What makes people more vulnerable to Post-Traumatic Stress Disorder (PTSD) following a traumatic event, and how can PTSD be prevented? The Diagnostic and Statistical Manual of Mental Disorders (DSM) IV defines an individual with Post Traumatic Stress Disorder (PTSD) as having been exposed to a traumatic event in which both of the following have occurred; firstly, the person either experienced or witnessed an event that involved “actual or threatened death or serious injury, or a threat to the physical integrity of self or others”. Secondly, the person’s exhibited response had to be one of “intense fear, horror or helplessness”. In addition to these criteria, the individual persistently re-experiences the event. This includes recurrent and intrusive recollections of the event which cause distress, persistent avoidance of stimuli that could be associated with the event, intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event, etc. Some of the symptoms of PTSD bear similarities with those of depression; withdrawal from social circumstances is common as well as a restricted range of affect and problems sleeping. As with any disorder, not everyone who suffers a traumatic event will develop PTSD, some people are more susceptible to suffering from this after experiencing said traumatic experience; this essay will explore the factors as to why that is, including research from both a biological and social point of view. As an extension of this, this essay will explore ways in which PTSD can possibly be prevented. From a biological point of view, there is high potential that vulnerability to Post Traumatic Stress Disorder can be genetic. Yehuda’s 1999 research for instance, found that there is an increased prevalence of PTSD in the adult children of Holocaust survivors, despite the fact that they did not experience the trauma themselves nor did they report a greater exposure to life- threatening events as a result of their family’s history. Family studies in this area support Yehuda’s findings; these are indicative of genetics playing a role in susceptibility to PTSD. For instance, studies involving twins appear to show that approximately 30% of the risk for developing PTSD is accounted for by genetic factors (Koenen et al., 2008, Vernon & Livesly, 2002) although some studies have given higher estimates such as recent research by Sartor et al., 2011. These studies between twins and parent/offspring provide results that indicate a link between genetics and a vulnerability to PTSD. As well as studies into genetics in general, there is also specific research in this field into endocrine factors. Main endocrine features of PTSD include abnormal regulation of Cortisol and thyroid hormones; however there is a fair bit of dispute surrounding these findings across studies. The hypothalamic-pituitary-adrenal (HPA) axis is the central coordinator of the neuroendocrine stress response systems; therefore it has been an important focus of research regarding individuals with PTSD. When confronted with stressful/traumatic situations, neurons in the hypothalamic paraventricular nucleus (PVN) release corticotropin-releasing hormone (CRH), in turn, this then leads to the production and release of adrenocorticotropin (ACTH) from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex; these control metabolism as well as immune and brain function, thereby managing physiological behavior to cope with stressors. Although stressors in general activate the HPA axis, studies in combat veterans with PTSD demonstrate decreased levels of cortisol concentrations (as detected in urine or blood) in comparison with healthy controls and other comparator groups. This finding, though consistent in other studies using PTSD patients from other populations such as Holocaust survivors, refugees, and abused persons, is not consistent across all...
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http://www.medicalnewstoday.com/articles/261598.php - published 6/7/2013, retrieved 10/11/2013
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