What causes acute stress disorder?

Acute stress disorder facts. acute stress disorder causes.
Acute stress disorder facts

Not everyone who experiences a traumatic event or who is exposed to the consequences of a traumatic event develops acute stress disorder (ASD). For instance, roughly one in four rescue workers during 9/11 developed ASD [11], and approximately 20% of those who experienced a traumatic event [8]. Why do some people develop ASD and others don’t? To answer this question, we need to look at the acute stress disorder causes: genetic and environmental factors. One of the acute stress disorder causes, the environmental factors, stress the importance of family cohesion and expressiveness to reduce the likelihood of developing ASD, and later PTSD [2],[8]. Understanding what causes people to develop ASD (and later PTSD) helps professionals to develop tools and treatments to reduce the impact of traumatic events. This page focuses on the acute stress disorder causes and highlights a few risk factors as well.

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Acute stress disorder causes – genetics

There is a growing body of evidence suggesting that both PTSD and ASD symptoms are moderately heritable [6],[9]. For instance, genes regulating the hypothalamic-pituitary-adrenal (HPA) axis affect the stress response after exposure to a traumatic event [5]. A strong stress response is associated with more ASD and PTSD symptoms. Also, genetic factors can influence the risk of exposure to some form of trauma, perhaps through individual differences in personality which in turn affect environmental choices [4]. This is in line with another study; a twin study suggests that exposure to assaultive trauma is moderately heritable, and exposure to non-assaultive trauma is not heritable [6]. Another twin study found a large genetic correlation between reward responsiveness and stress perception [7], which can explain the comorbidity of PTSD and alcohol/drug abuse & dependency. According to this study, an increased perception of stress makes some people more prone to find sedatives that reduce their perceived stress.


Another study reports that the serotonin transporter polymorphism (5-HTTLPR) and stressful life events interact to predict endocrine stress reactivity in a non-clinical sample. These results underpin the potential moderating role of HPA-axis hyper-reactivity as a premorbid risk factor to increase the vulnerability for depression if these people have low serotonin transporter efficiency and a history of severe life events [1]. There is a reasonable overlap of depression and ASD symptoms.
In other words, one of the acute stress disorder causes is heritability: there is a strong link between certain genetic components and ASD symptoms and typical responses after a traumatic event. NOTE: just inheriting one of the above mentioned factors does not mean that this person will develop ASD after a traumatic event. Environmental factors also play a huge role in the development of ASD.

Acute stress disorder causes – environment

Environmental factors in an individual’s life can affect the development of acute stress disorder. People with pre-existing Major Depression increases the risk for subsequent exposure to traumatic events twofold, and increases the risk for ASD and PTSD among exposed people threefold [3]. This suggests that people who were diagnosed with depressive disorder are more likely to develop acute stress disorder. Also other environmental factors contribute to the likelihood of ASD after experiencing a traumatic event:


A twin study found a large environmental correlation between reward responsiveness and stress perception; individual-specific environmental factors that increase perceived stress may negatively affect the ability to modulate behaviour as a function of reinforcers [7].


Family cohesion and expressiveness significantly reduce the psychological distress and ASD symptoms [2]. Also, strategies to maintain control over a situation, such as worrying and punishment, and poor social support are predictors of acute stress disorder and later PTSD. These coping strategies inhibit emotional processing and that can lead to ASD and PTSD [8]. These findings are in line with the findings of study [10], where an individual’s perceived coping self-efficacy (CSE, the ability to manage posttraumatic recovery) is a strong predictor of distress shortly after the traumatic even (two to eight weeks after the event).

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.