Without understanding the biological reason why, experts in drug and alcohol treatment have long understood that individuals in recovery should steer clear of the people and places that surrounded them during the period of time when they were active drug users. Scientists at the University of Cambridge are now starting to explain at least one mechanism in the brain that would explain why the people and places connected with past drug use could instigate a relapse. Researchers working at the Behavioral and Clinical Neuroscience Institute believe at least part of the answer lies in the amygdala, which neuroscientists know is the area in the brain responsible for processing the emotional aspects of memory involved in drug cravings.
Relapse Can Be Avoided Since Memory Is Not Concrete
Brain researchers have come to learn that memory can easily be manipulated with the right knowledge. In the past, they believed that memory was fixed, much like the words in a book. The current understanding, however, is that memory may be more akin to a computer document. It can be saved and remembered for future reference but also changed or deleted altogether.
It is at the point of recall that University of Cambridge researchers feel that memory is the most vulnerable to change. They believe the knowledge moves from an invariable to a variable state during the recollection process. The hope, therefore, is that the link between the external cue (the person or place linked with drug use) and the knee-jerk reaction of craving the drug can be undone at the moment of memory recall through targeted prescription drug intervention. In essence, researchers are attempting to render the external cues that trigger relapse powerless to make addicts crave their past drug of choice.
How Close Is Science to Controlling the Cravings That Lead to Relapse?
In a recent animal study, scientists paired the cue of a light with ingesting addictive drugs, until just seeing the light was enough to trigger the animals to seek out the substance. Then animals were given propranolol while being exposed to the light cue, and after only a single treatment, the animals no longer sought out the drug. This is believed to work because propranolol affects the same brain receptors that are activated in emotional memories and assist in creating new ones. Essentially, the propranolol ends up blocking the old emotional association and stops the animal from craving the drug in reaction to a particular environmental cue.
Researchers believe human trials with propranolol for alcohol recovery may start within two years. Since propranolol is already approved for human consumption, scientists believe it has a high probability of eventually being used in alcohol treatment to avoid relapses.
How do you think a pill that could impede environmental triggers for relapse would change the face of alcohol recovery? Your thoughts are welcome below.