Trauma
May 17, 2022
TLDR: Trauma's Biological Impact - Understanding Inflammation
This article examines how trauma and early life stress affect immune function and inflammation. Key points include:
Early life adversity creates lasting changes in immune system function
Trauma exposure increases inflammatory markers in the body
Chronic stress accumulates as "allostatic load" over time
Inflammation affects brain reward and threat processing
Gut health plays crucial role in trauma-related inflammation
Wise Mind Nutrition emphasizes the importance of:
Using anti-inflammatory nutrition to support healing
Taking a trauma-informed approach to dietary changes
Implementing lifestyle medicine strategies
Understanding biological impacts of stress
The article concludes that effective trauma recovery requires addressing inflammation through nutrition while maintaining a trauma-informed perspective.
[Read full article for detailed research on inflammation pathways and healing strategies]
The immune system regulates the inflammatory cascade. Immune dysregulation may be one pathway that explains the link between early life adversity and elevated rates of morbidity and mortality. Early life immune activation sensitizes traumatized individuals to the effects of subsequent stressors [1]. Thus, greater stress sensitivity resulting from early life adversity may put people at greater risk for multiple forms of immune dysregulation [2].
Specifically, epigenetic changes following early life adversity have been proposed to increase the production of monocytes and macrophages with strong pro-inflammatory tendencies [3]. Along with many other roles, these immune cells are a primary source of cytokines, which are immunomodulating agents. Common examples include interleukins (IL) and tumor necrosis factors (TNF). Did you know that targeted nutrition interventions can significantly reduce inflammation? Be here for it.
In a meta-analysis of 36 studies, trauma exposure was associated with elevated levels of C-reactive Protein (CRP), IL-1-beta, IL-6, and TNF-α [4]. In this report, the presence of psychiatric symptoms was a significant predictor of increased effect sizes for IL-1-beta and IL-6. In a New Zealand birth cohort followed for 32 years, maltreated children had graded increases in the risk for clinically relevant CRP 20 years later, independent of co-occurring early life risks, stress in adulthood, smoking, and physical activity [5].
Allostatic Load
Early stress research by Bruce McEwen identified “allostatic load” as the cost of chronic exposure from repeated environmental challenges, as a biological mechanism leading to a wide range of diseases [6]. A later definition described allostatic load as the “price of adaption that can lead to disease over long periods” [7]. Social environments have major impacts on human physiology by influencing the process of adaptation or allostasis.
In a longitudinal study from Scotland, higher allostatic load scores were not associated with an increased risk of all-cause mortality after five years however became significant after ten [8], highlighting how such impacts can accrue gradually over time. These investigators also found that allostatic load was not associated with specific causes of death, suggesting broad wear and tear across multiple physiological systems. To corroborate these findings, a longitudinal study of adults showed that those who experienced any type of abuse in childhood demonstrated steeper rises in inflammation over time [9].
Inflammation and the Brain
Prolonged influences on the biological stress system during development may increase individual susceptibility to later mental health disorders. Several recent reviews have proposed that gut-based immune responses leading to inflammation are likely to play a role in altered reward processing and reactivity, suggesting a potential role of neuroinflammation in both depression and addictions [10–12]. More specifically, inflammatory mediators can act on cortico-amygdala (threat) and cortico-basal ganglia (reward) circuitries in a manner that predisposes individuals to self-medicating behaviors such as smoking and drug use [13].
Management of stress responses in the body can be improved through contemplative practices. As we have outlined in this article, chronic stress can have strong biological causes and consequences. Improvements across multiple biological body systems can be achieved through lifestyle medicine approaches such as intentional movement, and eating patterns higher in fruits and vegetables and omega-3 fatty acids. Because of the adverse behavioral consequences of trauma, it could be argued that gut health is public health!
Trauma-Informed Nutrition
At Wise Mind Nutrition, we utilize the latest science on anti-inflammatory eating to offset the potential harms of stress, trauma, and adversity. Our recommendations are designed to support your immune system to foster the healing process. We believe in healing and our experience suggests that gut-based nutrition interventions can be a critical part of that. The language that we use is also trauma-informed. Is it time to start the healing process?
Trauma-informed nutrition is the here and now. This approach recognizes how trauma impacts multiple body systems and uses food as part of the healing process. It also recognizes the strengths of the individual and makes sure that interventions are appropriate and not triggering. Nutrition can be deliberate and intentional without being too complicated or associated with pass/fail approaches. This is the essence of Wise Mind Nutrition.
References
1. Danese A, Lewis SJ (2017) Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma? Neuropsychopharmacol 42:99–114
2. Fagundes CP, Glaser R, Kiecolt-Glaser JK (2013) Stressful early life experiences and immune dysregulation across the lifespan. Brain Behav Immun 27:8–12
3. Miller GE, Chen E, Parker KJ (2011) Psychological stress in childhood and susceptibility to the chronic diseases of aging: Moving toward a model of behavioral and biological mechanisms. Psychological Bulletin 137:959–997
4. Tursich M, Neufeld RWJ, Frewen PA, Harricharan S, Kibler JL, Rhind SG, Lanius RA (2014) Association of trauma exposure with proinflammatory activity: a transdiagnostic meta-analysis. Transl Psychiat 4:e413–e413
5. Danese A, Pariante CM, Caspi A, Taylor A, Poulton R (2007) Childhood maltreatment predicts adult inflammation in a life-course study. Proc National Acad Sci 104:1319–1324
6. McEwen BS, Stellar E (1993) Stress and the Individual: Mechanisms Leading to Disease. Archives of Internal Medicine 153:2093–2101 7. McEwen BS (1998) Stress, Adaptation, and Disease: Allostasis and Allostatic Load. Annals of the New York Academy of Sciences 840:33–44
8. Robertson T, Beveridge G, Bromley C (2017) Allostatic load as a predictor of all-cause and cause-specific mortality in the general population: Evidence from the Scottish Health Survey. Plos One 12:e0183297
9. Renna ME, Peng J, Shrout MR, Madison AA, Andridge R, Alfano CM, Povoski SP, Lipari AM, Malarkey WB, Kiecolt-Glaser JK (2020) Childhood abuse histories predict steeper inflammatory trajectories across time. Brain Behav Immun. https://doi.org/10.1016/j.bbi.2020.11.012
10. Dooley LN, Kuhlman KR, Robles TF, Eisenberger NI, Craske MG, Bower JE (2018) The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation. Neurosci Biobehav Rev 94:219–237
11. Fung TC, Olson CA, Hsiao EY (2017) Interactions between the microbiota, immune and nervous systems in health and disease. Nat Neurosci 20:145–155
12. Kohno M, Link J, Dennis LE, McCready H, Huckans M, Hoffman WF, Loftis JM (2019) Neuroinflammation in addiction: A review of neuroimaging studies and potential immunotherapies. Pharmacol Biochem Behav 179:34–42
13. Nusslock R, Miller GE (2016) Early-Life Adversity and Physical and Emotional Health Across the Lifespan: A Neuroimmune Network Hypothesis. Biological Psychiatry 80:23–32
