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Unveiling the Impact of Trauma: A Psychoneuroimmunological & Biopsychosocial Perspective

“Trauma” — a term that resonates through our minds, echoing with feelings of distress, fear, and dread. Defined by the American Psychological Association as an emotional response to a distressing event like an accident, rape, or natural disaster, trauma, if not adequately addressed, can have far-reaching consequences (American Psychological Association, 2020). We can now also define Complex Trauma, also known as Developmental trauma, which refers to chronic, interpersonal trauma experienced during crucial periods of a child's brain development, often leading to long-term cognitive, emotional, and social impacts (van der Kolk, 2005). These traumas can include but are not limited to abuse, neglect, and exposure to domestic violence (Felitti et al. 1998). These profound effects transcend the psychological realm, extending their grip to neuroimmunological and biopsychosocial facets of human health. In this article, we will delve into the intricacies of how trauma affects the body from a psychoneuroimmunological and biopsychosocial perspective.

The Psychoneuroimmunological Impact of Trauma

Psychoneuroimmunology (PNI) is a relatively new interdisciplinary field that studies the intricate interactions between the nervous, endocrine, and immune systems (Ader, 2007). Trauma can trigger a cascade of events in this trinity, altering the body's stress response and immune function.

A seminal study by Danese et al. (2007) discovered that individuals exposed to trauma, particularly during childhood, had heightened levels of inflammatory markers such as C-reactive protein and interleukin-6. These changes were associated with a higher risk of developing physical health problems such as cardiovascular disease and autoimmune disorders. The researchers hypothesised that this was due to the body's "fight-or-flight" response being activated persistently, leading to chronic inflammation (Danese et al. 2007).

Neurologically, trauma can stimulate the hypothalamic-pituitary-adrenal (HPA) axis — the body’s central stress response system (Ehlert, 2013). This can result in increased cortisol production, an essential stress hormone. In the short term, cortisol can be beneficial, enhancing immunity and inflammation. However, long-term exposure can lead to a state of cortisol resistance, reducing the body’s immune response and leaving individuals more susceptible to illnesses (Miller, Chen, & Zhou, 2007).

The Biopsychosocial Impact of Trauma

The biopsychosocial model proposed by Engel (1977) comprehensively explains how trauma can affect a person's biological, psychological, and social dimensions. Trauma, especially chronic or repetitive, can impact not only physiological health but also mental health, leading to conditions such as post-traumatic stress disorder (PTSD), depression, and anxiety disorders (Bremner, 2006).

From a social perspective, trauma can disrupt an individual's capacity to establish and maintain relationships. The social disconnection can lead to feelings of isolation and loneliness, exacerbating the individual's psychological distress and contributing to the onset of mental health disorders (Cacioppo & Cacioppo, 2014).

The biopsychosocial model encourages a holistic approach in understanding and treating the impact of trauma. It calls for the integration of physical, psychological, and social factors rather than focusing solely on the biological aspects of disease.

Conclusion

Trauma, as we've learned, exerts extensive effects on the human body, navigating through a labyrinth of interconnected systems and resulting in significant health implications. From a psychoneuroimmunological standpoint, trauma can result in persistent inflammation and compromised immune function. From a biopsychosocial perspective, trauma leaves its mark on the individual's psychological well-being and social interactions.

To fully understand and treat the profound impact of trauma, health care professionals & psychological practitioners must consider a holistic, interdisciplinary approach that accounts for the complex interactions between an individual's psychological state, neurological responses, immune function, and social well-being.



Written By Joanna Stokoe MNCIP (Accred)

References

American Psychological Association. (2020). Trauma. https://www.apa.org/topics/trauma

Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., Koss, M. P., & Marks, J. S. (1998). Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. American Journal of Preventive Medicine, 14(4), 245-258.

van der Kolk, B. A. (2005). Developmental trauma disorder. Psychiatric Annals, 35(5), 401-408.

Ader, R. (2007). Psychoneuroimmunology. Current Directions in Psychological Science, 16(4), 185-189. https://doi.org/10.1111/j.1467-8721.2007.00505.x

Bremner, J. D. (2006). Traumatic stress: effects on the brain. Dialogues in clinical neuroscience, 8(4), 445. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181836/

Cacioppo, J. T., & Cacioppo, S. (2014). Social relationships and health: The toxic effects of perceived social isolation. Social and personality psychology compass, 8(2), 58-72. https://doi.org/10.1111/spc3.12087

Danese, A., Pariante, C. M., Caspi, A., Taylor, A., & Poulton, R. (2007). Childhood maltreatment predicts adult inflammation in a life-course study. Proceedings of the National Academy of Sciences, 104(4), 1319-1324. https://doi.org/10.1073/pnas.061036210

Ehlert, U. (2013). Enduring psychobiological effects of childhood adversity. Psychoneuroendocrinology, 38(9), 1850-1857. https://doi.org/10.1016/j.psyneuen.2013.06.007

Engel, G. L. (1977). The need for a new medical model: a challenge for biomedicine. Science, 196(4286), 129-136. https://doi.org/10.1126/science.847460

Miller, G. E., Chen, E., & Zhou, E. S. (2007). If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. Psychological bulletin, 133(1), 25. https://doi.org/10.1037/0033-2909.133.1.25

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