What causes acute stress disorder?
Not everyone who experiences a traumatic event or is exposed to its aftermath develops acute stress disorder (ASD). For example, during 9/11, roughly one in four rescue workers developed ASD [11], and approximately 20% of individuals exposed to a traumatic event also experienced ASD [8]. This raises an important question: why do some people develop ASD while others do not? To answer this, we must explore the causes of acute stress disorder, which include both genetic and environmental factors.
Among these causes, environmental factors highlight the critical role of family cohesion and expressiveness in reducing the likelihood of developing ASD, and later, PTSD [2][8]. Understanding these underlying causes enables professionals to create effective tools and treatments to minimize the impact of traumatic events. This article delves into the genetic and environmental causes of acute stress disorder and outlines key risk factors.
A hostile or toxic work environment can create significant psychological stress, which may escalate into a traumatic event for some individuals. Constant exposure to bullying, harassment, or unreasonable demands can erode emotional well-being, making employees feel unsafe or devalued. Over time, such experiences can lead to acute stress responses, particularly if the individual perceives a loss of control or support in the workplace. If you would like a therapist to help you address these issues, you can book a no obligation consult with us here for free.
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Genetic Causes of Acute Stress Disorder
Research increasingly shows that both PTSD and ASD symptoms have a moderate genetic basis [6][9]. For example, genes regulating the hypothalamic-pituitary-adrenal (HPA) axis, which governs the body’s stress response, influence the severity of symptoms after exposure to a traumatic event [5]. A stronger stress response is associated with higher rates of ASD and PTSD symptoms.
Additionally, genetic factors may indirectly influence the likelihood of experiencing trauma. Personality traits, which are partly hereditary, can shape environmental choices, potentially increasing the risk of traumatic exposure [4]. Supporting this, a twin study revealed that exposure to assaultive trauma is moderately heritable, while exposure to non-assaultive trauma is not [6].
Another study found a strong genetic correlation between reward responsiveness and stress perception [7], which may explain the frequent comorbidity of PTSD with alcohol and drug dependence. People who perceive stress more intensely are more likely to use substances to alleviate their stress.
Furthermore, research indicates that a serotonin transporter polymorphism (5-HTTLPR) interacts with stressful life events to predict stress reactivity. This underscores the role of HPA-axis hyperreactivity as a premorbid risk factor, increasing vulnerability to depression among individuals with low serotonin transporter efficiency and a history of severe life events [1]. Since there is a significant overlap between depression and ASD symptoms, this genetic link may partially explain the development of ASD.
In summary, heritability plays a substantial role in ASD development. However, inheriting certain genetic factors does not guarantee that a person will develop ASD after a traumatic event. Environmental influences are equally critical in shaping outcomes.Environmental Causes of Acute Stress Disorder
Environmental factors also significantly affect the likelihood of developing ASD. For instance, individuals with pre-existing major depression are twice as likely to be exposed to traumatic events and three times as likely to develop ASD or PTSD after exposure [3]. This highlights the importance of addressing pre-existing mental health conditions to mitigate ASD risk.
Other environmental factors that contribute to ASD include:- Stress Perception: A twin study found that individual-specific environmental factors increasing stress perception negatively impact one’s ability to adapt behavior based on rewards or reinforcers [7].
- Family Cohesion: Strong family cohesion and expressiveness are protective factors, reducing psychological distress and ASD symptoms [2].
- Coping Strategies: Ineffective coping strategies, such as excessive worrying and self-punishment, are predictors of ASD and PTSD. These strategies hinder emotional processing and recovery [8].
- Social Support: Poor social support networks significantly increase the likelihood of ASD, while perceived coping self-efficacy (CSE)—the ability to manage post-traumatic recovery—has been shown to be a strong predictor of reduced distress in the weeks following trauma [10].
Conclusion
In short, the development of ASD is influenced by both genetic and environmental factors. Risk factors such as poor coping strategies, inadequate social support, and heightened stress perception increase the likelihood of ASD. Conversely, protective factors like strong family cohesion, expressiveness, and effective coping self-efficacy can help prevent ASD.
If you would like a therapist to help you with these issues, you can book a no obligation consult with us here for free.
In other words: Certain environmental factors increase the likelihood of developing ASD, such as the coping strategies ‘worrying’ and ‘punishment’ and having a poor support network, whereas other environmental factors can reduce the likelihood of developing ASD, such as a good family cohesion and expressiveness, and the ability manage posttraumatic recovery.
Literature
- [1] Alexander, N., Kuepper, Y., Schmitz, A., Osinsky, R., Kozyra, E., & Hennig, J. (2009). Gene–environment interactions predict cortisol responses after acute stress: implications for the etiology of depression. Psychoneuroendocrinology, 34, 1294-1303.
- [2] Shaw, R. J., Deblois, T., Ikuta, L., Ginzburg, K., Fleisher, B., & Koopman, C. (2006). Acute stress disorder among parents of infants in the neonatal intensive care nursery. Psychosomatics, 47, 206-212.
- [3] Breslau, N., Davis, G. C., Peterson, E. L., & Schultz, L. R. (2000). A second look at comorbidity in victims of trauma: The posttraumatic stress disorder–major depression connection. Biological psychiatry, 48, 902-909.
- [4] Stein, M. B., Jang, K. L., Taylor, S., Vernon, P. A., & Livesley, W. J. (2002). Genetic and environmental influences on trauma exposure and posttraumatic stress disorder symptoms: a twin study. American Journal of Psychiatry, 159, 1675-1681.
- [5] Amstadter, A. B., Nugent, N. R., Yang, B. Z., Miller, A., Siburian, R., Moorjani, P., … & Smoller, J. W. (2011). Corticotrophin-releasing hormone type 1 receptor gene (CRHR1) variants predict posttraumatic stress disorder onset and course in pediatric injury patients. Disease Markers, 30, 89-99.
- [6] Afifi, T. O., Asmundson, G. J., Taylor, S., & Jang, K. L. (2010). The role of genes and environment on trauma exposure and posttraumatic stress disorder symptoms: a review of twin studies. Clinical psychology review, 30, 101-112.
- [7] Bogdan, R., & Pizzagalli, D. A. (2009). The heritability of hedonic capacity and perceived stress: a twin study evaluation of candidate depressive phenotypes. Psychological medicine, 39, 211-218.
- [8] Holeva, V., Tarrier, N., & Wells, A. (2001). Prevalence and predictors of acute stress disorder and PTSD following road traffic accidents: Thought control strategies and social support. Behavior Therapy, 32, 65-83.
- [9] Stein, M. B., Jang, K. L., Taylor, S., Vernon, P. A., & Livesley, W. J. (2002). Genetic and environmental influences on trauma exposure and posttraumatic stress disorder symptoms: a twin study. American Journal of Psychiatry, 159, 1675-1681.
- [10] Benight, C. C., & Harper, M. L. (2002). Coping self‐efficacy perceptions as a mediator between acute stress response and long‐term distress following natural disasters. Journal of traumatic stress, 15, 177-186.
- [11] Fullerton, C. S., Ursano, R. J., & Wang, L. (2004). Acute stress disorder, posttraumatic stress disorder, and depression in disaster or rescue workers. American Journal of Psychiatry, 161, 1370-1376.