PSYCH 634 Week 6 Biology of Psychological Disorders Example

"Is It a Chemical Imbalance?" Genes, Inflammation, Sleep and the Serotonin Debate in One Patient's Depression

[Student Name]

University of Phoenix

PSYCH/634: Biological Basis of Behavior

Week 6 Assignment

[Instructor Name]

[Date]

The patient, her history and the sleep center are composites written for a model paper; research findings come from the sources listed.

Psychological disorders arise from interactions among genes, brains, bodies and lives. Biology contributes to every disorder, but rarely in the simple form popular explanations suggest. This final paper examines what biology can explain about one patient's depression.

The Patient

Teresa Vigil is thirty-nine and teaches fifth grade in Tucson. A year ago she began waking at three or four in the morning, unable to return to sleep. She came to our sleep center for evaluation; her study showed no apnea but fragmented sleep and early awakening. Over the following months she lost interest in activities she enjoyed, felt worthless and exhausted and struggled to plan lessons. Her physician diagnosed major depression and prescribed an antidepressant, and she began therapy. At a follow-up visit, she asked me, "Is it just a chemical imbalance? My doctor said my serotonin is low."

Genes and Heritability

Sullivan et al. (2000) pooled the twin research on major depression and put heritability near 37 percent; most of the rest traced to experiences each twin had alone, while growing up in the same house added little. Family studies also showed that relatives of people with depression have higher risk. Heritability of thirty-seven percent means that genetic differences account for a moderate share of the differences in depression among people in the populations studied; it does not mean that Teresa's depression is thirty-seven percent genetic. Large genetic studies since then have identified many common variants, each with a tiny effect, rather than a single depression gene.

Teresa's mother had depression, which suggests some inherited vulnerability, but her own experiences, including a divorce two years ago and the stress of teaching after the pandemic, also matter.

The Serotonin Story

The idea that depression results from low serotonin became popular in the 1990s, partly through marketing of selective serotonin reuptake inhibitors. Moncrieff et al. (2023) conducted an umbrella review of systematic reviews and meta-analyses examining the serotonin theory, including studies of serotonin and its breakdown products in body fluids, receptor and transporter levels, depletion experiments and genetic studies. They found no consistent evidence that depression is associated with or caused by lower serotonin activity. The authors argued that the chemical imbalance explanation should not be presented to patients as established.

The review prompted debate. Critics noted that antidepressants do help many people, and that a drug's effectiveness does not depend on depression being caused by a deficit of the chemical the drug affects. Aspirin relieves headaches without headaches being caused by a lack of aspirin. Antidepressants may work through other mechanisms, such as changes in emotional processing, neural plasticity or stress systems, which take weeks to develop.

An antidepressant can help without depression being a shortage of the chemical it targets.

Inflammation and the Immune System

Another line of research links depression to the immune system. Miller and Raison (2016) reviewed evidence that inflammatory signals, such as cytokines released during infection or chronic stress, can act on the brain to produce symptoms including fatigue, low mood, poor sleep and withdrawal, which may have helped ancient humans conserve energy and avoid others during illness. A subset of people with depression show elevated inflammatory markers, and some treatments that target inflammation have shown benefits in people with high inflammation. The authors emphasized that inflammation contributes to depression in some people, not all.

Chronic stress, poor sleep and obesity all raise inflammation, linking this pathway to others in Teresa's life.

Stress Hormones

Earlier in the course, we saw how chronic stress alters the stress hormone system. Many people with depression show changes in this system, such as disrupted cortisol rhythms. Teresa's divorce and work stress fit a pattern in which prolonged stress interacts with vulnerability to produce depression.

Sleep as Cause and Consequence

Teresa's insomnia began before her depression. Baglioni et al. (2011) meta-analyzed longitudinal studies following people without depression at the start and found that those with insomnia had about twice the risk of developing depression later than those without sleep problems. Insomnia is also a common symptom of depression and often persists after mood improves, raising the risk of relapse.

This evidence suggests that treating insomnia directly may help prevent or reduce depression, and Teresa's sleep physician referred her for cognitive behavioral therapy for insomnia alongside her depression treatment.

Brain Circuits and Plasticity

Imaging studies of depression, interpreted with the cautions discussed earlier in the course, point to changes in networks linking the prefrontal cortex, hippocampus and amygdala, the same circuits involved in emotion regulation and stress. Prolonged stress and depression have been associated in some studies with reduced hippocampal volume, and some treatments, including antidepressants, exercise and therapy, may promote neural plasticity in these circuits. These findings are group averages with considerable overlap between people with and without depression, so no scan can diagnose Teresa, but they suggest that recovery involves the brain relearning, not simply refilling a missing chemical.

Life Events and Biology Together

Biology does not act in a vacuum. Depressive episodes often follow a loss or a humiliating blow, and people who start out more vulnerable, through family history or biology, are the ones most likely to tip into depression afterward. Teresa's divorce, her mother's history of depression and her year of broken sleep illustrate how these strands can braid together. Social support, purposeful work and physical activity can push in the other direction, which is why treatment often combines medication or therapy with changes in daily life.

How the Pieces Fit

Teresa's depression likely reflects several interacting factors: inherited vulnerability, a period of intense stress, disrupted sleep and perhaps immune and stress hormone changes. No single factor explains it, and different patients with the same diagnosis may have different combinations. This complexity also explains why treatments that work for one person may not work for another.

Answering Teresa's Question

I am not her clinician, but I suggested she ask her physician about how her medication works and what else contributes to depression. A more accurate explanation than "low serotonin" might be: "Depression involves changes in brain circuits for mood, stress and sleep, influenced by genes and life events. Medication, therapy and better sleep can each help those circuits recover." Teresa said that this explanation made more sense to her and felt less like something was broken inside her.

Reflection on the Course

Six weeks of neuroscience have altered how I watch the monitors at night. I began by learning how opioids silence the neurons that drive breathing, and I end by seeing depression as many systems interacting. Along the way I learned to distrust colorful brain scans, to respect what stress does to the body and to see sleep as tied to almost everything. Most of all, I learned to ask what the evidence actually shows.

Conclusion

Biology contributes to depression through genes, stress systems, immune signals and sleep, but the evidence does not support a simple chemical imbalance. Communicating this complexity honestly helps patients understand their illness and their treatment options.

References

Baglioni, C., Battagliese, G., Feige, B., Spiegelhalder, K., Nissen, C., Voderholzer, U., Lombardo, C., & Riemann, D. (2011). Insomnia as a predictor of depression: A meta-analytic evaluation of longitudinal epidemiological studies. Journal of Affective Disorders, 135(1-3), 10-19. https://doi.org/10.1016/j.jad.2011.01.011

Miller, A. H., & Raison, C. L. (2016). The role of inflammation in depression: From evolutionary imperative to modern treatment target. Nature Reviews Immunology, 16(1), 22-34. https://doi.org/10.1038/nri.2015.5

Moncrieff, J., Cooper, R. E., Stockmann, T., Amendola, S., Hengartner, M. P., & Horowitz, M. A. (2023). The serotonin theory of depression: A systematic umbrella review of the evidence. Molecular Psychiatry, 28(8), 3243-3256. https://doi.org/10.1038/s41380-022-01661-0

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