Trauma also provokes enduring changes in the body’s primary stress circuitry, the HPA axis. The HPA axis governs the release of stress hormones (like cortisol and adrenaline) in response to threat. In acute trauma, the HPA axis kicks into high gear – the hypothalamus releases corticotropin-releasing hormone (CRH), the pituitary releases ACTH, and the adrenal glands flood the body with cortisol and adrenaline to mobilize a fight-or-flight response. In chronic trauma and PTSD, this system can become dysregulated. Researchers such as Yehuda (2002) have documented abnormal cortisol patterns in trauma survivors, including blunted or low cortisol levels in some PTSD populations despite high CRH, suggesting the system may become “tuned” to expect constant threat and adjust its baseline output accordingly. Such individuals can have a hypersensitive stress response — minor triggers produce exaggerated hormonal surges — or alternatively, a cortisol output that is erratic and not well-calibrated to current conditions.
Over time, chronic HPA activation contributes to wear-and-tear on the body (allostatic load), while low baseline cortisol might impair one’s ability to recover from stress. The key point is that traumatic experiences recalibrate the stress-hormone axis: survivors often live with a body chemistry primed for alarm. Maté (2011) emphasizes that childhood trauma fundamentally alters a child’s developing stress mechanisms, leaving them more reactive to stress throughout adult life. In this way, trauma’s imprint is not merely psychological; it is a physical reality of an altered neuroendocrine state. Elevated inflammatory markers, altered immune function, and stress-related illnesses common in trauma survivors may all be downstream effects of an overworked HPA axis (Heim et al., 2000; Yehuda et al., 1996).