**6.2 Biological factors**

Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stressrelated neuropsychiatric disorders, while Nutt (2000) has suggested that individuals develop PTSD due to neuroendocrine dysregulation. Furthermore, impaired feedback regulation of relevant stress responses, especially immune activation/inflammation, may, in turn, contribute to stress-related pathology that includes alterations in behavior, insulin sensitivity, bone metabolism, and acquired immune responses (Raison & Miller, 2003). Because the hypothalamic-pituitary gland-adrenal axis (HPA) regulates hormone reactions during stress, PTSD severity seems to decrease when individuals exposed to traumatic


Risk Factors and Hypothesis for Posttraumatic

Stress Disorder (PTSD) in Post Disaster Survivors 147



Risk Factors and Hypothesis for Posttraumatic

Stress Disorder (PTSD) in Post Disaster Survivors 149



Cited from Su et al. (2011) under permission

Table 1. Summary of Chi-Chi earthquake papers related to psychiatry (PubMed search through June 2009) (cited from Su et al., with permission)

Risk Factors and Hypothesis for Posttraumatic

motivated forgetting.

Stress Disorder (PTSD) in Post Disaster Survivors 151

events experience decreased stress levels. Thabet & Vostanis, (2000) and Gurvits et al. (1997) found more positive soft neurological signs in PTSD participants than in participants who experienced similar trauma but did not develop PTSD. Many trauma victims complain of memory impairment, such as difficulty remembering daily activities, frequent compulsive recall of the traumatic event in detail, memory gaps, island-like memory, difficulties with declarative memory, and intrusive memories. Anderson et al. (2004) used functional magnetic resonance imaging (MRI) to identify the neural systems involved in keeping unwanted memories out of one's awareness. Controlling unwanted memories is associated with increased dorsolateral prefrontal activation (DLPF), reduced hippocampal activation, and impaired retention of those memories. Both prefrontal cortical and right hippocampal activations predicted the magnitude of forgetting. These results confirm the existence of an active forgetting process and establish a neurobiological model for guiding inquiry into

There are still gaps in our understanding of the genetic underpinnings of PTSD. For example, while Stein et al. (2002) have found moderate hereditary factors in individuals

Meyer et al. (1999) indicated that some psychiatric symptoms and disorders are risk factors for PTSD (Meyer, Taiminen, Vuori, Aijälä, Helenius, 1999). For example, certain personality traits, such as neuroticism and introversion, are associated with an increased risk of PTSD (Lewin, Carr, & Webster, 1998; McFarlane, 1988) while some studies indicate that certain psychiatric disorders may be predictive of chronic PTSD (Engdahl, Dikel, Eberly, & Blank, 1998; McFarlane & Papay, 1992). Then again, other studies have examined the long-term course of PTSD. A longitudinal analysis of the mental health of school children after the great Hanshin Awaji earthquakes indicated that some survivors' psychological reactions emerged early and disappeared early (i.e., within two years after the disaster); however, this is contrary to findings from other studies (Shioyama et al., 2000). Lazaratou et al. (2008) have found that greater numbers of PTSD symptoms emerged during the first 6 months after the earthquake and were associated with a greater impact on the victims' lives 50 years after the event. Uemoto et al. (2000) posited that the best predictor of recovery from chronic PTSD was the initial level of post-traumatic reaction immediately after the accident. However, few

with PTSD symptoms, no single gene that causes PTSD has been identified.

data are available on the long-term effects caused by a disaster (Chou et al., 2007).

Inadequate social support after the trauma adds to the risk of developing PTSD (Chou et al., 2004a; Wang et al., 2000). Not surprisingly, higher levels of post-disaster life events are also related to the risk of developing PTSD (Chang, Connor, Lai, Lee, & Davidson, 2005). Similarly, social stressors such as economic or marital issues or a disruption of one's daily life, including relocation, the death of an intimate partner, or other significant loss problems

Hobfoll's conservation of resources (COR) model has been well supported by previous studies on natural disasters (Sumer, Karanci, Berument, & Gunes, 2005). According to

**6.3 Psychological factors and psychiatric symptoms** 

**6.4 Post-trauma social resource factors** 

**7. Hypothesis for PTSD** 

are associated with a greater risk for developing PTSD.

Cited from Su et al. (2011) under permission

through June 2009) (cited from Su et al., with permission)

Table 1. Summary of Chi-Chi earthquake papers related to psychiatry (PubMed search

events experience decreased stress levels. Thabet & Vostanis, (2000) and Gurvits et al. (1997) found more positive soft neurological signs in PTSD participants than in participants who experienced similar trauma but did not develop PTSD. Many trauma victims complain of memory impairment, such as difficulty remembering daily activities, frequent compulsive recall of the traumatic event in detail, memory gaps, island-like memory, difficulties with declarative memory, and intrusive memories. Anderson et al. (2004) used functional magnetic resonance imaging (MRI) to identify the neural systems involved in keeping unwanted memories out of one's awareness. Controlling unwanted memories is associated with increased dorsolateral prefrontal activation (DLPF), reduced hippocampal activation, and impaired retention of those memories. Both prefrontal cortical and right hippocampal activations predicted the magnitude of forgetting. These results confirm the existence of an active forgetting process and establish a neurobiological model for guiding inquiry into motivated forgetting.

There are still gaps in our understanding of the genetic underpinnings of PTSD. For example, while Stein et al. (2002) have found moderate hereditary factors in individuals with PTSD symptoms, no single gene that causes PTSD has been identified.
