| Course | ADC 655 Neurobiology of Addiction |
|---|---|
| Module | Module 8 |
| Paper type | Genetics and critical appraisal paper |
| Length | About 1,058 words, 6 pages |
| Format | APA 7 student paper |
| School | Aspen University |
| Program | Psychology and Addiction Studies |
| Updated | October 2026 |
Free sample paper for ADC 655 Module 8
Genes, Brains and Choices: What Neurobiology Means and Does Not Mean for Treatment
Student Name
Psychology and Addiction Studies Program, Aspen University
ADC 655: Neurobiology of Addiction
Instructor Name
Month Day, Year
Genes, Brains and Choices: What Neurobiology Means and Does Not Mean for Treatment
For her final session with the psychoeducation group at the Colorado Springs program these papers have followed, Nadia wanted to answer the question that had run underneath all the others: if addiction is in the brain and the genes, what is left for a person to do? Nadia, the program and its clients are fictional. This paper reviews the genetic evidence and the debate about the brain disease model to prepare her answer.
What Genetic Research Has Found
Agrawal et al. (2012) reviewed genetic research on addiction from a translational perspective. Twin and family studies consistently show that addiction risk is substantially heritable, with estimates for different substances ranging roughly from a third to more than half of the variation in risk. Much of this genetic risk is shared across substances, and some is shared with related traits such as impulsivity. Yet searches for specific genes have found relatively few with robust effects. The clearest examples involve genes for alcohol-metabolizing enzymes, whose variants make drinking unpleasant for some people and protect them, and nicotine receptor genes linked to heavy smoking. Most genetic risk appears to come from many genes, each with a very small effect, interacting with environment. The authors emphasized that genetic findings are not yet useful for predicting individual risk or choosing treatment, though they may become so.
A Critique of the Brain Disease Model
Hall et al. (2015) asked whether the brain disease model of addiction is supported by evidence and whether it has delivered on its promises. They acknowledged that drug use changes the brain, but argued that much of the evidence comes from animals given high doses or from imaging studies that compare people at one point in time, which cannot establish whether brain differences caused addiction or resulted from it. They noted that most people with addiction recover, often without treatment, which they found hard to reconcile with a view of addiction as a chronic brain disease. They also argued that the model had not produced the new treatments its advocates predicted and that evidence on whether it reduces stigma was mixed, since describing addiction as a brain disease may reduce blame but increase pessimism about recovery.
A Defense
Volkow et al. (2016) argued that neuroscience had transformed the understanding of addiction, identifying the brain changes that underlie the addiction cycle and explaining why recovery is difficult. They pointed to treatments, including medications for opioid and alcohol use disorders, whose use the model supports, and argued that the model justifies providing treatment rather than punishment. They emphasized that brain changes are not permanent and that the model is compatible with recovery and with personal responsibility for engaging in treatment.
What Neurobiology Implies
| Claim | Supported | Not supported |
|---|---|---|
| Drug use changes reward, stress and control systems | Yes, across animal and human research | That the changes are permanent |
| Genes influence risk | Yes, substantially | That genes determine outcomes or that genetic tests can predict individuals |
| Craving and relapse have biological bases | Yes | That clients have no control over their behavior |
| Medications can help | Yes, for some substances | That medication alone is sufficient |
| Treatment rather than punishment is justified | Supported by evidence on outcomes | That neuroscience settles questions of responsibility |
Genes, Environment and Recovery
Genetic risk interacts with environment. A person with high genetic risk who grows up in a supportive environment and avoids early heavy use may never develop addiction, while a person with lower risk exposed to trauma and easy access may. For people already in treatment, genetic risk does not determine recovery. It may help explain why some found drugs especially rewarding or hard to stop, which can reduce self-blame, but treatment response depends on many factors beyond genes.
Nadia's Closing Message
Nadia planned a message that held both views. She would tell the group that their brains had changed in real ways: the wanting system had grown louder, the stress system had become touchier and the brakes had weakened, and genes had made some of them more vulnerable than others. None of that was their fault, and none of it was the whole story. Most people with addiction recover. Brains change again with time, treatment, medication where it helps, new routines and people who matter. Knowing how the brain works does not take away choices; it shows which choices help most: avoiding cues early, managing stress, staying on medication, getting help after a slip.
Neuroscience and Stigma
Whether neuroscience reduces stigma depends on how it is used. Explaining that craving has biological roots can relieve shame, as Nadia saw with Marcus earlier in the course. But describing people as having broken brains can increase fear and pessimism, both among clients and among those around them. The most helpful framing combines biology with recovery: the brain adapted to drugs, and it can adapt again.
Looking Back Across ADC 655
Eight modules have traveled from reward circuits and drug actions through the addiction cycle, animal models, imaging, stress and relapse to genetics. Its consistent lesson is that neurobiology explains why addiction is hard to overcome and points to useful treatments, but it does not reduce people to their brains. Good practice uses neuroscience to reduce shame and guide treatment while keeping clients' agency and recovery at the center.
Questions for Further Study
Several questions remain open for counselors who want to keep reading. How far do genetic findings help predict who will respond to which treatment? Agrawal et al. (2012) noted that most identified genetic effects are small and that their combined predictive value is still limited. Can the brain disease model reduce stigma without making people feel their condition is permanent? Hall et al. (2015) argued that it can backfire. And how can neuroscience education be built into treatment so that it supports a client's sense of agency rather than replacing it? Each question links research to everyday practice.
Conclusion
Agrawal and colleagues show that addiction risk is substantially heritable but spread across many genes of small effect. Hall, Carter and Forlini question how far the brain disease model is supported and whether it has delivered, while Volkow, Koob and McLellan defend its contributions. Weighing both, Nadia's message to her group affirms that the brain changes in addiction are real and that recovery, through choices the science helps inform, is common.
References
Agrawal, A., Verweij, K. J. H., Gillespie, N. A., Heath, A. C., Lessov-Schlaggar, C. N., Martin, N. G., Nelson, E. C., Slutske, W. S., Whitfield, J. B., & Lynskey, M. T. (2012). The genetics of addiction: A translational perspective. Translational Psychiatry, 2(7), Article e140. https://doi.org/10.1038/tp.2012.54
Hall, W., Carter, A., & Forlini, C. (2015). The brain disease model of addiction: Is it supported by the evidence and has it delivered on its promises? The Lancet Psychiatry, 2(1), 105-110. https://doi.org/10.1016/S2215-0366(14)00126-6
Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374(4), 363-371. https://doi.org/10.1056/NEJMra1511480
Reading the ADC 655 Module 8 assignment instructions
The final module of ADC 655 usually asks for a paper on genetic approaches and on implications of neurobiology for treatment. Follow the Module 8 instructions in your Aspen course; the counselor and clients are invented. Review genetic findings, including what is and is not known about specific genes. Present the brain disease model with its strongest critique and defense. Weigh implications for treatment, policy and stigma, using a table if it helps. Draw together themes from the course. Craft a message for clients that is accurate and useful. Cite every source in APA 7, and present the debate fairly rather than taking a side without argument. Note where the two sides agree, since common ground is often the most useful part for practice.
How this ADC 655 Module 8 example is built
Nadia, the composite counselor, prepares a closing session for a group that has learned about reward circuits, the addiction cycle and relapse. Agrawal and colleagues' Translational Psychiatry review describes heritability and the few genes firmly linked to addiction, such as alcohol-metabolizing variants. Hall, Carter and Forlini's Lancet Psychiatry article argues that the brain disease model overstates evidence and has not delivered promised treatments. Volkow, Koob and McLellan's review argues that neurobiology has improved understanding and treatment. A five-row table weighs implications. Nadia's closing message holds both views: the brain changes are real, and so is the capacity to change. A reflection draws the course's modules together.
Reading the ADC 655 Module 8 grading rubric
Closing papers earn credit for accurate summary of genetic evidence, fair treatment of debate and a synthesis that serves practice. This example reports what genetic research has and has not found, avoiding claims of addiction genes and explaining why genetic tests cannot yet guide treatment. It presents the critique and defense of the brain disease model in their authors' terms. The implications table distinguishes what neurobiology supports from what it does not, which keeps the conclusion within the evidence. The client message is honest and hopeful without overclaiming. The paper draws on earlier modules to show integration. It notes where critics and defenders agree, which keeps the debate from becoming a false choice.
Common ADC 655 Module 8 mistakes, and how to avoid them
Genetics papers often overstate what genes determine. Explain heritability and the small effects of individual genes, and how genes interact with environment. Present debates fairly; the brain disease model has strong defenders and serious critics, and both deserve their best arguments. Weigh implications for stigma carefully, since evidence suggests disease framing can reduce blame while increasing pessimism. Bring the course together rather than adding new topics. Write a message for clients that you could actually say, and test it on a colleague before using it. Avoid messages that suggest clients are helpless or that their brains are broken beyond repair.
Write yours, or have the desk draft it
This paper is an original model document written by our desk, not a submitted student paper and not an official Aspen University document. Read it for the moves, then write your own to the instructions in your classroom. If you want one built to your exact prompt and rubric, the first custom sample is free and arrives in 24 to 48 hours.
More ADC 655 and Psychology and Addiction Studies sample papers
- ADC 655 Module 1: The Brain's Reward System
- ADC 655 Module 2: How Drugs Act on the Brain
- ADC 655 Module 3: The Stages of the Addiction Cycle
- ADC 655 Module 4: Animal Models of Addiction
- ADC 655 Module 5: Neuroimaging in Addiction
- ADC 655 Module 6: Stress, Withdrawal and Craving
- ADC 655 Module 7: Relapse Research
- PAC 320 Module 3: Assessment Tools
- PSY 620 Module 6: Collaboration With Families and Schools
- ADC 515 Module 8: Prevention and Treatment Targeting Implicit Cognition
- PAC 330 Module 2: Alcohol
ADC 655 Module 8 questions, answered
What does ADC 655 Module 8 usually ask for?
Aspen's ADC 655 ends with genetics and implications for treatment in this module, so a paper on genetic findings and a critical look at what neurobiology means for practice is typical. Consult your Module 8 prompt.
Is there an addiction gene?
No single gene; Agrawal and colleagues describe addiction risk as substantially heritable but spread across many genes of small effect, with only a few firmly identified.
Is addiction a brain disease?
The question is debated: Volkow, Koob and McLellan defend the brain disease model, while Hall, Carter and Forlini argue it overstates the evidence and has not delivered promised benefits.
Where can I find a free ADC 655 Module 8 sample paper?
This page holds the full paper: genetic findings, the brain disease model debate, a table of implications and a closing message for clients.
Does the brain disease model reduce stigma?
Evidence is mixed; disease framing may reduce blame while increasing pessimism about recovery, as critics including Hall, Carter and Forlini note.