PTSD and Alcohol Addiction

Biology of the Stress Response
by National Institute of Health

(Page 3 of 4)

Why does alcohol preference increase after stress, rather than during stress? The biology of the stress response gives us a clue. Exposure to uncontrollable stress elicits the familiar "fight or flight" response. Fear prompts the release of corticotropin-releasing hormone (CRH), which in turn stimulates the release of proopiomelanocortin (POMC), a large molecule that is broken up into several parts including adrenocorticotropic hormone (ACTH), which is responsible for the familiar "fight or flight" response, and beta-endorphin, which may have the survival advantage of numbing pain if the organism is attacked. The ACTH limb of the stress response increases arousal. The betaendorphin limb causes a reduction in emotional and physical pain.

The Role of Endorphins in PTSD and Alcohol Drinking

The model presented above suggests that uncontrollable trauma in humans and other mammals should lead to a release of endorphins and increased numbing. Research has shown that when animals are presented with inescapable shocks, their pain response decreases. The reduced pain response is attributable to an increased release of endogenous opioids. When rats were given naltrexone, which blocks the effects of endorphins, the numbing effects of uncontrollable trauma were also blocked. Furthermore, after uncontrollable trauma naltrexone produced an opiatelike withdrawal reaction suggesting a withdrawal from one's endorphins. Although exposure to controllable trauma, produces a modest analgesia, it is brief and there is no endorphin withdrawal following the traumatic experience. This shows that endorphin activity increases in response to uncontrollable trauma, but not in response to the same traumatic event if it can be controlled, a finding with important implications for understanding endorphin activity associated with PTSD.

Human studies have also shown that traumatic events can increase endorphin activity. For example, patients with PTSD will experience numbness or analgesia when simply exposed to reminders of the trauma. 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 (the trauma reminder produced analgesia). However, when the opioid receptors were blocked with naloxone, an injectable opioid receptor blocker, there was no analgesia. 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.

Endorphin Compensation Hypothesis

Chronic stimulation of the stress response leads to two compensatory responses. First, ACTH tends to inhibit the further release of CRH. Second, chronic stimulation of opioid receptors leads to an increase in an opposing system that has anti-opioidlike effects. Over time, the opposing system gets stronger and this leads to a lessening or habituation of the endorphin system. But when the trauma is over, the net result is a deficit in endorphin functioning and a resultant endorphin withdrawal. Like traumatic events, alcohol use can increase endorphin activity. In this way, drinking can compensate for the endorphin withdrawal that follows a traumatic experience. The endorphin compensation hypothesis (ECH) suggests that when people drink alcohol after traumatic events, the alcohol makes up for the lack of endorphin activity. According to this hypothesis, rats exposed to uncontrollable shocks should consume more alcohol than rats exposed to controllable shocks to compensate for the lack of endorphin activity that occurs after experiencing uncontrollable shocks. This explains why alcohol consumption would increase after the trauma, not before (in anticipation) or during the trauma, as predicted by the tension-reduction hypothesis.

Some people who either experience several traumatic events or continually reexperience the same event, as people with chronic 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. During the rebound withdrawal, craving for alcohol should increase. 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.

Women's Increased Risk for Trauma-Induced
Emotional Distress and Alcoholism

The association between PTSD and alcoholism is particularly strong for women. In adults, the rates for co-morbid PTSD and substance use disorders are two to three times higher for females than males, with 30 to 57 percent of all female substance abusers meeting the criteria for PTSD. Women's increased risk for co-morbid PTSD and substance dependence is related to their higher incidence of childhood physical and sexual abuse. For example, in a group of adolescents, a history of sexual abuse increased the risk of problem drinking to 20 times the normal rates of alcohol abuse for both sexes. However, females were much more likely to have been sexually abused than males and consequently the symptoms of PTSD were more common for female than male alcohol abusers.

These early experiences of physical or sexual abuse can have a life-long effect. Early experience with trauma (a history of childhood sexual or physical abuse) also heightens a person's susceptibility to severe PTSD symptoms as an adult. For example, victims of childhood physical and sexual abuse are at higher risk for developing PTSD symptoms following traumatic events in adulthood.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.