Effects of Stress on Alcohol Consumption

Stress and Alcohol Use. Animal studies indicate that stress increases alcohol consumption when the stress, whether physical or social, is chronic, unavoidable, and uncontrollable. Evidence from human and animal studies indicates that alcohol has profound anxiolytic effects. In rodents, tolerance to the anxiolytic effects of low or moderate doses of ethanol was shown to develop rapidly and, as such, may explain the augmented consumption of alcohol required to maintain its tension-reducing effects.

In addition, adverse experiences early in life, such as maternal separation, have been found to be associated with excessive alcohol consumption in monkeys as well as in humans. Furthermore, prenatal factors, such as maternal stress and drugs or alcohol consumption during pregnancy, can dysregulate physiological and behavioral stress responses in adulthood. Such findings suggest that early life experiences can result in long-lasting psychobiological changes that may manifest as enhanced alcohol consumption in order to achieve tension reduction.

Consistent with the stress-response dampening model, it is a common and long-held assumption that alcohol is often used as a means of coping with stress. Recently, however, with the observation that alcohol may or may not dampen physiological responses to stress, new theories have evolved. One that is consistent with many observations and the effectiveness of new pharmacological treatments for alcoholism is the endorphin compensation hypothesis.

This hypothesis proposes that alcohol is consumed following the termination of stress because the presence of stress increases levels of the endogenous opioid ß-EP. Alcohol is sought for its ability to increase ß-EP levels and compensate for the deficit that results when the stress has been removed. Consistent with this hypothesis is the use of naltrexone, an opiate antagonist, in the treatment of alcoholism.

Sleep and Alcohol Use. Sleep disturbance is a common complaint of alcohol- dependent patients. Various studies have demonstrated a strong association between poor sleep and psychological factors, especially in relation to perceived stress and associated increases in CRH and cortisol, the hypothalamic and adrenal products of the HPA axis. Both hormones are known to lead to arousal and sleeplessness in human subjects and experimental animals.

The daily sleep-wakefulness cycle is synchronous with circadian patterns of body temperature in humans and animals such that maximum body temperatures occur during the active portion of each day and minimum body temperatures occur during the inactive or sleep portion. In rodents, the daily active period corresponds with the dark phase of the daily light-dark cycle while sleep occurs during the light phase.

Acute administration of ethanol was found to alter the rodent’s circadian body temperature and activity rhythms in a dose- and time-dependent manner. Chronic exposure to ethanol has also been shown to alter the amplitude of the rat’s circadian body temperature and activity rhythms. Confirmation of these findings in translational studies on human subjects could provide a further basis for alcohol-induced sleep disturbances.

Trauma and Alcohol Use. Despite the controversy as to whether or not alcohol is used to minimize the impact of stress or to compensate for some post-stress condition, there is an abundance of correlational data linking increases in alcohol use with exposure to or the experience of traumatic or uncontrollable stressful events. For example, studies have demonstrated that there is an increase in social indices of alcohol use (such as arrests for driving while intoxicated) following disasters.

Not only are changes in a population’s alcohol consumption associated with traumatic events that affect a community (e.g., natural disasters), but a high percentage of those seeking treatment for alcoholism are survivors of abuse or suffering from posttraumatic stress disorder or other anxiety disorders. Although it may be difficult to determine a direct relationship between victimization and alcohol misuse, attempts to define whether or not alcohol abuse preceded, coincided with, or followed trauma have consistently found that trauma did, in fact, precede alcohol misuse.

Furthermore, trauma severity is positively correlated with alcohol consumption and the severity of alcohol-related problems. There is reason to believe that, whereas stress plays a role in the etiology of all drug dependence, the drug selected by men is more likely to be alcohol. Thus, there appears to be a gender difference in the drug of choice for the individual struggling with the aftermath or presence of stressful life conditions.

Traumatic Brain Injury and Alcohol Use. Traumatic brain injury (TBI) and its sequelae are of pivotal importance in the young generation (e.g., in victims of car accidents and in deployed soldiers and war veterans) with consequences ranging from physical disabilities to long-term behavioral and social deficits. Close to 25% of TBI cases are associated with alcohol abuse, and alcoholism may, in and of itself, complicate long-term TBI recovery.

A growing body of evidence raises the possibility that alcohol intoxication or dependence in combination with TBI may lead to increased deleterious effects on cognitive functioning. Moreover, serious alterations in neuroendocrine and immune regulation have been noted following chronic alcohol use and TBI in animal models and humans that can impair recovery and rehabilitation efforts after brain injury. However, the role of alcohol as an interactive or additive agent in these findings has not been fully assessed.

Alcoholism, Stress, and Relapse. Stressful life events have long been thought to play a role in the return to alcohol use following cessation of problematic drinking behavior. The role of stress in relapse has received much attention, with more recent reviews concluding that less severe psychosocial stress may not increase the likelihood of relapse, whereas severe acute stressors and chronic stressors perceived as highly threatening may contribute to an increased risk of relapse. In considering the role of stress in relapse, however, the capabilities of the individual must be considered.

The impact of even severe stress and whether this leads to relapse are mediated by both protective and risk factors that render the individual more or less likely to return to problematic alcohol use. Risk factors that may increase the likelihood of relapse to substance abuse include the persisting physiological symptoms of abstinence (e.g., HPA axis dysfunction, characterized by a blunted ACTH response to a challenge with CRH).

The role of stress has been the focus of many alcoholism treatments. Most notably, the relapse prevention model introduced by Marlatt and George in 1984 proposes that the goal of treatment for addictive behaviors must be to develop the means for coping with stressful situations. In order to change addictive patterns, situations that are high-risk for relapse need to be identified and methods for coping with such situations developed.

According to the model, cessation of addictive behavioral patterns can be achieved through the mastery of handling such high-risk situations. The relapse prevention model has been the focus of much research, although empirical support for its effectiveness is difficult to obtain. Despite research suggesting that relapse does occur in situations identified as being high-risk, the subjective nature of such retrospective reports calls any definitive conclusions into question.