The use of these drugs will also make it difficult for patients to enter 12-step programs like AA and NA, which have been found to be helpful (Hubbard and Martin, 2001, p. 29), because these programs aim for complete sobriety. There is still a dearth of information bearing directly on the functions of alcohol and drug ingestion in relation to PTSD; few studies have attempted to test the self-medication hypothesis directly (Follette et al., 1998, p. 229). It is known however that treating the drug use problem first, followed by PTSD treatments, is more effective than treating PTSD first, followed by drug treatments, or, by simultaneous treatment (Follette et al., 1998, p. 231).

There are alternative theories about the relationship of PTSD and drug abuse/dependency. According to classical conditioning theories of relapse, stimuli that reliably precede administration of alcohol or drugs may come to elicit a variety of possible substance-related conditioned responses (“cravings”). Exposure to these “triggers” and the conditioned emotional and physical response increased the likelihood of substance consumption. Because substance abusing/dependent individuals with PTSD often drink or use drugs in the presence of traumatic reminders, memories, or PTSD symptoms, these trauma-related stimuli may also come to elicit urges to drink or use substances (Rohsenow et al., 1990). Some researchers have investigated this hypothesis in women with some success (Peirce et al., 1996), but it is a fairly unexplored hypothesis that has yielded little in the way of successful treatment strategies.

Another simpler hypothesis is that since anxiety is increased as a symptom of PTSD, that people with normal levels of anxiety sensitivity begin to consume alcohol and other drugs to reduce the anxiety. High anxiety sensitivity has been linked to higher levels of alcohol consumption (Stewart et al., 1995) in people without PTSD, so it is plausible that normal levels of anxiety producing stimuli in an otherwise normal person with PTSD may drive them to substance abuse/dependence. This theory is appealingly simple, and it informs us as to why reducing anxiety-causing fixtures in a PTSD patient’s life can help prevent relapse.
Most recent developments in treatment combine some form of exposure therapy for PTSD with an empirically supported treatment for substance use disorder (Coffey, 2005).

It is vital to begin substance use treatments before the treatment of concurrent PTSD (Follette et al., 1998, p. 231), which seems to undermine the belief that PTSD is a primary diagnoses. Too many problems are encountered during PTSD treatments with substance abusers/dependents unless initial efforts towards sobriety are made. Practitioners have difficulty engaging the patient, drug therapies will probably not be adhered to, and exploration of trauma-related issues may be harmful to the patient who is currently abusing a substance (Reilly, 1994).

A general treatment strategy outlined by Follette et al. (1998, p. 237-243) would include using assessment to direct the treatment process, and assessment should be ongoing. The patient needs to be monitored carefully to detect any trends or events that are creating anxiety or possibly triggering the PTSD symptoms. A therapeutic relationship must be forged between the therapist, the client and any other groups helping the client. People with PTSD often have interpersonal difficulties associated with flat affect and other symptoms of PTSD, so the confrontational style of many self-help groups, particularly those of the 12-step variety, may be problematic. In this case, the therapist should direct the patient into the most appropriate groups, since AA and NA have been found to be helpful (Hubbard and Martin, 2001, p. 29). The next step in the treatment plan is to build motivation and set goals. This may involve different interviewing techniques, and Miller and Rollnick’s method (1991) is recommended by Follette et al (1998). It is based on providing helpful extended discussion of motivation enhancement methods based on five broad principles: (1) express empathy, (2) develop discrepancy (amplify in the client’s mind the discrepancy between current behavior and future goals), (3) avoid argumentation, (4) roll with resistance, and (5) support self-efficacy. Once the interviewing process has been completed, managing exposure to alcohol, drugs, and cues has to be undertaken. This may involve modifying the social environment. Often the spouse can be of great help in this process (Kosten, 1987). Finally implementing relapse prevention methods and training skills for risky situations must be undertaken. A summary of steps for therapy recommendations was published by Follette et al. (1998) on pages 246 and 247.

In conclusion, PTSD co-morbid with substance abuse/dependency is a relevant, but treatable problem. Its etiology and causes are largely unexplained, and the working hypotheses are inadequate, but some effective treatment therapies have emerged empirically. The future holds hope of finding even more effective, specific, treatment approaches, and hopefully a better understanding of the relationship of PTSD and substance abuse/dependency.


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