PS440 Unit 2 Models of Psychopathology Paper Example

A Gene That Did Not Replicate and a Grief That Did Not Lift: A PS440 Unit 2 Models of Psychopathology Paper

[Student Name]

Purdue University Global

PS440: Psychopathology

Unit 2 Models of Psychopathology Paper

[Instructor Name]

[Date]

The guest, her family and the crisis center are composite; the models and studies cited are real.

The Case

Kelsey, 26, works nights as a nursing assistant in a long-term care home in Rapid City, South Dakota. She came to our 24-hour crisis care center on a Sunday night after telling a coworker that nothing seemed worth getting up for anymore. She had no plan and agreed to a short stay.

Her history explains why the staff took her seriously. Four months earlier her mother died of breast cancer after a year in which Kelsey cared for her at home between night shifts. Since the funeral Kelsey has slept poorly, lost twelve pounds, stopped answering friends and felt, in her words, like a burden to everyone. She had one previous depressive episode at 17, after her parents' divorce, which lifted with counseling. Her mother had been treated for depression for years, and her maternal grandfather died by suicide. Her boyfriend moved to Sioux Falls for work in the spring.

The crisis center's counselor diagnosed a recurrent major depressive episode. This paper uses several models to explain why Kelsey became depressed now, and what each model contributes and leaves out.

The Diathesis-Stress Framework

Diathesis-stress models hold that disorder results from the combination of a vulnerability, the diathesis, and a stressful experience that activates it. Monroe and Simons (1991) reviewed how this idea had been used in depression research and argued that it needed more precision. They urged researchers to define the diathesis clearly, to distinguish severe life events from minor hassles and to recognize that people can help generate some of their own stress. They also discussed evidence that later episodes of depression may need less stress to begin than first episodes.

Kelsey's case fits the framework at several points. Her family history suggests a vulnerability. Her mother's illness and death, combined with exhausting caregiving and her boyfriend's move, are severe stressors. Her first episode followed a major loss, and her second followed another. The framework also invites a question it cannot answer alone: what exactly is Kelsey's diathesis?

The Biological Diathesis and a Cautionary Tale

The most famous attempt to name a specific diathesis came from Caspi et al. (2003). Following a birth cohort in New Zealand, they reported that stressful life events predicted later depression more strongly in participants carrying the short form of a serotonin transporter promoter variant than in those homozygous for the long form. The finding was published in Science, cited thousands of times and taught as a model of gene-environment interaction.

It did not hold up. Border et al. (2019) tested the most studied candidate genes for depression, including this serotonin transporter variant, in samples far larger than earlier studies. They found no support for any of the candidate genes, alone or in interaction with stress. Their conclusion was that the early findings were most likely false positives produced by small samples.

The serotonin transporter story taught a generation of students how genes and stress interact, and then taught them how a finding can fail.

That does not mean genes are irrelevant. Depression clearly runs in families, and twin studies attribute a moderate share of the risk to genetic factors. But the inherited part of the risk appears to be spread thinly across a very large number of genes, each nudging risk by a tiny amount, rather than from one variant a clinician could test. For Kelsey, her family history is the best available measure of her biological vulnerability, and it tells us nothing about a single gene.

A Cognitive Diathesis

Beck (2008) described how his cognitive model of depression developed. Its core claim is that people vulnerable to depression hold negative beliefs, or schemas, about themselves, often formed early, which become active under stress and bias how they interpret events. Once active, the schemas produce quick, unexamined thoughts that she is worthless, that others will leave and that nothing will improve, and those thoughts deepen low mood. Beck also connected the model to research on how the brain processes negative information.

Kelsey's language points to such schemas. She describes herself as a burden and says that she should have noticed her mother's cancer sooner, though she was not her mother's doctor. At 17 she said similar things about her parents' divorce. The cognitive model suggests that a belief formed in childhood, that she is responsible for keeping her family together and fails when it breaks, was reactivated by her mother's death. It also suggests a treatment target: those beliefs can be identified and tested in therapy.

Social Circumstances

The models above focus on the individual. Kelsey's social situation matters just as much. She lost her main source of support, her mother, and her secondary one, her boyfriend, within the same few months. Night shifts disrupt sleep and isolate her from friends on regular schedules. Nursing assistants are paid modestly, and Kelsey took unpaid leave to care for her mother, which left her in debt. These conditions are not just background. They are part of why her stress was so severe and why she had so few resources to manage it.

Her coworkers noticed changes before she did. They saw her stop eating lunch, take extra shifts to avoid going home and cry in the supply room. Workplaces like hers are often where depression is first visible, and they rarely have a way to respond.

What Each Model Contributes

Taken together, the models give a fuller explanation than any one of them. The diathesis-stress framework organizes the case: vulnerability plus severe stress. Family history and the genetic research suggest a real but diffuse biological vulnerability, and the failed candidate gene research warns against claiming more precision than the science allows. The cognitive model identifies a psychological vulnerability with a clear treatment target. Social circumstances explain the size of the stress and the lack of buffers.

The models also point to different parts of treatment. Cognitive therapy can address her beliefs about being a burden. Medication may help given her recurrent episodes and family history. Practical help, such as a change from night shifts and a grief support group, addresses the social side.

Conclusion

Kelsey's second depression is best explained by a combination of family vulnerability, a negative self-schema from adolescence and a year of loss and exhaustion. The diathesis-stress model frames that combination, and the story of the serotonin transporter gene is a reminder that the biological part of the explanation should be stated with care. No single model would have explained why she arrived at our door on that Sunday night.

References

Beck, A. T. (2008). The evolution of the cognitive model of depression and its neurobiological correlates. American Journal of Psychiatry, 165(8), 969-977. https://doi.org/10.1176/appi.ajp.2008.08050721

Border, R., Johnson, E. C., Evans, L. M., Smolen, A., Berley, N., Sullivan, P. F., & Keller, M. C. (2019). No support for historical candidate gene or candidate gene-by-interaction hypotheses for major depression across multiple large samples. American Journal of Psychiatry, 176(5), 376-387. https://doi.org/10.1176/appi.ajp.2018.18070881

Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington, H., McClay, J., Mill, J., Martin, J., Braithwaite, A., & Poulton, R. (2003). Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene. Science, 301(5631), 386-389. https://doi.org/10.1126/science.1083968

Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress theories in the context of life stress research: Implications for the depressive disorders. Psychological Bulletin, 110(3), 406-425. https://doi.org/10.1037/0033-2909.110.3.406