Stress increases alcoholism

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A number of sociocultural studies indicate that stress may increase the risk of alcoholism. In other words, an individual’s ability to cope with stressful situations may indicate his or her vulnerability to alcoholism.

A study in Alcoholism: Clinical & Experimental Research has found that individuals with a family history of alcoholism exhibit a dysfunction in their stress response prior to the development of alcohol dependence, while individuals without a family history of alcoholism exhibit a dysfunction in their stress response following the development of alcohol dependence.

“It is not well understood how stress increases alcohol consumption, or what the relationship is between stress and alcohol,” said Christina Gianoulakis, a professor in the department of psychiatry at McGill University and corresponding author for the study. 

"One of the questions we wanted to ask is whether alcohol induces a number of biological responses that help the individual cope with a stressful situation. If that is the case, then the alteration of the activity of biological systems by both alcohol and stress may help us to understand the relationship between stress and alcohol. One such biological system is that of brain and pituitary £]-endorphin.”

Both Gianoulakis and Maurice Dongier, professor emeritus in the department of psychiatry at McGill University, agree that the effect of stress on £]-endorphin is clear and well defined. “Stress increases the release of £]-endorphin by both the pituitary gland and the brain,” said Dongier. “But the effect of alcohol is not as clear. It is, in fact, somewhat contradictory.”

Gianoulakis said that a specific response may depend on the dose of alcohol as well as the species involved. “For example, in experimental animals such as rats, all doses of alcohol increase the release of £]-endorphin,” she said. “However, in humans low doses of alcohol have either no or a small effect on £]-endorphin release, whereas high doses of alcohol are needed to induce a significant increase in £]-endorphin release.”

For this study, four groups of individuals participated: social and heavy drinkers with a family history of alcoholism (considered “high risk") and without a family history of alcoholism (considered “low risk"). Each participant was given either a placebo or alcohol (0.50g ethanol/kg) drink; researchers then measured their responses to both drinks as well as a stress test performed 30 minutes following ingestion. The stress test had two components: arithmetic computations, and a competition for monetary reward. Plasma £]-endorphin levels were also measured prior to and for 3.5 hours after the stress test.

Results indicate that there are differences in both the basal plasma £]-endorphin levels as well as the response of the pituitary £]-endorphin to stress as a function of an individual’s family history of alcohol problems.

“There are two major findings in this study,” said Gianoulakis. “In participants with a family history of alcoholism, the lower activity of the pituitary £]-endorphin system indicated by the low basal plasma £]-endorphin levels and the lower £]-endorphin response to stress predate the development of alcoholism, and alcohol dependence does not induce a further decrease in the activity of the pituitary £]-endorphin system. However, in subjects without a family history of alcoholism, alcohol dependence induces a decrease of the activity of pituitary £]-endorphin, as indicated by the lower basal plasma £]-endorphin levels and the lower £]-endorphin response to stress.” In other words, said Gianoulakis, in high-risk individuals, dysfunction in the activity of the pituitary £]-endorphin system predates the development of alcoholism; while in low-risk individuals, dysfunction develops following alcohol dependence.

“The second important finding is that when participants of all four groups ingested a small amount of alcohol, the equivalent of about two standard drinks, the stress task performed 30 minutes after the drink did not increase the release of £]-endorphin,” said Gianoulakis. “Thus, prior alcohol consumption blocked or decreased the £]-endorphin response to stress regardless of family history of alcoholism and presence of alcohol dependence.”

Gianoulakis added it was important to note that stress dysfunction can both act as a mediator of alcohol dependence and occur as a consequence of alcohol dependence. “The major objective of a biological response to stress is to help that individual cope with a stressful situation,” she said. “A low response to stress may compromise an individual’s ability to cope, so that he or she feels the need to search for alternative ways to cope with stress, one of which could be drinking, eventually leading to alcohol dependence. Conversely, we also found that alcohol dependence can induce a decrease of then £]-endorphin response to stress in individuals without a family history of alcoholism, eventually compromising their responses to stress and his or her ability to cope with stressful situations. They may cope with subsequent stress by increasing alcohol consumption, which not only prevents recovery of the stress response but may also induce a further dysfunction of the stress response.”

Both Gianoulakis and Dongier said that one group in particular V individuals with a family history of alcoholism V needs to be aware of their potentially greater risk of developing alcohol problems.

“Individuals with a family history of alcoholism exhibit a dysfunction of the stress response prior to the development of alcohol dependence,” said Gianoulakis. “These individuals may have a greater vulnerability to stressful situations, and should try to avoid drinking alcohol in the face of stress, as well as develop alternative behavioural skills for coping with stress.”

http://www.mcgill.ca

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