ADC 655 Module 7 Relapse Research Example

Three Doors Back to Use: What Relapse Research Shows About Drugs, Cues and Stress

Student Name

Psychology and Addiction Studies Program, Aspen University

ADC 655: Neurobiology of Addiction

Instructor Name

Month Day, Year

Three Doors Back to Use: What Relapse Research Shows About Drugs, Cues and Stress

After nine weeks at the Colorado Springs residential program these papers follow, Jay, whose words about using to feel normal opened an earlier module, was preparing to go home. He was stable on buprenorphine and determined, but worried: "What's going to set me off?" Jay, Nadia and the program are fictional. This paper reviews what relapse research has found and how it shaped his plan.

Three Triggers in the Laboratory

Shaham et al. (2003) reviewed the reinstatement model of relapse. Animals trained to self-administer a drug undergo extinction, in which drug seeking goes unrewarded until it fades. Researchers then test what revives seeking. Three kinds of trigger have proved reliable across drugs and laboratories. Drug priming, a small dose of the drug itself, reinstates seeking. Cues previously paired with the drug, such as a light or tone, reinstate it. And stressors, such as brief footshock, reinstate it. The authors noted that these triggers correspond to the precipitants of relapse that people describe: a single use, reminders of use and stress. The model has been used to identify brain circuits for each trigger and to screen potential medications.

A Common Pathway

Kalivas and Volkow (2005) reviewed research on the brain basis of drug seeking. They described addiction as a pathology of motivation and choice, in which the value of drugs rises and the value of other rewards falls. Central to their account is a pathway from the prefrontal cortex to the nucleus accumbens that uses glutamate, the brain's main excitatory messenger. Animal studies suggested that activity in this pathway is required for reinstatement by drug, cues and stress alike, making it a possible final common pathway for drug seeking. Repeated drug use alters glutamate signaling in this pathway in ways that may make drug seeking harder to stop once triggered. They suggested that medications targeting glutamate might reduce relapse.

Evidence in People

Sinha et al. (2006) studied people with cocaine dependence in inpatient treatment. Before discharge, participants listened to personalized scripts describing a stressful situation from their own lives, a drug-related situation and a neutral situation, while their craving and stress hormones were measured. After discharge, participants whose stress scripts produced stronger craving and stronger stress hormone responses relapsed sooner and used more cocaine. The study gave human evidence that stress reactivity, measured in the laboratory, predicts relapse, consistent with the animal findings.

Matching Triggers to Strategies

Pain as a Stressor

For Jay, chronic knee pain was both a stressor and a reminder of how his opioid use began. Pain activates stress systems and can produce craving directly, especially in people whose opioid use started with prescriptions. His plan therefore treated pain management as relapse prevention: regular physical therapy, a non-opioid pain plan from his physician and an agreement to tell his prescriber about any flare rather than managing it alone.

Jay's Plan

Jay's plan addressed each trigger. For drug priming, he would continue buprenorphine, which occupies opioid receptors and reduces the effect of other opioids, and he agreed on what to do if he used: call his outpatient counselor the same day rather than conclude he had failed. For cues, he would not visit the friend who had supplied pills, would ask his sister to remove old prescription bottles from his house and would rehearse a response to the pharmacy where he used to fill prescriptions. For stress, which for Jay centered on flares of knee pain and debt, he would use a pain management plan from his physician, keep his physical therapy appointments and meet with a financial counselor. Nadia noted that the most dangerous moments would be when two triggers came together, such as a pain flare during a stressful week.

When Triggers Combine

The laboratory isolates triggers; life combines them. A person may face a stressful argument in a place full of cues, or take a single drink at a party where old friends are using. The convergence of triggers on a common pathway suggests that combinations may be especially dangerous. Relapse prevention plans should therefore identify the situations where triggers are likely to coincide and arrange extra support for them in advance.

Medications and the Glutamate Pathway

Kalivas and Volkow's account of glutamate signaling has encouraged research on medications that act on this system. Some candidates showed promise in animals and early human studies, though none has yet become a standard treatment. The search illustrates how relapse research moves from laboratory findings toward clinical tools, and how slow and uncertain that path can be.

Limits

Animal reinstatement differs from human relapse in important ways. Animals do not choose abstinence, and extinction is not the same as a person's decision to stop. Human studies of predictors, like Sinha and colleagues', are valuable but measure risk in groups rather than certainty for individuals.

Rehearsing the First Week Home

Nadia asked Jay to walk through his first week at home day by day. Monday brought the drive past the pharmacy where he used to fill early prescriptions, a cue. Wednesday brought a physical therapy appointment that always left his knee aching, a stressor tied to pain. Friday brought a card game with a cousin who still used, where a priming offer was likely. For each day they wrote one step: a different route, a call to his sponsor after therapy and a decision to skip the card game for a month, matching the three triggers that Shaham et al. (2003) described.

Conclusion

Shaham and colleagues' review shows that drug priming, cues and stress revive drug seeking in animals, Kalivas and Volkow describe a glutamate pathway through which these triggers may act and Sinha and colleagues show that stress reactivity predicts relapse in people. Jay's plan addresses all three triggers, with particular attention to moments when they coincide.

References

Kalivas, P. W., & Volkow, N. D. (2005). The neural basis of addiction: A pathology of motivation and choice. American Journal of Psychiatry, 162(8), 1403-1413. https://doi.org/10.1176/appi.ajp.162.8.1403

Shaham, Y., Shalev, U., Lu, L., de Wit, H., & Stewart, J. (2003). The reinstatement model of drug relapse: History, methodology and major findings. Psychopharmacology, 168(1-2), 3-20. https://doi.org/10.1007/s00213-002-1224-x

Sinha, R., Garcia, M., Paliwal, P., Kreek, M. J., & Rounsaville, B. J. (2006). Stress-induced cocaine craving and hypothalamic-pituitary-adrenal responses are predictive of cocaine relapse outcomes. Archives of General Psychiatry, 63(3), 324-331. https://doi.org/10.1001/archpsyc.63.3.324