A PSY 108 Module 4 position paper on nature versus nurture in depression, covering heritability from twin research, stressful life events, gene-environment correlation, a failed candidate gene replication and a defended position, in APA style. Searches like "psy 108 module 4 assignment", "psy108 module 4 nature versus nurture position paper" and "psy 108 module 4 example" land here.
The PSY 108 Module 4 example, in full
Not Nature or Nurture but Nature Through Nurture: A Position on the Causes of Depression
[Student Name]
Southern New Hampshire University
PSY 108: Introduction to Psychology
Module Four Position Paper
[Instructor Name]
[Date]
Not Nature or Nurture but Nature Through Nurture: A Position on the Causes of Depression
Introduction and Position
Depression is one of the most common psychological disorders, and people often ask whether it is inherited or caused by life experiences. My position is that the question, posed as a choice, has no good answer. Evidence shows that genes and environment both contribute substantially to depression, and that they do not add together like separate ingredients. Genetic differences shape how people respond to and even select their environments, and environments shape whether genetic risk is expressed. The more useful question is how the two work through each other.
Evidence for Nature
The strongest evidence for genetic influence comes from twin studies. Identical twins share essentially all their genes, while fraternal twins share about half on average, so if identical twins are more alike in a trait than fraternal twins, genetic influence is implied. Sullivan et al. (2000) combined twin studies of major depression and estimated its heritability at about 37 percent. Heritability refers to the share of differences among people in a population that is associated with genetic differences; it does not mean that 37 percent of any one person's depression is genetic.
Depression is not unusual in this respect. Polderman et al. (2015) analyzed twin studies covering thousands of human traits from five decades of research and found an average heritability of 49 percent. Plomin et al. (2016) listed among the most replicated findings in behavioral genetics that all psychological traits show significant genetic influence, that no trait is entirely heritable and that the heritability of traits reflects many genes, each of small effect. Depression fits all three findings.
What Heritability Does Not Mean
Heritability figures are easy to misread. A heritability of 37 percent does not mean that depression is 37 percent inevitable for someone with an affected parent, and it does not mean that the environment matters little. Heritability is a population statistic that describes where differences among people come from under the conditions studied. If environments changed, for example if stressful life events became much rarer, the figure could change too. A trait can also be highly heritable and still respond strongly to the environment: height is very heritable, yet average height rose across the twentieth century as nutrition improved. Genetic influence describes a tendency, not a fixed outcome.
Evidence for Nurture
The same twin research is also strong evidence for environmental influence. If heritability is about 37 percent, then most of the variation in depression is associated with something other than genes. Sullivan et al. (2000) found that this environmental influence came mainly from experiences unique to each individual, rather than from the family environment that siblings share.
Stressful life events are among the best-studied of those experiences. Kendler et al. (1999) followed twins and found a substantial causal relationship between stressful events, such as a death in the family, divorce or job loss, and the onset of major depression. Using the twin design, they could compare twins who experienced an event with co-twins who did not, which helped separate the effect of the event from the effect of shared genes and family background. Life events do not merely coincide with depression; for many people, they help set it off.
How Nature and Nurture Become Entangled
The same study also showed why the two cannot be neatly separated. Kendler et al. (1999) estimated that about a third of the association between stressful events and depression was not causal, because people who were predisposed to depression were also more likely to experience certain stressful events. This is gene-environment correlation: genetic differences, for example in temperament, influence the environments people encounter and create, such as conflict in relationships. In that case, part of what looks like nurture is partly nature expressed through the environment.
The reverse also occurs. Whether genetic risk leads to depression may depend on the environment. A person with higher genetic risk who has strong social support and few major stressors may never become depressed, while the same risk combined with repeated losses may lead to illness. This is why I describe depression as nature working through nurture.
The Strongest Counterargument
The most influential challenge to this view came from a claim that a single gene determined how people respond to stress. Caspi et al. (2003) reported that people carrying a particular version of a serotonin transporter gene variant were more likely to become depressed after stressful life events than people with other versions. The finding was widely taught as proof that one gene moderates the effect of the environment, and it seemed to offer a simple answer to the nature versus nurture question.
Larger studies did not support it. Border et al. (2019) tested this and other widely studied candidate genes for depression, including their interactions with environmental factors, in samples of up to several hundred thousand people and found no support for the historical candidate gene hypotheses. The result fits the broader finding that genetic influence on depression is spread across many variants of small effect rather than concentrated in one. The failed replication strengthens my position: there is no single switch in nature that decides how nurture affects us.
Implications for Prevention
If depression develops through the interplay of genetic tendency and life experience, prevention does not have to wait for genetic tests that can identify who is at risk; such tests do not exist for depression in any useful form. The environmental side offers practical targets now. Stressful events cannot always be prevented, but their impact can be reduced through social support, early help after losses and skills for managing difficult emotions. Family history remains useful information, since it signals higher risk and a reason to watch for early signs, but it should prompt support rather than resignation.
Conclusion
Depression has substantial genetic influence and substantial environmental influence, and the two are intertwined through gene-environment correlation and interaction. Asking which one causes depression forces a false choice. Recognizing this has practical value. It argues against fatalism, since genetic risk is not destiny, and against blame, since depression is not simply a failure to cope with life. It also supports the approach psychology already takes in practice: reducing environmental stressors, building support and treating depression effectively regardless of where the risk began.
References
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
Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between stressful life events and the onset of major depression. American Journal of Psychiatry, 156(6), 837-841. https://doi.org/10.1176/ajp.156.6.837
Plomin, R., DeFries, J. C., Knopik, V. S., & Neiderhiser, J. M. (2016). Top 10 replicated findings from behavioral genetics. Perspectives on Psychological Science, 11(1), 3-23. https://doi.org/10.1177/1745691615617439
Polderman, T. J. C., Benyamin, B., de Leeuw, C. A., Sullivan, P. F., van Bochoven, A., Visscher, P. M., & Posthuma, D. (2015). Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature Genetics, 47(7), 702-709. https://doi.org/10.1038/ng.3285
Sullivan, P. F., Neale, M. C., & Kendler, K. S. (2000). Genetic epidemiology of major depression: Review and meta-analysis. American Journal of Psychiatry, 157(10), 1552-1562. https://doi.org/10.1176/appi.ajp.157.10.1552
How this PSY 108 Module 4 example is structured
The paper states its position in the introduction, then presents evidence for genetic influence, evidence for environmental influence and evidence that the two interact. It addresses the strongest counterargument, the appeal of single-gene explanations, and concludes by restating the position and what it means for how people think about depression.
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PSY 108 Module 4 questions, answered
What does the PSY 108 nature versus nurture paper require?
Students are usually asked to choose a behavior or trait, examine evidence for genetic and environmental influences on it and take a position on how nature and nurture contribute, supported by research and written in APA style.
What does heritability mean?
Heritability is the proportion of differences among people in a trait, within a particular population, that can be attributed to genetic differences. It does not describe how much of one person's trait is genetic, and it can change when environments change.
Is there a gene for depression?
No single gene causes depression. Genetic influence appears to come from many genetic variants, each with a very small effect, and large studies have not confirmed earlier claims that particular single genes strongly shape risk.