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Many researchers believe that people are prompted to drink because of alcohol’s stress-relieving effect. However, while alcohol may temporarily relieve such symptoms, chronic drinking can exacerbate the adverse effects of stress instead. In fact, it may leave the brain in a state of permanent physiological stress.

Scientists are gaining a better understanding of how a process called neuroadaptation sets the stage for alcohol addiction. So, let’s look at how neuroadaptation works.

Chronic Alcohol Use Interferes with Brain Cell Communication

Networks of brain cells perform the brain’s essential functions which include storing information, regulating basic body functions, and directing behavior. These brain networks require communication from cell to cell by means of chemical messengers called neurotransmitters. Neurotransmitters are released into narrow gaps, or synapses, between cells. Next, these neurotransmitters cross the synapse and activate proteins called receptors. Receptor activation, in turn, leads to a series of molecular interactions within the receiving cell.

Some of the molecular interactions are short–term. They remain localized to the area of the cell containing the receptors. But other interactions result in lasting changes. Furthermore, such changes can occur at multiple locations throughout the cell. Such changes are exhibited through protein expression, structure, and composition.

The short–term acute effects of alcohol, including intoxication, are caused primarily by temporary and reversible changes in specific receptors and the associated molecules. That said, with repeated or chronic alcohol exposure, long–lasting changes occur in receptors and the series of chemical interactions they signal.

Neuroscientists have discovered that these changes in receptors are only one example of many permanent changes in the brain caused by alcohol. They suspect there are changes at many different levels. These would include the genetically directed production of critical proteins as well as physical changes in the structure of the cells on both sides of the synapse. In other words, there are changes in both the signaling and the receiving cell.

It’s these changes that scientists refer to as neuroadaptation. Furthermore, they now believe that neuroadaptation is associated with the development of alcohol tolerance in the individual, or the need to drink more alcohol to achieve the same level of intoxication that the individual is accustomed to and desires. But they also link neuroadaptation with both the symptoms of withdrawal and the cravings that can lead to relapse—even after long periods of abstinence.

Treatments Neuroscience Might Suggest

Scientists are striving to develop medications that target both the acute responses to alcohol and the neuroadaptations that can accompany chronic drinking. These would help by targeting specific receptor types, impacting the series of chemical reactions set off by receptor activation, or through the production of critical protein enzymes which are involved in these processes within cells. Of course, not everyone will respond to these drugs in the same way. After all, different subtypes of alcoholics have different genetically determined traits shaping their response to alcohol—as well as underlying their vulnerability to alcohol problems. As a result, a variety of drugs might be needed to target treatment--according to a person’s individual biology.

Fortunately, treatment techniques which foster coping skills, problem-solving skills, and social support have been shown to play a pivotal role in the successful treatment of the alcoholic as well. Yes, these can help the recovering alcoholic to deal more effectively with stress. As a result, even without medication, the recovering alcoholic may be able to avoid relapse, something which has so longed been a problem for this group of people. As we learn more and more about the brain, it seems we can provide more people with more hope that what were once devastating problems may be more successfully managed, if not eliminated.