A recent study conducted by researchers at the Swiss Federal Institute of Technology Lausanne (EPFL) has shed light on why some individuals develop post-traumatic stress disorder (PTSD) following exposure to trauma, while others do not. The study findings have significant implications for the development of more targeted treatments for PTSD.
PTSD is a mental health disorder that can occur after experiencing or witnessing a traumatic event. The condition is characterized by symptoms such as intrusive thoughts, avoidance behaviors, sleep disturbances, and hypervigilance. Understanding why certain individuals develop PTSD while others don’t is crucial for early identification and effective treatment.
The EPFL study focused on the body’s stress hormone response as a contributing factor to PTSD vulnerability. The levels of glucocorticoids, a type of steroid hormone, released into the bloodstream vary greatly among individuals when they experience stress. Low levels of glucocorticoids are frequently observed in PTSD patients after trauma exposure.
Glucocorticoids, particularly cortisol, the primary stress hormone, work with specific parts of the brain to regulate mood, motivation, and fear. The brain releases cortisol in response to perceived danger after the fight-or-flight response. However, it has been challenging to establish whether low glucocorticoid levels and a smaller hippocampus, the region of the brain involved in memory formation, are risk factors or consequences of trauma exposure.
To investigate the link between reduced stress hormone response and PTSD symptoms, the researchers used genetically modified rats that mimicked humans with a diminished cortisol response. They observed the volume of different brain regions, trained the rats to associate fear with a cue, monitored their sleep patterns, and measured their brain activity.
The study revealed that decreased responsiveness to glucocorticoids led to several vital vulnerability traits for PTSD, including impaired fear extinction, reduced hippocampal volume, and disturbances in rapid-eye-movement sleep (REMS). Fear extinction is the process by which a conditioned fear response diminishes over time, and REMS is crucial for memory consolidation. Both of these traits are often impaired in individuals with PTSD. The researchers concluded that these traits are interconnected rather than independent risk factors.
In further experiments, the rats were given cognitive-behavioral therapy to reduce their learned fears. Following that, corticosterone, the murine version of cortisol, was administered to the rats. The study found that excessive fear and REM sleep disturbances decreased, and the levels of norepinephrine, a neurotransmitter associated with the fight-or-flight response, returned to normal.
The findings of the study provide evidence of a direct implication of low glucocorticoid responsiveness in the development of PTSD and its associated symptoms. This suggests that glucocorticoid treatments may be beneficial for individuals with reduced glucocorticoid responsiveness.
The study’s results have significant implications for the development of targeted treatments for PTSD. By understanding the biological link between stress hormone response and PTSD symptoms, researchers can potentially develop interventions that specifically address the underlying hormonal dysregulation in individuals with PTSD.
Overall, this study highlights the importance of considering individual differences in stress hormone response in understanding the development and treatment of PTSD. By targeting the body’s stress response system, researchers may be able to provide more effective interventions for individuals with PTSD.
1. Source: Coherent Market Insights, Public sources, Desk research
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