For a long time, it was thought our genes were static, that they couldn’t be changed or altered. While this is partially true, under the right conditions they can turn on or off, just a like a light switch. For example, when you have an infection, the genes governing the production of inflammatory cytokines (chemical messengers) that help co-ordinate the immune response are switched on to help you fight off the infection. If the process were to continue, this highly inflammatory state could lead to detrimental outcomes, so once the danger period has passed the genes governing the production of these specialised proteins switch off and production ceases. But what if, under the right conditions, this process continued? Chronic inflammation, however low grade, will create health issues if sustained over time.
The response to traumatic events is similar, at least in some aspects, to an invading pathogen. Stress causes activation of the hypothalmic pituitary adrenal (HPA) axis, stimulating the release of adrenaline, cortisol and noradrenalin. Inflammatory cytokines are released to help the body deal with the potential for injury. If the stimulus continues the cycle gets caught in a loop – and it’s this chronic activation of the HPA axis that causes dysregulation in many biochemical reactions throughout the body (5).
Early life influences: How trauma affects our genes.
Early life trauma (ELC) influences gene expression during critical stages in neurodevelopment increasing the risk of developing major depressive disorder (MDD), and other mental health conditions, later in life (1). Epigenetic changes in gene expression have been noted in response to levels of maternal care, or neglect, in rats. In humans, exposure of the growing foetus to maternal stress has been shown to result in emotional and behavioural abnormalities (2). One study found that a surge in cortisol associated with the stress response altered expression in over 1000 genes (1).
Does this mean that exposure to trauma at an early age dooms us to the possibility of experiencing mental health issues later in life? Not necessarily. It’s not just negative experiences that have the ability to alter epigenetic expression. Evidence shows that positive genome interaction via nutrition, lifestyle modification and psychotherapy can support HPA axis regulation, reduce the inflammatory response and other epigenetic changes associated with ELT (3)(4). Early identification of those at risk may assist in prophylactic treatment and mitigation of the negative effects of stress and trauma during childhood.
Awareness is the key to healing.
We are only just beginning to understand how mental health affects physical health and vice versa. However, it is very clear that our previous ignorance to what is now evidence-based fact has been damaging to the wellbeing of previous generations. Consider soldiers returning from war, the cycle of abuse within families, the removal of Indigenous people from their lands, bullying at school and in the workplace. Trauma does not have to occur during childhood in order to have a lasting impact on human health. The first step in managing our wellbeing in a more proactive fashion is not considering what may go wrong in the future, but what can be corrected now to prevent the cycle from continuing.
(1) Hoffmann, A., Sportelli, V., Ziller, M., & Spengler, D. (2017, August 4). Epigenomics of major depressive disorders and schizophrenia: Early life decides. International Journal of Molecular Sciences. MDPI AG. https://doi.org/10.3390/ijms18081711
(2) Glover V. (2011). Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective. Journal of child psychology and psychiatry, and allied disciplines, 52(4), 356–367. doi:10.1111/j.1469-7610.2011.02371.x
(3) Vinkers, C.H., Geuze, E., van Rooij, S.J.H. et al. Successful treatment of post-traumatic stress disorder reverses DNA methylation marks. Mol Psychiatry (2019). https://doi.org/10.1038/s41380-019-0549-3
(4) Burdge, G. C., Hoile, S. P., & Lillycrop, K. A. (2012). Epigenetics: are there implications for personalised nutrition?. Current opinion in clinical nutrition and metabolic care, 15(5), 442–447. doi:10.1097/MCO.0b013e3283567dd2
(5) Cattaneo, A., Macchi, F., Plazzotta, G., Veronica, B., Bocchio-Chiavetto, L., Riva, M. A., & Pariante, C. M. (2015, March 31). Inflammation and neuronal plasticity: A link between childhood trauma and depression pathogenesis. Frontiers in Cellular Neuroscience. Frontiers Media S.A. https://doi.org/10.3389/fncel.2015.00040