| Course | PAC 110 Addiction Theories |
|---|---|
| Module | Module 2 |
| Paper type | Biological theory evaluation |
| Length | About 1,071 words, 6 pages |
| Format | APA 7 student paper |
| School | Aspen University |
| Program | Psychology and Addiction Studies |
| Updated | October 2026 |
Free sample paper for PAC 110 Module 2
In the Family, Not in the Cards: What Genetic and Brain Research Can and Cannot Tell a Client About His Drinking
Student Name
Psychology and Addiction Studies Program, Aspen University
PAC 110: Addiction Theories
Instructor Name
Month Day, Year
In the Family, Not in the Cards: What Genetic and Brain Research Can and Cannot Tell a Client About His Drinking
Tom is forty-four, an electrician and the father of two teenagers, and he came to Millbrook Counseling Center after his second arrest for driving under the influence. His father drank himself out of three jobs, and his grandfather died of liver disease. In his intake interview Tom said, half joking, that he never had a chance: "It's in the blood." His fear for his own children was not a joke. Tom's comment raises the question this module asks: what do biological and genetic theories actually say about addiction, and what can a social worker responsibly tell a client about them? Like Ray in the first module, Tom is a composite, and Millbrook is invented; every study cited is real.
What Heritability Means
Researchers estimate the role of genes in a condition by comparing relatives who share different amounts of genetic material. In a twin design, the question is whether identical pairs resemble each other more closely on a trait than fraternal pairs do, since the first share almost their entire genome and the second roughly half. An adoption design asks whether adoptees look more like the birth family or the family that raised them. Verhulst et al. (2015) combined the results of twin and adoption studies of alcohol use disorder in a meta-analysis. They estimated the heritability of alcohol use disorder at about half, with shared family environment accounting for a much smaller share and the remainder due to experiences unique to each person. The estimate was similar for men and women.
Heritability is easily misunderstood. It estimates the share of differences between people in a given population that tracks differences in their genes. A heritability of one half says nothing about what portion of Tom's own drinking came from his genes, and it carries no promise about how his life will turn out. Heritability can differ across environments, and no single gene determines addiction; many genes each contribute small effects.
The Brain in Addiction
Volkow et al. (2016) summarized decades of research into a model of addiction as a cycle of three stages, each tied to particular brain circuits. In the binge and intoxication stage, drugs produce large surges of dopamine in the brain's reward system, centered in the basal ganglia, and cues linked to use gain power to trigger craving. In the withdrawal and negative affect stage, the reward system becomes less responsive and stress systems in the extended amygdala become more active, so that people feel irritable, anxious and low when not using. In the preoccupation and anticipation stage, the prefrontal regions that support planning and self-control function less effectively, making it harder to resist the urge to use. The authors argued that these changes explain why addiction persists despite harm and why relapse is common, and they defended the brain disease model while noting that not everyone who uses drugs becomes addicted.
A Different Reading of the Same Changes
Lewis (2018) accepted that addiction involves real brain changes but disputed calling them disease. He argued that the brain changes in response to every strong and repeated experience, and that the changes seen in addiction resemble those that occur when people learn to pursue any highly rewarding goal, including falling in love. In his view, addiction is a form of deep learning that develops in a person's particular circumstances, often in response to stress or isolation, and many people stop without treatment as their circumstances change. Lewis suggested that calling addiction a disease may encourage passivity and that framing it as learning points toward recovery as further development.
| Question | What biological research shows | What it leaves open |
|---|---|---|
| Does addiction run in families? | Yes; heritability around half | Which genes, and how they interact with environment |
| Is addiction inevitable for people with family history? | No; many relatives never develop it | Why some with high risk do not |
| Does use change the brain? | Yes; reward, stress and control circuits change | Whether changes are disease or learning |
| Can the brain recover? | Many changes partly reverse with abstinence | How long, and for whom |
| Do medications help? | For some substances, yes | Why responses differ so much |
| Does biology explain recovery without treatment? | Only partly | The role of life changes and meaning |
Strengths and Limits for Practice
The biological theories have real strengths. They explain why addiction clusters in families, why craving and relapse persist and why medications help some people. They can relieve shame by showing that people did not simply choose their condition. But they have limits. They say little about why most people with a family history never develop addiction, why many recover without treatment or why addiction rates differ so much across communities and eras. They can also be heard as fate, which may discourage clients from trying. A client who believes his genes decided the matter may see little point in learning new ways to handle stress, rebuilding relationships or changing where he spends his evenings, even though those are the changes most likely to help. Biological explanations also say little about the social conditions, such as unemployment, isolation and easy access to alcohol, that shaped Tom's drinking and his father's before him.
Talking With Tom
For Tom, the research offers a more accurate message than the one he arrived with, and a more hopeful one. It also gives him something to do with his worry about his son and daughter, who are fifteen and seventeen and who have watched him struggle. His family history raises his risk; it does not seal his fate. His brain has changed through years of heavy drinking, which helps explain his craving and his trouble stopping, and many of those changes ease with time sober. A social worker might put it this way: Tom inherited a vulnerability, not a sentence. For his children, the same research suggests that knowing their family history, delaying first use and talking openly about drinking are reasonable protective steps.
Conclusion
Genetic studies show that addiction is substantially heritable, and brain research shows how use changes the circuits of reward, stress and self-control. Verhulst and colleagues, Volkow and colleagues and Lewis together show both the power and the limits of these findings. For practice, biology explains risk and persistence but not destiny, and how a helper describes it can strengthen or weaken a client's belief that change is possible.
References
Lewis, M. (2018). Brain change in addiction as learning, not disease. New England Journal of Medicine, 379(16), 1551-1560. https://doi.org/10.1056/NEJMra1602872
Verhulst, B., Neale, M. C., & Kendler, K. S. (2015). The heritability of alcohol use disorders: A meta-analysis of twin and adoption studies. Psychological Medicine, 45(5), 1061-1072. https://doi.org/10.1017/S0033291714002165
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 PAC 110 Module 2 assignment instructions
For the second module, PAC 110 turns to the body: an assignment here commonly wants the biological and genetic theories explained clearly and then judged, not simply repeated. The Module 2 prompt in your Aspen course is the authority; the client here is invented. Explain what heritability means and what it does not mean. Describe the brain systems involved, using a current review rather than a textbook summary. Present at least one serious critique of the biological account. Separate what the evidence supports from what it leaves open. Apply the theory to a client or case and show how it would shape what you say. Cite every source in APA 7 and use precise terms, such as risk rather than cause.
How the PAC 110 Module 2 example is put together
Tom's question, whether he was born to drink, opens the paper. Verhulst, Neale and Kendler's Psychological Medicine meta-analysis supplies the heritability estimate of about half and the small role of shared environment. Volkow, Koob and McLellan's New England Journal of Medicine review explains the binge and intoxication stage, the withdrawal and negative affect stage and the preoccupation and anticipation stage, each with its circuits. Lewis's article in the same journal argues that these changes are what learning looks like in a brain under strong motivation. A six-row table lists what biology explains and what it does not. The final sections show how to talk with Tom about risk without implying fate.
Reading the PAC 110 Module 2 grading rubric
Biological theory papers earn credit for accurate explanation, for correct use of terms like heritability and for critical judgment. This example defines heritability as a population estimate and explains why half heritable does not mean half of Tom's drinking was genetic. It presents the brain disease account in its strongest current form and then a serious alternative from a neuroscientist, so the critique is not a strawman. The table makes clear what the evidence settles and what remains open. The section on talking with Tom applies theory to practice, which the course requires, and the paper's language, risk rather than destiny, shows care with how biological findings reach clients.
Common PAC 110 Module 2 mistakes, and how to avoid them
Students often write that addiction is genetic or that people are born addicts, which misstates the research. Heritability describes variation in a population, not the share of one person's behavior caused by genes. Another weakness is describing brain changes without saying whether they cause addiction or follow from use. Include a critique, such as Lewis's learning account, and evaluate it rather than dismissing it. Avoid detailed neuroanatomy that does not serve the argument. Show how the theory would shape practice, including how you would explain inherited risk to a client. Keep claims tied to sources and avoid popular phrases like hijacked brain unless you explain what they mean.
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 PAC 110 and Psychology and Addiction Studies sample papers
- PAC 110 Module 1: Models of Addiction Across History
- PAC 110 Module 3: Learning and Behavioral Theories
- PAC 110 Module 4: Cognitive and Psychodynamic Approaches
- PAC 110 Module 5: Social and Environmental Theories
- PAC 110 Module 6: Theories of Change and Motivation
- PAC 110 Module 7: Systems of Psychotherapy in Addiction Practice
- PAC 110 Module 8: Integrating Theory Into Personal Practice
- PAC 230 Module 8: Reducing Adverse Health Outcomes in Families
- PAC 310 Module 5: Boundaries and Dual Relationships
- PAC 201 Module 6: Emotional and Social Development
- PAC 415 Module 8: Reflection on Practical Wisdom
PAC 110 Module 2 questions, answered
What does PAC 110 Module 2 usually ask for?
Aspen's PAC 110 covers biological and genetic theories in this module, so explaining them, weighing their evidence and applying them to practice is typical. Check your Module 2 prompt.
Is alcoholism genetic?
Partly. Verhulst, Neale and Kendler's meta-analysis estimated that about half of the variation in alcohol use disorder in a population is heritable; environment accounts for the rest.
What are the three stages of addiction in the brain?
Volkow, Koob and McLellan describe binge and intoxication, withdrawal and negative affect, and preoccupation and anticipation, each linked to different brain circuits.
Where can I find a free PAC 110 Module 2 sample paper?
This page shows it in full: genetic and brain theories of addiction weighed through one client's family history, with a table of what biology explains.
Is addiction a disease or learning?
Researchers disagree. Volkow and colleagues defend the brain disease model, while Lewis argues the same brain changes reflect deep learning.