Co-Occurring Post-Traumatic Stress Disorder and Alcohol Use Disorder in U S. Military and Veteran Populations Alcohol Research: Current Reviews
In one case study of an OEF/OIF veteran, researchers examined the effectiveness of concurrent treatment of PTSD and SUD using prolonged exposure (COPE) therapy.45 COPE involves 12, 90-minute sessions that integrate relapse prevention with prolonged exposure therapy. The veteran who received the therapy reported reduced alcohol use throughout treatment, scored in the nonclinical range for PTSD at the end of treatment, and maintained treatment gains at a 3-month follow-up. Finally, although preclinical work has resulted in considerable progress toward delineating the contributions of the HPA axis and noradrenergic systems to the pathophysiologic underpinnings of PTSD with comorbid substance dependence, few neurobiologic studies have been conducted in this patient population. The inclusion of subjects with this comorbidity may render such studies more complicated, but the data emerging from this work would better inform the clinical management of the difficult-to-treat symptoms of these frequently encountered patients. At the minimum, patients who participate in studies of PTSD or of substance dependence must be thoroughly evaluated for the presence of this comorbidity to permit adequate control of the effects of the comorbid condition on the neurobiologic processes under study. Evidence of noradrenergic dysregulation in both PTSD and in withdrawal from CNS depressants has prompted the use of the α2-adrenoceptor agonist clonidine in both disorders (57, 58).
There was no statistically significant main effect for prolonged exposure therapy on PTSD symptoms and no observed differences in the number of dropouts across conditions. In the same sample, prolonged exposure was more beneficial for those with non–combat-related traumas and higher baseline PTSD severity.39 Also, naltrexone was most beneficial for those with the longest duration of AUD. Some people who either experience several traumatic events or continually reexperience the same event, as people with chronic kundalini meditation PTSD do, will drink to reproduce the numbing effects experienced with increased levels of endorphins. The constant reexperiencing of the PTSD symptoms causes an initial increase in endorphin activity followed by a rebound withdrawal. One study conducted with Vietnam combat veterans with chronic PTSD showed that their alcohol use generally began after the onset of PTSD symptoms. For many of the patients, alcohol consumption continued to increase as their symptoms of PTSD increased (Bremner et al. 1996).
- Evidence indicates that concurrent treatment of PTSD and AUD can be safe and effective.30,39 Before reporting on concurrent treatment approaches, we describe evidence-based treatments targeting either PTSD or AUD.
- High doses of alcohol produce a characteristic inflammatory response in the brain, including activation of microglia and upregulation of proinflammatory signaling molecules.59 Further, this inflammatory response to alcohol is exacerbated in animals with a history of TBI.
- Factors contributing to addiction to alcohol and PTSD sufferers include the severity and type of PTSD the person experiences.
However, no differences were found on any of the primary variables of interest between those with complete versus incomplete data. Thus, it appears that the subset of participants who provided complete data were representative of the larger sample and comprise the sample analyzed below. Data were examined for compliance with the assumptions of analysis of variance (Tabatchnik and Fidell 2001). There were no univariate outliers on the PILL, and, although the variable distribution was skewed, it was insufficient to violate the assumptions of ANCOVA. Because of the underrepresented female sample, we performed post hoc analysis to confirm the consistency of the observed findings.
Biology of the Stress Response
Are there significant differences in the occurrence and trajectory of PTSD and AUD among racial and ethnic minorities? These questions, and others, should be addressed by further research to ultimately minimize the harm experienced by the millions of individuals who experience AUD and PTSD. The lifetime prevalence of severe AUD was about 14%, and the past 12-month prevalence was more than 3%. Less than 20% of respondents who experienced AUD in their lifetime ever sought treatment for the condition.
Treating Co-Occurring PTSD and AUD
Additionally, the conditional nature of the disorders, based on the exposure to an event or a substance, makes this a complex relationship for analysis, interpretation, and intervention for treatment. Our review of the literature on the pathophysiologic basis of comorbid PTSD and addiction selectively focuses on studies of the hypothalamic-pituitary-adrenal (HPA) axis and the noradrenergic system, as these have been most extensively studied in PTSD. It must be emphasized that many other neurobiological systems are involved in both the acute and chronic adaptation to stress and to substance use. These systems include the dopaminergic, γ-aminobutyric acid, benzodiazepine, and serotonergic systems, as well as the thyroid axis. Interactions among these systems in patients with comorbid PTSD and substance dependence are enormously complex. Thus, the potential relationships we discuss between the HPA axis, the noradrenergic system, and symptoms in patients with comorbid PTSD and substance use disorders should be viewed as one part of a far more complex whole.
She avoided numerous situations reminiscent of her earlier experiences, including her childhood home and movies and news items involving child abuse. She also avoided discussing her abuse history with others and attempted to suppress her own memories of what happened. She felt unable to control many of these PTSD symptoms except by drinking alcohol, but even alcohol provided only temporary relief. Unfortunately, this example is far too 254 massachusetts sober living homes transitional living ma common, as people like Margaret, after an experience of sexual or physical victimization, turn to alcohol to relieve symptoms of anxiety, irritability, and depression. In this paper we present a new model to help explain how trauma’s effects on psychological distress may influence alcohol consumption. As shown in the schematic, AUD and other mental health disorders occur across a spectrum from lower to higher levels of severity.
Behavioral Treatments for PTSD
We know the analgesia is attributable to a release of endorphins because drugs that block endorphins (opioid blockers) also block the analgesia in PTSD patients. In one study, Vietnam veterans with PTSD were shown a videotape of combat and asked to rate the pain intensity of a hot stimulus. After viewing the videotape the hot stimulus was less painful (i.e., the trauma reminder produced analgesia). However, when the 4 ways to relax without alcohol opioid receptors were blocked with naloxone, an injectable opioid receptor blocker, there was no analgesia (van der Kolk et al. 1989). The naloxone blocked the analgesia produced by the trauma reminder; and, with their opioid receptors blocked, patients with PTSD felt the pain as severely as did people who did not have PTSD. This finding shows that trauma reminders in PTSD patients activate the endorphin system.
Transcend participants also experienced improvements in SUD symptoms, including decreased alcohol consumption, decreased polysubstance drug use, and decreased episodes of drinking to intoxication. Although these findings are promising, they remain preliminary, as Transcend has yet to be evaluated in a randomized controlled trial. During chronic uncontrollable stress, norepinephrine turnover increases in specific brain regions, including the locus ceruleus, hypothalamus, hippocampus, amygdala, and cerebral cortex (51). Noradrenergic dysregulation has also been reported during states of withdrawal from chronic self-administration of alcohol and other abused substances.
PTSD and Alcohol: How Does Alcohol Affect PTSD Symptoms?
Prazosin was effective in decreasing alcohol use in one study (Simpson et al. 2015) but not in the other larger trial (Petrakis et al. 2016); prazosin was not effective in treating PTSD symptoms in either study evaluating its efficacy. The neurokinin-1 receptor antagonist aprepitant had no effect on PTSD symptoms or alcohol craving (Kwako et al. 2015). AUD and PTSD have shown a consistent comorbidity over many decades and in diverse populations. The strong relationship is present in representative surveys of the United States, throughout Europe, and in Australia.
LiRong Wang reports sub-award from Pharmacotherapies for Alcohol and Substance Use Disorders Alliance (PASA) funded by the Department of Defense. Treatment providers can connect you with programs that provide the tools to help you get and stay sober. Take our short alcohol quiz to learn where you fall on the drinking spectrum and if you might benefit from quitting or cutting back on alcohol. If you’re struggling with alcoholism and PTSD, American Addiction Centers (AAC) can help you find treatment. Contributors to this article for the NIAAA Core Resource on Alcohol include the writers for the full article, reviewers, and editorial staff. Participants unable to read or write provided a thumb print together with a signature from a witness confirming their voluntary participation.
The Relationship Between Alcohol And PTSD
For information about the terms governing the use of our website and how we handle data, please refer to our Terms of Use and Privacy Policy. Moreover, each condition comes with its own set of distressing symptoms, so the situation can be quite tenuous when they occur together. This, in turn, can lead to addiction and a comorbid diagnosis of PTSD and alcoholism. Although urinalysis is the predominant and often preferred biological method of assessment, SUD screening may also involve testing other bodily fluids, such as blood and saliva (Wolff et al., 1999). CDT testing is particularly useful when used in combination with other indicators such as liver enzymes (Aithal et al., 1998).
Do People Use Alcohol to Cope with PTSD?
The treatment of PTSD patients with alcohol dependence involves simultaneously addressing both disorders, because they seem to be intertwined. In therapy, patients learn to cope with their previous traumas and to handle situations that may remind them of the event. Because research shows that both alcohol use and trauma increase endorphin activity, opioid receptor blockers may be a useful part of treatment for PTSD. We speculate that as trauma-related memories brought up during therapy may cause a release of endorphins and subsequent emotional numbing, this may interfere with the patient’s ability to engage in therapy fully.
Amaro et al. (2007) compared a comprehensive women’s substance abuse and co-occurring disorder treatment model that included a 25 session TREM intervention to treatment-as-usual in 342 women with a trauma history and SUD. Women in the intervention group showed significantly greater reductions in drug use and PTSD symptoms at the 12-month follow-up as compared to women in usual care. However, the study had limitations such as lack of randomization and lack of biological measures to verify abstinence. Because the TREM intervention was delivered as part of a comprehensive treatment package, it was difficult to attribute outcomes to the trauma intervention component. High doses of alcohol produce a characteristic inflammatory response in the brain, including activation of microglia and upregulation of proinflammatory signaling molecules.59 Further, this inflammatory response to alcohol is exacerbated in animals with a history of TBI.
In one case study of an OEF/OIF veteran, researchers examined the effectiveness of concurrent treatment of PTSD and SUD using prolonged exposure (COPE) therapy.45 COPE involves 12, 90-minute sessions that integrate relapse prevention with prolonged exposure therapy. The veteran who received the therapy reported reduced alcohol use throughout treatment, scored in the nonclinical range for…