America is engulfed in an opioid epidemic. Whether this is depicted through the tens of thousands of lives claimed by the number of drug overdoses each year, the unprecedentedly high and increasing rates of opiate abuse, or the broadening demographic profile of the addict, it is clear that the current issue is one that requires serious attention. As informed by the negative attitudes toward drug addiction that have prevailed since the War on Drugs was declared, it is hypothesized that much of the contemporary predicament is a result of this misinformation that did not resolve, but exacerbated the drug crisis. Despite the concurrent emergence of evidence asserting that addiction is a disease, instead, the idea that drug addiction is a failure prevails.
As with many brain diseases, drug addiction displays both pathological alterations in the transmission of signals within the neural circuitries and the morphological defects associated with non-random regions of the brain. The alteration that is observed during opioid tolerance is the desensitization of mu opioid receptors to dopamine, resulting in the need of increased dosage of opiates to achieve the same high. During opioid dependence, key changes that are seen in the locus ceruleus and the mesolimbic reward system increase both the likelihood of an overdose event and withdrawal when an exogenous opioid is present or absent, respectively. There are two models that describe additional changes that occur during the transition from frequent abuse to addiction: (1) the “Changed Set Point Model” and (2) the “Cognitive Deficits Model.” All three variants of the “Changed Set Point Model” portray a shift in the physiological set points of dopamine and glutamate levels in the reward system and regions that control it. The “Cognitive Deficits Model” theorizes that the modifications localized to the prefrontal cortex are responsible for the ultimate transition.
Once the abuser is thrust into the addiction cycle, additional changes in the neural networks are observed. These changes are seen in each of the three phases: (1) Binge and Intoxication, (2) Withdrawal and Negative Affect, and (3) Preoccupation and Anticipation. In the first phase, a process called drug-induced neuroplasticity occurs, resulting in the amplification of signals originating from dopaminergic neurons. Next, during Withdrawal and Negative Affect phase, among other changes, the amygdala is shown to be re-wired in such a way that the addict is more sensitive to stress. And finally in the last phase, the changes that occur, secondary to processes similar to drug-induced, are indicated in the prefrontal cortex.
The current FDA-approved medication-assisted therapies include methadone, buprenorphine, and naltrexone. The single outstanding abstinence-based treatment is the 12-step program. In the evaluation of medical and non-medical interventions the relative efficacies were measured using the metrics: (1) rates of abstinence achievement, (2) rates of opioid use, and (3) retention in treatment. Individually, all therapies show moderate success when measured against each metric, which further validates the brain disease model for addiction, and also indicates that the future direction of addressing the opioid epidemic should point at combination therapies. What is most imperative now is for there to be more widespread recognition of the brain disease model for addiction.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/16772 |
| Date | 17 June 2016 |
| Creators | Chang, Kitae |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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