Bessel van der Kolk’s phrase the body keeps the score has become a familiar way of saying that trauma leaves a felt trace, even after the memory fades. What recent research adds to this idea is not just a metaphor. Early adversity appears to leave a measurable mark on the immune system, and this mark can quietly shape how a person feels and how well they respond to treatment years or decades later.
What biology shows
When the body is threatened, physically or emotionally, it mounts an inflammatory response: a coordinated set of chemical signals that mobilizes the immune system to protect and repair. This response is designed to be temporary. However, when a child grows up under chronic threat, abuse, neglect, or persistent caregiver unpredictability, the inflammatory system may fail to return to baseline fully. Instead, it can remain in a state of low-grade activation long after the original danger has passed.
This is not a fringe finding. A large meta-analysis pooling data from nearly 17,000 adults found that individuals with a history of childhood trauma had significantly higher circulating inflammatory markers decades after the adverse experiences occurred (Baumeister et al., 2016). Interestingly, different forms of adversity appeared to leave distinct biological signatures: physical and sexual abuse were more consistently associated with elevated C-reactive protein, whereas parental absence showed stronger associations with interleukin-6, suggesting that different adverse experiences may become biologically embedded through partially distinct pathways. An earlier systematic review reached a similar conclusion, identifying childhood maltreatment as a robust, albeit heterogeneous, predictor of immune dysregulation in adulthood (Coelho et al., 2014).
One proposed mechanism underlying these long-term effects involves epigenetic modification. Rather than altering DNA itself, chronic childhood stress may alter the expression of genes regulating inflammation and stress responsivity through processes such as DNA methylation. These biological adaptations may help explain how early adversity becomes “embedded” in physiology and contributes to persistent inflammatory activity across the lifespan (Provencal & Binder, 2015).
It is worth emphasizing, however, that this relationship is neither simple nor universal. A 2021 update by many of the same researchers reviewed newer studies and found considerably more heterogeneous findings than earlier reviews suggested. Several well-designed studies reported no significant association between childhood adversity and inflammatory biomarkers after accounting for factors such as body mass index, smoking, trauma subtype, and the inflammatory marker examined (Brown et al., 2021). Emerging evidence also suggests that biological embedding may vary by the developmental period during which adversity occurred and the individual’s sex, although these moderating effects remain an active area of investigation (Lacey et al., 2020; Davis et al., 2019). The most balanced conclusion, therefore, is that childhood adversity increases the probability of heightened inflammation in adulthood—it does not guarantee it, nor does inflammation constitute a diagnostic marker of trauma.
What this looks like in the therapy room
For clinicians, these findings matter less as laboratory results than as another way of understanding a familiar clinical presentation: the client with a significant trauma history who is persistently exhausted rather than overtly depressed, emotionally flat rather than tearful, and unable to experience motivation or pleasure as they once did. Clients and families often interpret such presentations, and sometimes clinicians, as evidence of laziness, poor motivation, or resistance to recovery. Chronic low-grade inflammation offers an alternative explanatory framework. It may alter reward processing, disrupt sleep regulation, and contribute to fatigue, anhedonia, and cognitive slowing by affecting the brain and immune system (Bower & Kuhlman, 2023).
For many clients, this perspective can substantially reduce self-blame. Understanding that a body shaped by prolonged early threat may continue to mount a background inflammatory response not because of a personal weakness but because of adaptive biological responses to chronic adversity can be an important component of trauma-informed psychoeducation. At the same time, clinicians should use this framework flexibly. For some individuals, biological explanations may reduce shame; for others, they may inadvertently reinforce beliefs that they are permanently “damaged” or biologically determined. Whether this psychoeducational approach is helpful depends on the client’s formulation, preferences, and clinical context.
What can be done
These findings do not suggest replacing psychotherapy with anti-inflammatory medication, nor do they imply that inflammatory biomarkers should become part of routine clinical assessment. Instead, they point towards several practical implications for psychological care.
Psychological interventions themselves appear capable of modestly reducing inflammatory activity. A meta-analysis of 19 randomized controlled trials found that psychological treatment produced small but statistically significant reductions in inflammatory biomarkers, with the most consistent effect observed for C-reactive protein (O’Toole et al., 2018). More recently, a network meta-analysis of 104 trials reported that structured cognitive therapies, lifestyle-focused interventions, and mindfulness-based programs each reduced pro-inflammatory markers, while mindfulness-based interventions additionally increased anti-inflammatory activity (Ballesio et al., 2023). These findings suggest that effective psychological treatment may influence both subjective psychological recovery and relevant biological processes.
The biological dimension is also worth discussing with clients, particularly those whose symptoms remain dominated by fatigue, cognitive slowing, and low energy despite pharmacological treatment. In this context, regular sleep, physical activity, and anti-inflammatory dietary patterns should not be viewed as generic lifestyle advice but rather as complementary interventions that may be used alongside psychotherapy.
Similarly, collaboration with primary care should be normalized for clients with extensive trauma histories and persistent somatic symptoms. This is not about pursuing inflammatory testing indiscriminately but about identifying potentially modifiable physical contributors while promoting genuinely integrated care.
Ultimately, naming the biological consequences of trauma may help reduce shame for many clients. Recognizing that exhaustion can have a plausible physiological basis, rather than reflecting insufficient effort or poor character, often creates space for greater self-compassion. Biological explanations do not replace the psychological work of processing traumatic experiences, but for some individuals, they can make that work feel more understandable, achievable, and hopeful.
References
Ballesio, A., Zagaria, A., Vacca, M., Pariante, C. M., & Lombardo, C. (2023). Comparative efficacy of psychological interventions on immune biomarkers: A systematic review and network meta-analysis (NMA). Brain, behavior, and immunity, 111, 424–435. https://doi.org/10.1016/j.bbi.2023.05.006.
Baumeister, D., Akhtar, R., Ciufolini, S., Pariante, C. M., & Mondelli, V. (2016). Childhood trauma and adulthood inflammation: a meta-analysis of peripheral C-reactive protein, interleukin-6 and tumour necrosis factor-α. Molecular psychiatry, 21(5), 642–649. https://doi.org/10.1038/mp.2015.67.
Bower, J. E., & Kuhlman, K. R. (2023). Psychoneuroimmunology: An Introduction to Immune-to-Brain Communication and Its Implications for Clinical Psychology. Annual review of clinical psychology, 19, 331–359. https://doi.org/10.1146/annurev-clinpsy-080621-045153.
Brown, M., Worrell, C., & Pariante, C. M. (2021). Inflammation and early life stress: An updated review of childhood trauma and inflammatory markers in adulthood. Pharmacology, biochemistry, and behavior, 211, 173291. https://doi.org/10.1016/j.pbb.2021.173291.
Coelho, R., Viola, T. W., Walss-Bass, C., Brietzke, E., & Grassi-Oliveira, R. (2014). Childhood maltreatment and inflammatory markers: a systematic review. Acta psychiatrica Scandinavica, 129(3), 180–192. https://doi.org/10.1111/acps.12217.
Davis, M. C., Lemery-Chalfant, K., Yeung, E. W., Luecken, L. J., Zautra, A. J., & Irwin, M. R. (2019). Interleukin-6 and Depressive Mood Symptoms: Mediators of the Association Between Childhood Abuse and Cognitive Performance in Middle-Aged Adults. Annals of behavioral medicine : a publication of the Society of Behavioral Medicine, 53(1), 29–38. https://doi.org/10.1093/abm/kay014.
Lacey, R. E., Bartley, M., Kelly-Irving, M., Bevilacqua, L., Iob, E., Kelly, Y., & Howe, L. D. (2020). Adverse childhood experiences and early life inflammation in the Avon longitudinal study of parents and children. Psychoneuroendocrinology, 122, 104914. https://doi.org/10.1016/j.psyneuen.2020.104914.
O’Toole, M. S., Bovbjerg, D. H., Renna, M. E., Lekander, M., Mennin, D. S., & Zachariae, R. (2018). Effects of psychological interventions on systemic levels of inflammatory biomarkers in humans: A systematic review and meta-analysis. Brain, behavior, and immunity, 74, 68–78. https://doi.org/10.1016/j.bbi.2018.04.005.
Provençal, N., & Binder, E. B. (2015). The effects of early life stress on the epigenome: From the womb to adulthood and even before. Experimental neurology, 268, 10–20. https://doi.org/10.1016/j.expneurol.2014.09.001.