Post-traumatic stress disorder (PTSD) commonly co-occurs with alcoholism and is characterized by abnormalities in the hypothalamic-pituitary adrenal (HPA) axis. However, the influence of interaction between these two disorders upon disruptions in the HPA axis is not well understood. A study in the June issue of Alcoholism: Clinical & Experimental Research has found that alcoholics without PTSD have a disconnect between their high emotional distress and low biological stress response to a stress-inducing test … and appear more likely to relapse during the month following the test.
"More than 50 percent of individuals with PTSD meet criteria for alcohol abuse or dependence at some time in their lives," said Kathleen T. Brady, professor of psychiatry and associate dean for clinical research at the Medical University of South Carolina and corresponding author for the study. "It is possible that individuals with PTSD use alcohol in an attempt to treat some of the symptoms associated with PTSD such as sleep disturbance, nightmares and unwanted thoughts of the traumatic event. It is also possible that using alcohol as a means of coping with traumatic events and memories prevents the development of more healthy coping strategies and may make an individual more vulnerable to the development of PTSD after a traumatic event has occurred."
"The HPA axis is a critical part of the body's stress response system," explained Bryon H. Adinoff, Distinguished Professor in the department of psychiatry at the University of Texas Southwestern Medical Center at Dallas. "One of the main functions of the HPA axis is to modulate the brain's response to stress. Many investigators have shown that patients with alcoholism or with PTSD have alterations in their biological stress response system. Given the importance of stress in both PTSD and alcoholism, how these two disorders interact upon the stress-response system may have an important role in the development and progression of both disorders. This study is the first to explore this interaction."
During acute stress, the HPA axis is activated, increasing adrenocortotropic hormone (ACTH), which in turn increases cortisol. During alcohol intoxication and alcohol withdrawal, ACTH and cortisol are also increased. When an alcoholic stops drinking, however, the ACTH and cortisol response to stress becomes impaired. This may be due to the body adapting to chronically elevated levels of cortisol. Similarly, in PTSD, the HPA axis appears to adapt to persistently elevated levels of cortisol. Thus, for both alcoholism and PTSD, chronic stimulation of the HPA axis leads to an adaptive "down-regulation" of the system.
For this study, researchers exposed 63 individuals (35 men, 28 women) to a widely used physical laboratory stressor called Cold Pressor Task (CPT), which requires subjects to submerge one hand in a cold water bath for up to one minute. Of the 63 participants, 35 had alcohol dependence only, and 28 had both alcohol dependence and PTSD. The two groups were equally divided between men and women. Subjective stress, craving, and ACTH and cortisol levels were measured before, immediately after, and then at five, 30, 60 and 120 minutes after the CPT. Alcohol use during the month following testing was also assessed.
"We found that for individuals with alcohol dependence without PTSD, alcohol craving and disruption of the HPA axis response were associated with more drinking in the follow-up period," said Brady. "This may mean that for these individuals, there is a meaningful relationship between the disruption of HPA axis function caused by excessive alcohol consumption and relapse. A decrease in the ACTH capacity to respond normally to a stressor may be positively associated with stress-related craving and drinking in alcohol-dependent individuals."
"In this group," added Adinoff, "some of these subjects experienced a lot of distress immediately after the cold pressure task. When someone reports feeling stressed, you would expect their ACTH hormone to rise. However, in some of the patients who reported feeling stressed, their ACTH hormone did not increase much. These patients – the ones who showed a disconnect between their high emotional distress and low biological stress response – were also more likely to drink over the next month compared to all of the other alcohol-only patients tested."
In other words, he summarized, the long-term, heavy use of alcohol leads to disruptions in the body's biological response to stress, which persist even during abstinence. "Because the body can no longer respond appropriately to stress, this may leave an abstinent alcoholic more vulnerable to effects of stress, which may place the person at greater risk for relapse," he said.
"Conversely, these relationships did not hold true for individuals with PTSD and alcohol dependence," observed Brady.
"It may be that the combination of alcoholism and PTSD so severely disrupts the HPA axis that anyone with both disorders who experiences stress does not have an appropriately robust hormone stress response," said Adinoff. "In other words, the combination of PTSD and alcoholism may have more profound, long-term effects on the HPA axis than just having alcoholism alone."
"In terms of clinical applicability," said Brady, "interventions that target coping with stress and decreasing stress may be useful in relapse prevention. For individuals with PTSD and other psychiatric comorbidity, triggers for relapse and biologic vulnerabilities to relapse may be different than for individuals without psychiatric comorbidity. We plan to investigate the impact of stress-management techniques as well as medications that impact the stress response on craving and relapse in individuals with and without psychiatric comorbidity."
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Cold Pressor Task Reactivity: Predictors of Alcohol Use among Alcohol-Dependent Individuals with and without Comorbid PTSD," were: Sudie E. Back, Angela E. Waldrop, Aimee L. McRae, Raymond F. Anton, Himanshu P. Upadhyaya, Michael E. Saladin, and Patrick K. Randall, all of the Medical University of South Carolina in Charleston, South Carolina. The study was funded by the National Institute on Alcohol Abuse and Alcoholism, the National Institute of Health, and the National Institute on Drug Abuse.
Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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