Friday, November 4, 2022

Effects of Childhood Trauma on the HPA Axis

Over two-thirds of children experiences at least one traumatic event before the age of 16. Childhood trauma is much more common and relevant than we may expect. SAMHSA (the Substance Use and Mental Health Services Administration), describes psychological, physical, or sexual abuse, community or school violence, national disasters or terrorism, sexual exploitation, neglect, and many more as examples of childhood traumatic events. Traumatic events in childhood have been linked to susceptibility to adult psychological and psychiatric conditions, and the main culprit is in dysregulation of the HPA (hypothalamic-pituitary-adrenal) axis.

A traumatic event negatively impacts the stress response system by inducing hyperarousal of the sympathetic nervous system. Hyperarousal of the stress response can cause physiological changes like increased blood pressure, heart rate, and respiration, changes to perceiving the environment, and outward behaviors like crying/shouting. The difference is that these behaviors tend to be advantageous to the stress response in adults, while they tend to be maladaptive in children because children lack the ability to readily protect themselves physically. There is also a notable difference between the normal stress response and one to a traumatic event, which is that following a traumatic event, the state of hyperarousal continues long after the trauma, causing disruptions in the HPA axis, limbic system, and prefrontal cortex. A child’s brain is very sensitive and susceptible to endocrine changes during a time of development, so it is crucial to consider the downstream effects of childhood trauma.

The HPA axis is accepted as the major neuroendocrine stress response system which helps an organism adapt in stressful times. During activation of the SNS, the hypothalamus first releases of corticotropin-releasing hormone (CRH) to increase alertness. Then, release of CRH signals to the pituitary to release adrenocorticotropic hormone (ACTH), which signals to the adrenal glands to release cortisol which helps the body adapt to stress. Stressors, either physical or nonphysical, lead to a temporary spike in cortisol which causes system dysregulation. Also, activation of the amygdala (which processes fear-inducing stimuli) causes an overproduction of CRH.

Overall, stressful situations in childhood effectively cause dysregulations of the HPA axis which lead into adulthood. It has been shown that children who experienced trauma like violence or abuse have dysregulated cortisol levels before they even reach adulthood. This is an important consideration because there are assumed links between cortisol dysregulation and adult psychiatric disorders such as major depressive disorder (MDD), PTSD, bipolar disorder, and psychosis.

‌Murphy, F., Nasa, A., Cullinane, D., Raajakesary, K., Gazzaz, A., Sooknarine, V., Haines, M., Roman, E., Kelly, L., O’Neill, A., Cannon, M. & Roddy, D.W. (2022). Childhood trauma, the HPA axis and psychiatric illnesses: A targeted literature synthesis. Frontiers in Psychiatry, 13(748372), 1-15. https://doi.org/10.3389/fpsyt.2022.748372.

Understanding Child Trauma. (n.d.). Www.samhsa.gov. https://www.samhsa.gov/child-trauma/understanding-child-trauma#:~:text=Child%20trauma%20occurs%20more%20than


1 comment:

  1. Not only is the affect of childhood trauma on the HPA axis disheartening in itself, perhaps even more insidious is the fact that trauma is now being found to affect the HPA axis development of children in utero.

    How? Radtke et. al recently investigated the effect of maternal intimate partner violence on the baby both prior to, and during pregnancy. The team followed 25 women, and 24 of their children to investigate methylation changes of the the NR3C1 gene, which encodes the glucocorticoid receptor. 10 different CpG sites on the GR promoter were observed for methylation levels both at time of birth, and 15 years down the line in offspring. A heavy correlation was found between maternal intimate partner violence during pregnancy, and increased methylation of the GR promotor of the NR3C1 gene. The effect? Increased catecholamines and glucocorticoids, which play a role in fetal HPA axis development (Radke, 2011). Not only were these changes associated with mental health issues in the child, but also changes in regions of the hippocampus and increased stress response. (Serpeloni et. al, 2017).

    References:

    Radtke, M., Ruf, M., Gunter, H., Dohrmann, K., Schauer, M., Meyer, A., Albert, T. (2011). Transgenerational Impact of Intimate Partner Violence on Methylation in the Promotor of the Glucocorticoid Receptor. Translational Psychiatry, 1(7). https://doi.org/10.1038/tp.2011.21

    Serpeloni, F., Radtke, K., Assis, S., Henning, F., Natt, D., Elbert, T. (2017). Grandmaternal Stress During Pregnancy and DNA Methylation of the Third Generation: An Epigenome-Wide Association Study. Translational Psychiatry 7, e1202. https://doi.org/10.1038/tp.2017.153

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