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Addiction, Abstinence and Relapse: Why the Drug Epidemic Refuses to Retreat

Written by Ashima Seth and Edited by Amy Huynh

Image by Steve Buissinne from Pixabay

We have all heard media outlets and political personages declare a war on drugs by stating that poor lifestyle choices and lack of willpower plague drug addicts. The truth that few people know is that drug addiction is a chronic relapse disease. A single exposure event to strong drugs such as cocaine, morphine or methamphetamines is enough to cause cravings and long-term dependency that can come back to haunt after decades of sobriety with a cue as minor as the sight of rolled paper. According to the National Institute on Drug Abuse (NIDA), relapse rates in the United States are as high as 40-60% [1]. How do drugs cause such dependence, and why is relapse so common?

To understand how addiction happens, we must first understand the neurobiology involved. The limbic system is the neural circuitry of the brain concerned with instinct, mood, and basic survival-oriented behaviors such as fear, procreation, pleasure, and seeking of food. This system is also closely associated with the reward circuitry of the brain, which has been found to incentivize certain behaviours by the release of dopamine—a neurotransmitter or a chemical used for communication between brain cells—commonly related to pleasure. The reward circuitry and limbic system are both closely connected to a region of the brain called the prefrontal cortex, which is involved in decision-making.

Most drugs have been found to cause addiction by hacking into this reward circuitry and causing either excessive release of certain neurotransmitters (usually dopamine), inhibition of neurotransmitter degradation, or prevention of neurotransmitter communication with other cells by blocking the pathway. As a result of these drugs flooding our reward system with ‘feel-good’ neurotransmitters, the limbic system recognizes drug-seeking behaviour as excessively pleasurable (oftentimes, more so than partaking in food or even sex). This also encourages the prefrontal cortex to make decisions that become more and more geared to seeking out more drugs—resulting in what society refers to as “poor life decisions” [2].

However, this is simply the beginning of what drugs do to the neural circuitry. Eventually, excess drug consumption results in cells becoming less sensitive to these drugs, driving addicts to take greater doses in order to achieve the same level of pleasure as before. This has been shown in several cases to lead to a fatal overdose [3].

Several drug addicts attempt to abstain and remain sober, and while a fair amount do succeed, almost an equal amount fail to do so in the long run. Researchers have found that the answer may lie not in modification of the genome (the complete set of genes in an organism’s cells), but rather in modification of the epigenome, which is an extensive and varied set of chemicals that tell genes what to do. While the genome of an organism is what it receives as a complex amalgamation of its ancestry, the epigenome is more dependent on the organism’s personal experiences and can determine which part of the genome gets expressed and which does not. Research studies found that drugs are actually capable of modifying the epigenome, resulting in a re-calibration of the neural circuitry in a way that recognizes cues associated with the drug long after the drug habit has been abandoned. As a result, when a former addict comes across the drug or a social setting reminiscent of past drug use, relapse occurs [4].

There is a dire need in today’s society to accept and treat substance abuse as a disease and not simply a lifestyle choice, for only then can we work towards eradicating it successfully.

References:

  1. “Treatment And Recovery”. Drugabuse.Gov, 2018, https://www.drugabuse.gov/publications/drugs-brains-behavior-science-addiction/treatment-recovery. Accessed 28 Oct 2018.
  2. Koob, G.F., Volkow, N.D. (2016). Neurobiology of addiction: a neurocircuitry analysis. Lancet Psychiatry, 3(8): 760-773.
  3. Buttner, A. (2011). Review: The neuropathology of drug abuse. Neuropathology and Applied Neurobiology, 37(2): 118-134.
  4. Becker, J.A.J., Le Merrer, J. (2016). Long-Term Transcriptional Consequences of Drug Exposure as Cues to Understand Vulnerability to Relapse: Advances and Perspectives. Journal of Studies on Alcohol and Drugs, 77(5): 692-695.
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