Relationship Between Exposure
to Traumatic Stress and Mental
Illness
A study on flood victims in Nepal
Bachelor Degree Project in Cognitive Neuroscience Basic Level 22.5 ECTS
Spring term 2020
Emelie Zakariasson
Acknowledgements
I would like to send my gratitude to all participants taking part in the study, who shared their experiences of the flood in 2019. Thank you to the University of Skövde, SIDA, and the Swedish Council for Higher Education, for granting me a minor field study scholarship. Without the funding from the scholarship, this trip to Nepal would not have been possible. I also wish to express my sincere gratitude to my supervisor on site in Nepal, Mrs. Radhika Shrestha, for providing me the most excellent scholarly support. It is because of you that this study could be carried out.
I would also like to express my gratitude to my supervisor Pilleriin Sikka for your
professional guidance and valuable knowledge that you have shared with a kind and warm heart. You have been giving me much of your time ang guidance throughout this process. To Rebecca Linder, thank you for all the courage and support.
I also want to thank all of my loving and supportive family and friends who always cheer me on and believe in me.
And to my newfound family in Nepal, Raju Malla and Bimala Malla. Raju, thank you for all academic support and happy times with much laughter. And Bimala thank you for the unconditional love and warmth you greeted me with. The kindness of you both will always follow me and you will always have a special place in my heart.
Abstract
Traumatic experiences, such as natural disasters, do not only cause people to suffer from material and financial losses, but they can lead to a maladaptive regulation of the stress response and to the onset of stress-induced psychopathology. Traumatic stress has been shown to alter brain structures and functions involved in the stress response. It has also been linked to the dysregulation of the hypothalamic-pituitary-adrenal axis, an overactive
sympathetic nervous system with elevated cortisol and norepinephrine levels. These
neurobiological alterations can make some individuals more vulnerable to the development of depression and anxiety disorders. A dose-response relationship between trauma severity and psychopathology has been found in previous research. Research has also revealed that a person’s perceived ability to cope with hardship, coping self-efficacy (CSE), is related to decreased vulnerability or resilience to stress. In the study carried out in the framework of this thesis, associations between the severity of traumatic exposure and CSE with
posttraumatic stress disorder, depression, and generalized anxiety disorder were examined in a sample (N = 105) of Nepalese flood victims. Participants (18-90 years old) answered a questionnaire carried out via interview. Results showed that there were no significant correlations between flood related trauma severity and depression or anxiety. However, findings showed that higher CSE was associated with fewer depressive symptoms. Future studies in Nepal should directly investigate this association as well as possible interventions aimed at enhancing CSE and whether such interventions can reduce symptoms of depression.
Keywords: traumatic stress, PTSD, depression, anxiety, coping self-efficacy,
Table of Contents
1. Introduction ... 4
2. Definitions of Trauma and Stress ... 6
2.1 Traumatic Experience ... 6
2.2 Stress ... 6
2.2.1 Acute and chronic stress. ... 7
3. Neurobiology of the Stress Response ... 7
4. Trauma and Psychopathology ... 8
4.1 Trauma and Psychopathology in Nepal ... 9
5. Trauma and Neurobiological Implications ... 10
5.1 The Neurobiology of Trauma ... 10
5.2 The Neurobiology of PTSD ... 11
5.3 The Neurobiology of Depression ... 13
5.4 The Neurobiology of Generalized Anxiety Disorder ... 14
6. Vulnerability and Resilience to Stress ... 15
6.1 Coping Self-Efficacy ... 15
6.1.1 Coping self-efficacy and its neurobiology. ... 16
7. Aim and Hypotheses of the Present Study ... 17
8. Method ... 18
8.1 Participants ... 18
8.2 Procedure ... 18
8.3 Measures... 19
8.3.1 Demographic questions. ... 19
8.3.2 Experience of natural disasters. ... 19
8.3.3 Traumatic exposure severity scale (TESS). ... 19
8.3.4 Primary care PTSD screen (PC-PTSD-5). ... 20
8.3.5 Patient health questionnaire (PHQ-9). ... 21
8.3.6 Generalized anxiety disorder scale (GAD-7). ... 21
8.3.7 Coping self-efficacy scale (CSES). ... 22
8.4 Statistical Analyses ... 22
9. Results ... 23
10. Discussion ... 27
11. Conclusion ... 30
12. References ... 31
Appendix A – English Version of the Questionnaire Package ... 40
1. Introduction
“Traumatic events challenge an individual's view of the world as a just, safe and predictable place”
– American Psychology Association, APA Dictionary of Psychology Every year natural disasters like earthquakes, floods, and hurricanes affect almost 160 million people and kill nearly 90000 people worldwide. These catastrophic events suddenly disrupt not only the day-to-day lives of individuals but give rise to long-term effects on the health and well-being of the affected population (World Health Organization, 2020).
The country of Nepal is located in the South-East Asian region and is a so-called low-and middle-income country, with 21.6% of its population living below the poverty line and 80% is at risk of being affected by a natural disaster (Kc, Gan, & Dwirahmadi, 2019; UNDP Nepal, 2019). In July 2019, a flash flood hit Nepal and caused 12000 households to be displaced and 13800 households to need acute assistance. For 176800 people, food security became threatened and it was estimated that 117 people died (Nepal Food Security
Monitoring System, 2019).
In the aftermath of a traumatic experience, such as a natural disaster, mental illness in the affected population can occur and last over a year after the incident (Elal & Slade, 2005). According to research by Grant, Beck, Marques, Palyo, and Clapp (2008) traumatic experiences are highly correlated with posttraumatic stress disorder (PTSD), major depressive disorder (MDD), and generalized anxiety disorder (GAD) (Grant et al., 2008). Evidence indicates a dose-response relationship between the severity of traumatic
experiences and PTSD, depression, and anxiety among people who have experienced natural disasters (Goenjian et al., 2000). However, it is not clear whether it is the cumulative effect of the traumatic experience or certain exposure-related factors that are associated with mental health outcomes (Elal & Slade, 2005).
The development of psychiatric disorders, such as PTSD, depression, and anxiety, has a genetic predisposition. However, stressful (especially traumatic) life experiences can
dysregulate the adaptive stress response system, leading to psychopathology (McEwen, 2008; Sapolsky, 2015). Traumatic stress has been associated with structural and functional changes in various brain areas such as the amygdala, hippocampus, and prefrontal cortex. It is also associated with alterations in the production of hormones such as cortisol and norepinephrine (Bremner, 2006, 2008).
2004). One psychological factor is the way in which the individuals believe that they can cope with their stress or trauma. In a review of studies, Benight and Bandura (2004) showed that individuals with higher coping self-efficacy (CSE) are more likely to have a sense of personal mastery and control. This often leads to adaptive coping, such as more active coping behaviors(e.g., problem solving or seeking support). On the contrary, individuals being lower in the same trait can perceive traumatic experience to be more threatening and they can use more maladaptive coping behaviors, such as becoming more passive in their way of coping (e.g., avoidance or denial) (Benight & Bandura, 2004). Research has shown the buffering effects of CSE when dealing with the experience of natural disasters in American, European, and Australian samples (Benight et al., 1999; Pritchard & Gow, 2012; Sumer, Karanci, Berument, & Gunes, 2005).
Mental health in low-and-middle-income countries, is under-researched in areas such as studies on trauma victims, depression, anxiety, and mental health interventions (Sharan, Levav, Olifson, de Francisco, & Saxena, 2007). The National Planning Commission in Nepal has reported that it is important to carry out such research at both national and sub-national levels. International support is needed for Nepal to reach its Sustainable Development Goals (SDG) 2030 (National Planning Commission, 2015). Target 3 of the SDG for Nepal includes research that maps mental illness in the population and work that promotes the decrease of mental health diseases, such as depression and anxiety. It is thus important to perform research to address this gap. It is also beneficial to further expand knowledge about the relationship between CSE and psychopathology since such research is lacking with natural disaster victims in Nepal. This could lead to the development of mental health interventions targeting CSE in vulnerable populations in Nepal.
The first aim of the current thesis is to present a theoretical overview regarding traumatic stress and its relationship with stress-induced psychopathology, such as PTSD, depression, and anxiety. In the framework of this thesis, an empirical study was conducted in a Nepalese village that was affected by a flash flood in the summer of 2019. The aim of the study was to investigate trauma severity and its associations with symptoms of PTSD, depression, and anxiety. Additionally, the aim was to examine the associations between CSE and symptoms of PTSD, depression, and anxiety.
alterations from stress-induced psychopathology, namely PTSD, depression, and anxiety will also be described. The main focus will be on studies using functional magnetic resonance imaging (fMRI) and positron emission tomography (PET). Some vulnerability and resilience factors of the stress response will be described. This will be followed by a brief description of CSE and some of its neurobiological implications. After the theoretical background, the method of the current study will be presented, followed by the results and discussion of the findings.
2. Definitions of Trauma and Stress 2.1 Traumatic Experience
In the Diagnostic and Statistical Manual of Mental Health Disorders, Edition 5 (DSM-5; American Psychiatric Association, 2013), the definition of trauma includes “actual or
threatened death, serious injury, or sexual violence” (p. 271). Trauma is required to be a personal experience, personally witnessing trauma happening to someone else, or learning that it happened to family or friends (American Psychiatric Association, 2013). Many people experience various types of traumatic stressors, e.g., natural disasters. Since trauma is a severe form of a stressor, it neurobiologically affects these individuals (Heim & Nemeroff, 2009).
2.2 Stress
Stress is a physiological response to stressors or stressful stimuli (Fink, 2016). Stressors can either be physical (e.g., injury) or psychological (e.g., experiencing strain from daily hassles). Hans Selye defined stressors as something that threatens the internal physiological balance of the body, referred to as “homeostasis” (Robinson, 2018). Lazarus and Folkman (1984) added a cognitive aspect to stress by suggesting that stress occurs when the demands exceed the perceived ability to cope with the stressor (Lazarus & Folkman, 1984). Thus, the stressor (stimulus) causes the brain to react and evaluate the stressor and its possible impact. This is called the stress perception. In turn, this leads to the activation of the stress response, with the physiological characteristics of the fight-or-flight system (Dhabhar, 2018).
More recent research has shifted focus from the nature to the duration of the stress response (Dhabhar, 2018).
2.2.1 Acute and chronic stress. Acute stress can last between minutes and hours, and in
this phase of the stress reaction, the body promotes responses from neural, autonomic, immune, and memory systems. After the body has responded to the stressor, the nervous and endocrine systems quickly adapt and set the body back to homeostasis, or allostasis, as described by McEwen. When allostasis is called upon too often or is inefficiently managed, allostatic load is reached (Dhabhar, 2018; McEwen, 2008; McEwen et al., 2015).
Allostatic load is a state where the cumulative effect of multiple stressors can lead to the dysregulation of and failure to shut off the stress response for weeks or months, often referred to as chronic stress (Dhabhar, 2018; McEwen, 2003). The concept of allostatic overload has been described as the culminative pathophysiology that can result from excessive stress and the dysregulation of the stress response. Thus, both allostasis and allostatic load are concepts of stress that describe the biological adaptive and maladaptive responses to stressors,
respectively (McEwen et al., 2015).
Acute stress can lead to the development of the acute stress disorder, the symptoms (e.g., arousal and irritable mood) of which last between three days and up to a month after the traumatic incident (Bryant, 2018). The prolonged effects of allostatic load or chronic stress can lead to depression, chronic anxiety disorders, and PTSD (McEwen, 2003; 2017).
3. Neurobiology of the Stress Response
A comprehensive overview of the neurobiology of stress is out of the scope of this thesis. However, a brief overview is given for providing context.
The sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal axis (HPA-axis) are the two key systems that are involved in the stress response. The SNS prepares the organs of the body for action, often referred to as the fight-or-flight response or the tend-and-befriend response seen in females. These stress responses are characterized by increased blood pressure, heart – and breathing rate to deliver glucose and oxygen to the muscles (Taylor et al., 2000; Wirth, 2015). The SNS will activate the adrenal medulla, which releases a blend of catecholamines, usually the stress hormones epinephrine and
norepinephrine (Christopher, 2004).
stress response (Herman et al., 2016). Glucocorticoid receptors are widely distributed in the brain, especially in the hippocampus, therefore the hippocampus can sense too high levels of cortisol and inhibit the HPA-axis. This is called the negative feedback mechanism and it protects against cortisol overproduction (Lovallo, 2016; McEwen & Gianaros, 2010). The parasympathetic nervous system then suppresses the activation of the SNS and sets the body and organs back into a resting state, characterized by decreased heart- and breathing rate (Herman et al., 2016).
For the psychological stress response, the amygdala is important for threat detection and fear conditioning, and it can turn on stress hormones and increase heart rate. The PFC and especially the dorsolateral prefrontal cortex (dlPFC), has a top-down control over the emotional response to the stressor. Hippocampus provides context to the given stressor and forms declarative memories of the stressful or threatful event (McEwen & Gianaros, 2010; McEwen & Morrison, 2013; McEwen et al., 2015). However, these brain regions do not function in isolation during the acute stress response, but as parts of functional brain
networks. fMRI studies have revealed that during heightened levels of stress-induced cortisol, increased connectivity within the salience network (SN) occurs. With core regions such as amygdala, anterior insula, and dorsal anterior cingulate cortex, the SN (especially anterior insula) is important for detecting behaviorally relevant stimuli and coordinating a neural response to it. The default mode network (DMN), which is important for higher cognition such as self-referential and autobiographical memory, shows decreased functional
connectivity. DMN consists of core regions such as the medial prefrontal cortex (mPFC), hippocampus, and posterior cingulate cortex (PCC). Lastly, the central executive network (CEN), which is centered on the dlPFC, is important for executive functions and has shown altered functional connectivity (Van Oort et al., 2017; Zhang et al., 2019).
4. Trauma and Psychopathology
Meta-analysis has revealed that among trauma-exposed civilians and military samples, trauma exposure severity was one of the factors that were linked to symptom severity in PTSD (Brewin, Andrews, & Valentine, 2000). Trauma exposure severity was also found to be significantly correlated with PTSD severity among 3271 civilian survivors of the
September 11 terrorist attack after 2-3 years (DiGrande, Neria, Brackbill, Pulliam, & Galea, 2011).
In a longitudinal study by Goenjian et al. (2000), three different Armenian groups that had experienced either mild earthquake, severe earthquake, or severe violence were examined for psychopathology 1.5 years and 4.5 years after the trauma. Results from both time
intervals showed that trauma severity was significantly correlated with PTSD, depression, and anxiety in the earthquake groups. Results also showed no significant differences in the level of psychopathology between the groups that had experienced either severe earthquake or severe violence. The severity of the trauma, rather than the type of trauma itself, was seen to impact the level of psychopathology in their sample (Goenjian et al., 2000).
4.1 Trauma and Psychopathology in Nepal
There is little research on traumatic stressors and mental health outcomes in developing countries, although some research conducted in Nepal is available on the subject. A study that was conducted 10 months after the earthquake in 2015 revealed that 24.1% of the 291 adults included in the sample had PTSD (Adhikari Baral & Bhagawati, 2019). Another study, performed 8-12 months after the earthquake, showed that 46.7% suffered from mild to severe anxiety and 56.3% from mild to severe depression (Bhandari et al., 2018).
In a sample of 223 participants from a village one year after earthquake exposure, 9% screened positive for PTSD, and 33% for mild to severe depression. In the same sample, results indicated an association between the severity of the trauma exposure, as measured with Traumatic Exposure Severity Scale (TESS), and symptoms of PTSD and depression. The category “exposure to the grotesque” (e.g., exposure to body parts) was associated with increased resilience (e.g., ability bounce back after stress) in the sample (Schwind et al., 2019).
5. Trauma and Neurobiological Implications
Chronic dysregulation of the stress response induced by trauma can make individuals “psychologically traumatized” and a maladaptive regulation of multiple stress-mediating response systems can occur after a psychological “shock” (Sherin & Nemeroff, 2011). When the brain experiences a traumatic stressor, it is exposed to abnormal levels of glucocorticoids and norepinephrine, leading to both altered dendric development and synaptic density in the brain. This results in an abnormal neural architecture and connectivity of the brain. As a result, stress-induced psychopathology can occur (Bremner, 2006; McEwen, 2008; McEwen et al., 2015). The following sections will contain a brief overview of the neurobiological alterations in trauma-exposed individuals, PTSD, depression, and anxiety. A comprehensive review of the literature is out of the scope of this paper, but some main findings will be pointed out, involving the core regions and networks of the stress response system.
5.1 The Neurobiology of Trauma
There is scarce research on alterations in the neural functional patterns shortly after traumatic exposure and what changes in the brain that are caused by the trauma exposure itself (Nilsen et al., 2016). However, some studies have compared trauma-exposed individuals without PTSD to those with PTSD and to healthy control groups (HCG). In a resting-state fMRI study, trauma-exposed individuals had increased effective
connectivity from the mPFC to the amygdala when compared to a HCG. The trauma-exposed group also showed increased connectivity from the amygdala to dlPFC and decreased
connectivity in the reversed direction. These results suggest that trauma-exposed individuals exhibit less regulation of the amygdala from the dlPFC, causing a weaker top-down control (Chen et al., 2018).
Further, trauma-exposed individuals have displayed higher activation in the mPFC, thalamus, and anterior cingulate cortex (ACC) to script-driven imagery of traumatic memories, when compared to individuals with PTSD (Lanius et al., 2001).
to the reduced volume of cornu ammonis 3 and the dentate gyrus in the hippocampus (Stevens et al., 2017).
Amygdala is involved in the emotional valence of events, and during acute traumatic stress, glucocorticoids foster hypertrophy of the basolateral amygdala, which generates a stronger fear acquisition. Intensive fear and fear conditioning can also contribute to the distorted memories of the traumatic event (Bremner, 2006; Gonzalez & Martinez, 2014; Sapolsky, 2015).
In a PET study, increased activity in the right anterior insula of trauma-exposed individuals was found compared to both a PTSD group and a HCG. The anterior insula, which is important for emotional experiences and threat detection, has been commonly reported to be activated during fear conditioning. A heightened activation of this region has been suggested to be an indicator of trauma-exposed individuals without PTSD being more resilient to traumatic stress than the other groups (Jeong et al., 2019; Shin & Liberzon, 2009).
5.2 The Neurobiology of PTSD
The common symptoms of PTSD are a behavioral representation of stress-induced structural and functional changes in the brain. The DSM-5 criteria for PTSD include symptoms such as intrusion (e.g., flashbacks and intrusive memories), avoidance (e.g.,
trauma-related emotions and feelings), cognition and mood (e.g., negative affect), and arousal (e.g., hypervigilance and concentration deficits) (American Psychiatric Association, 2013). Evidence of functional alterations in PTSD includes core stress response structures such as the amygdala, hippocampus, and mPFC, which are presented under a dysregulated fronto-limbic circuitry model (Akiki, Averill, & Abdallah, 2017). This model suggests that the amygdala is overactive and hyperresponsive to threat-related stimuli, causing heightened arousal and exaggerated fear response in PTSD patients. This is aggravated by a dysfunction of the mPFC, which leads to decreased ability to inhibit the reaction from the amygdala leading to bottom-up control from the limbic system. Additionally, with decreased
hippocampal activity, a failure to identify that a non-threatening situation is safe contributes to symptoms of avoidance and re-experiencing (Akiki et al., 2017). However, the complexity of the manifestation of this disorder can not only be explained by alterations in local brain function, rather by a broader approach of functional integration between brain regions (Ke et al., 2018).
functional connectivity within the DMN, including the regions of ACC/vmPFC and hippocampus (Sripada et al., 2012). A decreased functional connectivity in the DMN has been suggested to be related to PTSD symptoms such as depersonalization and
autobiographical memory deficits (Lanius, Frewen, Tursich, Jetly, & McKinnon, 2015). Furthermore, the PTSD group showed increased cross-network connectivity, which included SN seed regions, having increased connectivity to DMN region of left hippocampus, and, in turn, DMN having increased connectivity to SN regions such as insula, putamen, and supplementary motor area. This can reflect an inappropriate activation of the SN during times of rest in PTSD individuals and further sustain symptoms of heightened arousal. Also,
increased activity within the SN in the PTSD group was found. This was shown as high functional connectivity between the anterior insula and both amygdala and striatum (Sripada et al., 2012). Not only is high functional connectivity within SN proposed to be linked to hyperarousal and hypervigilance in PTSD, but also to a greater HPA-axis responsivity to aversive stimuli (Lanius et al., 2015; Sripada et al., 2012). Within the PTSD group, symptom severity was correlated to decreased functional connectivity between vmPFC and left
hippocampus and increased connectivity within the anterior insular and within the amygdala (Sripada et al., 2012).
There are also structural alterations in the brain that have been connected to the disorder, e.g., atrophy of the hippocampus. In PTSD, a decreased volume of the hippocampus
negatively affects both extinction learning of fear memories and the negative feedback mechanism (Joshi et al., 2020; Sherin & Nemeroff, 2011). A reduced volume of the
amygdala, lateral orbitofrontal cortex, left rostral middle frontal cortex, and inferior parietal cortex also been shown in individuals with PTSD when compared to individuals without PTSD. Reduced volume in these regions is suggested to negatively affect executive control, emotional processing and memory deficits in the disorder (Eckart et al., 2011; Morey et al., 2012).
5.3 The Neurobiology of Depression
Acute and chronic stress is one of the critical environmental triggers for the development of depression, and excessive glucocorticoid levels in the brain can lead to the onset of
depressive behaviors and symptoms (Zhu et al., 2014). The comorbidity of PTSD, MDD, and GAD has been argued to stem from their common symptom overlap of excessive negative affect. Research on trauma-exposed individuals with MDD has revealed overlapping
affective symptoms with PTSD in the form of emotional numbing and hyperarousal (Price & Stolk-Cooke, 2015; Price et al., 2019). In the DSM-5, symptoms of depressed mood or loss of interest are core symptoms of MDD. Also, deficits in cognitive abilities such as
concentration, decision making and negative thought patterns (American Psychiatric Association, 2013).
Patients with MDD exhibit alterations in brain structure, such as a decreased volume of the hippocampus (Hamilton, Siemer, & Gotlib, 2008; Treadway et al., 2015). The chronic stress-induced hyperactivity of the HPA-axis seen in depressed individuals can stem from the deficits in the negative feedback mechanism (Zhu et al., 2014).
Findings from fMRI studies have revealed abnormal functional and connectivity patterns in certain networks in the brain in patients with MDD (Li et al., 2018). Increased resting-state functional connectivity within the affective network has been discovered, with increased functional connectivity between the insular cortex, orbitofrontal cortex, amygdala, subgenual PFC, and subgenual ACC. This has been proposed to be the underlying cause of the
dysregulation of emotions in depressed individuals, leading to excessive negative mood (dysphoria), a hallmark of the disorder (Li et al., 2018; Sheline, Price, Yan, & Mintun, 2010). A decreased functional connectivity in the cognitive control network has also been seen in individuals with MDD when compared to healthy controls. This included decreased connectivity in both thalamic-frontal circuits and between PFC and hippocampus, insula, and amygdala (Lui et al., 2011). This decrease in connectivity between fronto-limbic regions negatively affects cognitive control over emotional processing, which leads to an ineffective top-down control over the negative thoughts, e.g., causing depressed mood (Li et al., 2018). Common symptoms in depressed patients are loss of motivation and pleasure
Depressed individuals also commonly show enhanced connectivity in the DMN when compared to non-depressed individuals. This has been suggested to be associated with autobiographical memory deficits and a maladaptive rumination centering on negative thoughts, common symptoms of the disorder (Li et al., 2018; Sheline et al., 2010).
5.4 The Neurobiology of Generalized Anxiety Disorder
Environmental factors of allostatic load and trauma can contribute to the onset of GAD (Patriquin & Mathew, 2017). In contrast to the symptoms of avoidance and re-experiencing traumatic memories in PTSD, in GAD, the characteristic symptoms are uncontrollable worry and arousal associated with non-traumatic stressors (Milanak, Gros, Magruder, Brawman-Mintzer, & Frueh, 2013). The diagnostic criteria for GAD in the DSM-5 are heightened anxiety and worry that is present during most of the everyday activities (e.g., work, friends, and family). This should be sustained for a minimum of six months and followed by certain symptoms such as concentration problems, restlessness, and irritability (American Psychiatric Association, 2013).
In a study by Qiao et al. (2017), comparing individuals with GAD to a HCG in resting-state fMRI, the results showed that those with GAD exhibited increased functional
connectivity within the SN. There was also increased functional connectivity within the amygdala, thalamus, and the insula, and also heightened connectivity between the amygdala and both thalamus and insula. Hyperactivity of the amygdala has been considered to be a major contributor to the development of the disorder. Increased connectivity to the insula can cause individuals with GAD to regard neutral stimuli as threatening, and increased
connectivity to the thalamus can cause difficulties filtering out unimportant stimuli (Qiao et al., 2017).
Further, the same study showed that both PFC and middle temporal gyrus have decreased connectivity to the amygdala. This leads to a dysregulation of the top-down control (i.e., PFC control over amygdala) and reduced fear extinction, causing symptoms of worry and anxiety to be persistent in the disorder (Qiao et al., 2017). Lastly, increased connectivity in the PCC, which is the central node of DMN, was discovered in the GAD group when comparing to the HCG. This increased connectivity indicates enhanced processing of the external environment, leading to worry and tension even in a resting state (Qiao et al., 2017).
SNS/HPA-axis activity at baseline and lesser SNS/ HPA-axis activity after a mental
arithmetic challenge. Compared to the HCG, who exhibited symmetry in these stress systems, measured with saliva samples. Results suggest that GAD is characteristic by SNS/HPA-axis asymmetry (Reeves, Fisher, Newman, & Granger, 2016).
6. Vulnerability and Resilience to Stress
There are certain individual differences that help explain whether one develops an adaptive or maladaptive stress response to trauma and whether trauma-related stress leads to psychopathology (Christopher, 2004). An individual’s coping ability with the stressor can affect the intensity of the physiological arousal and the peak level and duration of elevated levels of stress hormones (Dhabhar, 2018). Vulnerability factors, such as previous psychiatric diagnosis and early childhood stress and trauma, can reduce the tolerance to increased
allostatic load later in life (Patriquin & Mathew, 2017). The most acknowledged contributor to psychopathology besides stress is genetics (Smoller, 2016).
It is also possible to enhance resilience towards (traumatic) stressors such as learning to use more adaptive coping strategies (Faye, McGowan, Denny, & David, 2018). CSE, as both a resiliency and vulnerability factor against (traumatic) stress will be briefly described next.
6.1 Coping Self-Efficacy
CSE is a concept that stems from social cognitive theory and refers to the individual’s belief in his/her own ability to use adaptive coping strategies and behaviors. The belief in one’s self-efficacy is not a general disposition, meaning that high self-efficacy in one domain does not automatically correlate the same amount of self-efficacy in other domains (Benight & Bandura, 2004; Chesney, Neilands, Chambers, Taylor, & Folkman, 2006; Rodkjaer et al., 2014).
Findings from several experimental studies propose that CSE plays a major role when facing traumatic stressors. In particular, CSE has a role as a cognitive mediator (e.g., judgment and evaluation) of the stressor and can affect the stress reaction from a top-down direction (Brown, Joscelyne, Dorfman, Marmar, & Bryant, 2012). It is shown that those higher in CSE use more adaptive (e.g., problem solving or seeking support) and less
maladaptive (e.g., denial or avoidance) coping strategies. Using adaptive coping when facing traumatic stress can lead to reduced stress levels and positive outcomes such as more
threatening than those higher in CSE. Over time, individuals higher in CSE are less vulnerable to distress and are better prepared to deal with hardships (Benight & Bandura, 2004; Rodkjaer et al., 2014).
CSE has also been studied with a trauma film paradigm, where those low in CSE recalled more central details and had more negative intrusion from the traumatic clip 24 hours later, compared to those higher in CSE. This suggest that higher CSE could have reduction in PTSD symptoms, less intrusive recollections of aversive memories and reduced attentional bias towards trauma related stimuli (Brown et al., 2012).
In various traumatic and stressful situations, CSE has been found to be one factor that impacts psychopathology after a traumatic event. Longitudinal studies on both an Israelian combat sample and an American sample of natural disaster victims, showed that lower CSE to be a significant factor for the outcome of PTSD symptoms (Benight & Harper, 2002; Solomon, Weisenberg, Schwarzwald, & Mikulincer, 1988). Research on how CSE relates to depression and anxiety in samples of victims of natural disasters is scarce. However, studies on the relationship between CSE and life-threatening diseases has shed some light on the topic. Research has found a negative relationship between the level of CSE and the outcome of depression symptom severity in samples of both cancer and HIV-survivors (Philip, Merluzza, Zhang, & Heitzmann, 2013; Rodkjaer et al., 2014). In a study on patients with early onset and established rheumatoid arthritis, CSE was negatively associated with both depression and anxiety, with the strongest correlation with anxiety (Benka et al., 2014).
6.1.1 Coping self-efficacy and its neurobiology. There is a lack of neuroimaging
research on CSE; therefore research using other neuroscientific methods is briefly reviewed instead.
In a study by Guo, Ni, Li, and Hong (2019), electrical activity in the cerebral cortex was measured with event-related potentials in athletes in a high-stressed performance group. This showed that individuals higher in CSE responded faster to the initial stressor (arithmetic problems with characteristics of uncontrollability and social-evaluated threat), and those lower in CSE showed a longer N100 peak latency. The amplitude of N100 was also
significantly larger for those higher in CSE, indicating a higher level of vigilance, adaptive strategies, and early warning information processing.
self-efficacy followed by exposure to the phobic trigger (spider). Blood samples showed that participants with lower CSE displayed a higher increase in epinephrine and norepinephrine when dealing with the phobic trigger. Mere thoughts about the inability to succeed with overriding demands caused dopac (a neuronal metabolite of dopamine) to rise to high levels, suggested reflecting the activity of dopamine neurons in the brain. During the experiment, the CSE was measured again in the participants. For those individuals that had been going from a lower CSE to a higher CSE during the study, had their catecholamine reactivity quickly dropped to a normal level when dealing with the phobic trigger. This supported the view of CSE being a cognitive mediator of the stress reaction (Bandura et al., 1985; Winner et al., 2017). In the study on hurricane victims, Benight et al. (1997) found that higher levels of CSE were found to be negatively correlated with emotional distress and symptoms of PTSD. One group in the same study was also HIV positive, and in that group, those with higher CSE showed lower norepinephrine to cortisol ratio than those with lower CSE, measured with urinary samples (Benight et al., 1997). Studies have shown that higher
norepinephrine/cortisol ratio has been found in individuals with PTSD (Dale, Weber, Cohen, & Brody, 2017).
These few studies seem to suggest that being lower in CSE can be a neurobiological vulnerability factor to stress whereas higher CSE can provide neurobiological resilience to stress.
7. Aim and Hypotheses of the Present Study
The present study focused on individuals living in a Nepalese village who had been exposed to a traumatic event, that is, a natural disaster in the form of a flash flood in the summer of 2019. The aim of the study was to investigate trauma severity and its associations with symptoms of PTSD, depression, and anxiety. Additionally, the aim was to examine the associations between CSE and symptoms of PTSD, depression, and anxiety.
mediator of depression and anxiety in samples with severe and life-threatening illnesses (Benka et al., 2014; Philip et al., 2013; Rodkjaer et al., 2014). Therefore, in the present study, it was predicted that among those who have experienced the traumatic event of the flood, those with higher levels of CSE would report fewer symptoms of flood related PTSD (Hypothesis 4), depression (Hypothesis 5), and anxiety (Hypothesis 6).
8. Method 8.1 Participants
A total of 108 individuals (female = 43; male = 65) participated in the study.
Participants’ age ranged from 18-90 years old, with a mean age of 41.12 (SD = 18.43). After excluding three participants due to incomplete answers in their questionnaires, 105
participants (female = 42; male = 63) were included in the final sample and analysis. Their age ranged from 18-90 years, with a mean age of 40.9 (SD = 18.48).
All participants were recruited from the flood affected area of “Siraha”, in province number 2.
8.2 Procedure
The study was carried out from March 21st to March 22nd , 2020. A convenience sample of individuals living in a rural area of Nepal called Siraha, who had been affected by the flood in 2019, was used. The intended sample size was 250 participants. The data were supposed to have been collected within a week, but due to the emergence of the COVID-19 pandemic, Nepal was suddenly put into lockdown, terminating the data collection after one and a half days.
To collect the data, six interviewers from a local college were hired. They were all familiar with the area and its specific dialect. On the morning of the 21st of March, the interviewers received a two-hour group session, carried out by two bilingual persons and the author of this thesis. During this session, the interviewers were explained all the instructions and statements of all the scales in the questionnaire and were given the opportunity to ask questions. The interviewers were then divided into three pairs and they practiced asking all the questions from each other in order to address any misconceptions before the data
collection. During all these steps, the author of this thesis supervised the process and helped with questions regarding the questionnaire.
2019. After that, the interviewers read the informed consent form to the participants, and the participants marked the box indicating their voluntary consent to take part in the study. The interviewers were instructed to not influence the respondents in any way. If there was a question from the respondent, they were only allowed to explain a statement according to the instructions received during the training session. The interviewers were instructed to inform the participants that they should answer according to what they themselves think and feel and that there were no right or wrong answers. The interviewer read each statement to the
participants and marked their answers in the questionnaire. All participants signed the consent form, and no one was offered compensation for participating in the study.
8.3 Measures
The questionnaire consisted of previously validated scales that were forward translated from English to Nepali by a bilingual person. After that, each statement was revised in cooperation between the author of this paper and the translator. Every statement was controlled for having the correct translation and meaning in Nepalese. For those statements that were incorrectly translated, changes were made by the bilingual person in collaboration with a third bilingual person. The translation procedure was originally planned to be done according to the back-translation method. Due to accelerating time pressure, as a result of the COVID-19 pandemic, the field visit had to be scheduled earlier, and the time for
back-translation was no longer possible (see Appendix A for the original English version and Appendix B for the Nepali version of the questionnaire).
8.3.1 Demographic questions. Sociodemographic variables that were included in the
questionnaire were age, gender, marital status, religion, ethnicity, education, occupation, place of residence, current living status, facilities, health, household monthly income, and family type.
8.3.2 Experience of natural disasters. Participants were asked whether and how many
times they have experienced each of the following natural disasters: earthquake, flood, bushfire, hurricane, landslide, and drought.
8.3.3 Traumatic exposure severity scale (TESS). In order to measure the exposure and
natural disasters. The items are categorized into five dimensions or subscales: resource loss, damage to home and goods, personal harm, concern for significant others, and exposure to the grotesque (e.g., exposure to body parts or odors from dead bodies). The scale measures the occurrence (TESS Occurrence scale) and distress (TESS Distress scale) of each of the items. For the occurrence, the respondent answers yes/no to each item, and every “Yes” is scored with 1 point and every “No” with 0 points. For those items that the respondents have experienced, they indicate how distressing the item has been for them on a scale from 1 (not at all) to 5 (extremely). The items that received a 0 for occurrence were also coded as 0 on the TESS Distress scale. It is possible to calculate the total score of the TESS scale as well as separate scores for TESS Occurrence and TESS Distress scales separately (Elal & Slade, 2005).
In this study, the TESS Occurrence score was calculated by summing up all the scores to each TESS Occurrence item (1 for “Yes” and 0 for “No). The TESS Distress score was calculated by summing up the scores (1 to 5) given to each TESS Distress item. Additionally, separate scores were calculated for each dimension or subscale (e.g., TESS Occurrence Resource Loss, TESS Distress Resource Loss) by using the same system.
Previous studies have shown an adequate internal consistency of the TESS Occurrence scale with a Cronbach's alpha of .78 and of the TESS Distress scale with a Cronbach’s alpha of .84. (Elal & Slade, 2005). Cronbach’s alphas of the TESS Occurrence and Distress scales in the current study were all in the range between .8 and .9 and considered to be good (see Table 3).
8.3.4 Primary care PTSD screen (PC-PTSD-5). The primary care PTSD screener
called PC-PTSD-5 (Prins et al., 2016) was used to measure the prevalence of PTSD symptoms. The scale includes 5 items that are consistent with DSM-5 criteria for PTSD. These 5 items are yes/no questions regarding the trauma’s impact over the past month. A cut-point of 3 “Yes” answers is suggested to be used as indicative for probable PTSD (Prins et al., 2016). In this study, the PTSD questions were related to the participant’s experience of the flood, e.g. “had nightmares about the flood or thought about the flood when you did not want to?” Every item that was responded to with “Yes” was coded with number 1 and statements with the answer “No” were coded with 0. The total score of the scale was calculated by summing up the scores for all 5 items.
study Cronbach’s alpha of the scale was <.5 and considered unacceptable (see Table 3). Therefore, the scale was not included in further analyses.
8.3.5 Patient health questionnaire (PHQ-9). The Patient Health Questionnaire (PHQ-9;
Kroenke, Spitzer, & Williams, 2001) was used to measure depression. The 9 items on the scale are taken from the criteria of depression in the Diagnostic and Statistical Manual of Mental Health Disorder, Fourth Edition (DSM-IV, Kroenke et al., 2001). The respondents answered each item based on their experience over the past 2 weeks, on a scale from 0 = Not at all, 1 = Several days, 2 = More than half of the days, to 3 = Nearly every day. A total score of the scale was calculated by summing up the score for each item. The total score can be used to categorize the severity of depression as follows: 0-4 = None-minimal, 5-9 = Mild, 10-14 = Moderate, 15-19 = Moderately severe, 20-27 = Severe (Kroenke et al., 2001).
The internal consistency of the PHQ-9 has shown to be good in a primary care study including 580 patients, with a Cronbach's alpha of .89. The scale also showed test-retest reliability of .84 within 48 hours, and that it discriminates well between persons with and without major depression (Kroenke et al., 2001). Cronbach’s alpha of the PHQ-9 in the current study was questionable, within the range between .6 and .7 (see Table 3).
8.3.6 Generalized anxiety disorder scale (GAD-7). To measure anxiety, the
Generalized Anxiety Disorder scale (GAD-7; Spitzer, Kroenke, Williams, & Löwe, 2006) was used. The respondents answered 7 items that are based on the DSM-IV symptoms of GAD. Scores are based on their experience over the past 2 weeks, on a scale from 0 = Not at all, 1 = Several days, 2 = More than half of the days, to 3 = Nearly every day. A total score of the scale was calculated by summing up the scores for each item. The total score can be used to categorize the severity of anxiety as follows: 0-4 = Minimal, 5-9 = Mild, 10-14 =
Moderate, 15-21 = Severe. A score of 10 and higher indicates a cut-point for the identification of a GAD patient (Spitzer et al., 2006).
8.3.7 Coping self-efficacy scale (CSES). The 26-item Coping Self-Efficacy Scale
(CSES; Chesney et al., 2006) was used to measure the perceived ability to cope with hardship. The 26 items are categorized into three subscales of different coping strategies: problem-focused coping, stop unpleasant emotions and thoughts, and get support from friends and family. The respondents answered, “When things aren’t going well for you, or when you’re having problems, how confident or certain are you that you can do the
following” regarding each of the 26 items. Each item was rated on a 11-point scale from 0 = cannot do at all, 5 = moderately certain can do to 10 = certain can do. By summing up the scores for all items, an overall CSES score was created. Participants had to answer a minimum 80 percent of the items to receive a score. The scores range from 0 to 260, and higher scores on the scale indicate higher CSE (Chesney et al., 2006).
Yanes, Humphreys, McInerney-Leo, and Biesecker (2017) found the scale to have a Cronbach's alpha .94 in a population of 62 parents of children with an undiagnosed disease (Yanes et al., 2017). Cronbach’s alpha of the CSES in the current study was within the range of .8 to .9 and considered to be good (see Table 3).
8.4 Statistical Analyses
All analyses were carried out with the IBM SPSS Statistics 25 software. First, the internal consistency of each scale was measured by calculating their Cronbach’s alphas. George and Mallery´s (as cited in Ustun & Tracey, 2020) rules of thumb were used in this study to determine the thresholds of internal consistency, i.e., unacceptable (alpha < .5), poor (.5 ≤ alpha < .6), questionable (.6 ≤ alpha < .7), acceptable (.7 ≤ alpha < .8), good (.8 ≤ alpha < .9) and excellent (alpha ≥ .9). Scales that measured a Cronbach’s alpha of <.5 were
unacceptable and, therefore, not included in the statistical analyses.
Next, a Kolmogorov-Smirnov test of normality assumptions (Steinskog, Tjøstheim, & Kvamstø, 2007) was conducted for all the remaining scales.
Due to the non-normal distribution of the variables (scores of scales), the non-parametric Spearman’s rank correlation (rs) was used to analyze the correlations between all the scales (TESS Occurrence, TESS Distress, CSES, PHQ-9, and GAD-7).
9. Results
Descriptive data regarding the demographic questions and the frequency of individuals having experienced different types of natural disasters are presented in Table 1. All of the respondents had experienced the flood in 2019 and a majority of the respondents were
married (83%) and illiterate (53%). The majority followed the Hindu religion (97%) and were of Madhesi Dalit (64%) ethnicity.
Table 1
Demographics of the Sample in Siraha, Province 2, Nepal (N=105)
Characteristic n (%) Characteristic n (%)
Gender Occupation
Female 42 (40.0) Agriculture 61 (58.1) Male 63 (60.0) Student 15 (14.3) Marital status Daily labor 13 (12.4) Married 88 (83.8) Service 3 (2.9) Single 16 (15.2) Business 4 (3.8) Other 1 (1.0) Other 9 (8.6) Religion Current living status
Hindu 97 (92.4) Living in my own house 101 (96.2) Buddhist 0 (0.0) Living displaced from my home 4 (3.8) Christian 1 (1.0) Family type
Muslim 7 (6.7) Joint family 72 (68.6) Other 0 (0.0) Nuclear family 33 (31.4) Ethnicity Facilities in my home b
Brahman/Chettri 0 (0.0) Toilet 67 (63.8) Madhesi janajatis 18 (17.1) Drinking water 79 (75.2) Madhesi Dalit 68 (64.8) Electricity 80 (76.2) Madhesi 17 (16.2) Access to health services
Other 2 (1.9) Health check-up 53 (50.5) Education Household monthly income
Illiterate / no education 56 (53.3) No response 34 (32.4) Primary a 19 (18.1) ≤ 10.000 NPR 33 (31.4)
Secondary a 3 (2.9) > 10.000 NPR 38 (36.2)
SEE a 8 (7.6) Health
+ 2 a 5 (4.8) I feel healthy 97 (92.4)
+ 2 or above a 14 (13.3) I do not feel healthy 8 (7.6)
Place of residence Natural disasters experienced b
Countryside 102 (97.1) Earthquake 101 (96.2) City 3 (2.9) Flood 105 (100.0) Bushfire 89 (84.8) Hurricane 93 (88.6) Landslide 36 (34.3) Drought 86 (81.9)
a Primary = 1-5 years, secondary = 6-8 years, SEE = secondary education examination (obligatory for
As can be seen in Table 1, all of the respondents had experienced flood. The number of times the participants had experienced floods ranged between 1-23, with a mean of 4.4 (SD = 4.3).
The number and percentage of participants who had experienced any of the various stressors due to the flood (as measured with the dimensions or subscales of the TESS Occurrence scale) are reported in Table 2.
Table 2
Number and Percentage of Participants Having Experienced Various Stressors Due to the Flood (as Measured with the TESS Occurrence Scale)
Dimension of TESS Occurrence n (%) Resource Loss/Being in Need (6 items) 91 (86.7) Damage to Home and Goods (3 items) 69 (65.7) Personal Harm (5 items) 58 (55.2) Concern of Significant Others (6 items) 80 (76.2) Exposure to the Grotesque (4 items) 84 (80.0)
Total score 105 (100.0)
Table 3 shows the internal consistency and descriptive statistics for each scale.
Table 3
Internal Consistency (Cronbach’s alpha) of Used Scales, Mean, SD, Theoretical, and Actual Range of Scores Measure Cronbach’ s alpha Mean (M) SD Theoretical range Actual range
TESS Occurrence Scale .80 9.17 4.76 0-24 1-23 Recourse Loss/Being in Need .64 3.02 1.77 0-6 0-6 Damage to Home and Goods .60 1.23 1.10 0-3 0-3 Personal Harm .69 1.16 1.40 0-5 0-5 Concern for Significant Others .57 1.96 1.53 0-6 0-6 Exposure to the Grotesque .51 1.80 1.26 0-4 0-4 TESS Distress Scale .83 27.48 16.79 0-120 1-79 Recourse Loss/Being in Need .71 8.93 6.37 0-30 0-27 Damage to Home and Goods .66 3.85 3.97 0-15 0-15 Personal Harm .65 3.30 4.17 0-25 0-19 Concern for Significant Others .53 5.67 4.82 0-30 0-21 Exposure to the Grotesque .59 5.73 4.65 0-20 0-17
PC_PTSD_5* .37 2.90 1.27 0-5 0-5
PHQ-9 .63 9.13 4.07 0-27 0-17
GAD-7 .53 7.35 3.26 0-21 0-19
CSES .87 128.54 32.42 0-260 56-225
The prevalence of depression and anxiety symptomology (as measured with PHQ-9 and GAD-7) are reported in Table 4.
Table 4
Prevalence of Symptoms of Depression and Anxiety in the Sample
Clinical Outcome n (%) Depression Symptomology None-minimal (0-4) 16 (15.2) Mild (5-9) 38 (36.2) Moderate (10-14) 40 (38.1) Moderately Severe (15-19) 11 (10.5) Severe (20-27) 00 (00.0) Anxiety Symptomology None-minimal (0-4) 23 (21.9) Mild (5-9) 59 (56.2) Moderate (10-14) 21 (20.0) Severe (15-21) 2 (1.9)
Table 5
Spearman’s Rank Correlation Coefficients Between the Scales
Measure PHQ-9 GAD-7 CSES
1. TESS Occurrence Total .070 .130 .012
2. TESS Occurrence - Resource Loss/Being in Need .115 .137 .000
3. TESS Occurrence - Damage to Home and Goods .088 .162 -.057
4. TESS Occurrence - Personal Harm .028 .090 -.173
5. TESS Occurrence - Concern for Significant Other .016 .056 .088
6. TESS Occurrence - Exposure to the Grotesque -.056 .065 .253**
7. TESS Distress Total -.010 .109 .196*
8. TESS Distress - Resource Loss/Being in Need .052 .115 .151
9. TESS Distress - Damage to Home and Goods .057 .144 .037
10.TESS Distress - Personal Harm -.034 .088 -.101
11. TESS Distress - Concern for Significant Other -.041 .013 .175
12. TESS Distress - Exposure to the Grotesque -.123 -.003 .313**
13. PHQ-9 .546** -.281**
14. GAD-7 .546** -.079
15. CSES -.281** -.079
16. Number of Experienced Floods .206* .062 .004 *. Correlation is significant at the 0.05 level (2-tailed)
**. Correlation is significant at the 0.01 level (2-tailed)
10. Discussion
In this study, victims of the traumatic event of a flash flood that hit a Nepalese village in the summer of 2019 were investigated. The first aim of the study was to investigate trauma severity and its associations with symptoms of flood related PTSD, depression, and anxiety. The second aim was to examine the associations between CSE and symptoms of PTSD, depression, and anxiety.
In the current sample, all participants had experienced the flood. And of the five different dimensions of traumatic experiences (as measured with TESS), the highest occurrences were reported for the categories of “resource loss/being in need" (86%), “exposure to the
grotesque” (80%), and “concern of significant other” (76%). A majority of the respondent had experienced severe outcomes from the flood, such as need of aid, experiencing other people suffer, and unable to locate family members.
The mean score of the TESS Occurrence in this study was nearly the same as Schwind et al. (2019) found in their earthquake sample in Nepal. The TESS Distress mean score was lower in the current study with 27.48 (SD = 16.79) when compared to Schwind et al. (2019) sample (with a mean score of 39.2; SD = 15.1).
Results from the depression screening in the current sample indicated that 85% of the participants had symptoms of mild to moderately severe depression and 78% had symptoms of mild to severe anxiety. When comparing to Schwind et al. (2019) study, these results are higher than the depression rates from the earthquake in Nepal. Anxiety levels in this sample (82%) were also higher than those from the Bhandari et al. (2018) earthquake sample (46.7%).
It was predicted that the current study would find a positive correlation between trauma severity and symptoms of depression (Hypothesis 2) and anxiety (Hypothesis 3). The results of this study did not support either hypothesis. This could be explained by the fact that TESS Distress scores were rather low, indicating that the respondents were not in that much distress by the flood. It seems that the participants have rather high levels of both depression and anxiety, but that this is related to other factors and not specifically to the flood.
to more adaptive coping behaviors. This could make them more resilient to stress and less likely to develop stress-induced psychopathology, such as depression (Brown et al., 2012; Philip et al., 2013; Rodkjaer et al., 2014; Viana Machado et al., 2020).
Due to the unacceptable internal consistency of the scale measuring symptoms of flood-related PTSD (PC-PTSD-5), it was not possible to use the scale in any of the analyses. As a result, it was not possible to test hypotheses one (H1) and four (H4). The unacceptable internal consistency could be caused by the fact that the scale consisted of only five items with
dichotomous yes/no answers, which can be problematic in small samples. Other possible explanations of this can be translation issues or the cultural perception of the items. Unexpectedly, exploratory analyses showed that CSES was positively correlated with TESS Distress and with the dimension of “exposure to the grotesque” regarding both
occurrence and distress. Presumably, it should be the other way around, i.e., high CSE should be associated with less distress in the face of stressors. Speculatively, it could be that the respondents had experienced high distress even though they possessed higher CSE. Or it could be that individuals with high experience of distress have evolved and come out from these experiences with higher CSE. This can be linked to posttraumatic growth, which includes personal growth and increased well-being after a traumatic event (Tedeschi & Calhoun, 2004). Interestingly, Schwind et al. (2019), who studied a sample that had experienced an earthquake in Nepal, also showed that resilience was positively correlated with the categories of “exposure to the grotesque”.
Exploratory analyses also showed associations between the number of times the participants had experienced floods and depressive symptoms. This is in line with research showing that cumulative effects of trauma exposure are linked to more psychiatric disorders and increased likelihood of persistent depressive symptoms (Suliman et al., 2009; Tanskanen et al., 2004). The multiple experiences of re-occurring floods could also be one factor that differentiates the results of this study from Schwind et al. (2019) study, as earthquakes have not regularly occurred in their sample in the same way as floods have re-occurred in Siraha. Also, both depression and GAD are common comorbid diseases to PTSD, and thus, one can speculate that it reflects a possible high prevalence of PTSD in this sample.
Although it is not possible to know why there were such high levels of psychopathology in the sample, some implications can be discussed. The knowledge of whether the
common mental disorders (Lund et al., 2010). Furthermore, the great majority of the
participants had not just only experienced floods many times, but also other natural disasters. Over 80% of the sample had experienced earthquakes, hurricanes, bushfires, and droughts at least one time previous to this study. This repeated exposure to severe traumatic events can be one explanation for the high levels of psychopathology in the sample. As previously described in the thesis, the cumulative experiences of severe stressors can lead to allostatic overload, with consequences like a dysregulation of the HPA-axis and elevated stress hormones, such as cortisol and norepinephrine. This can lead to alterations in the structure, function, and connectivity of brain areas and circuits linked to e.g., depression- and anxiety disorders (Bremner, 2006; McEwen, 2008; McEwen et al., 2015; McEwen, 2017). MDD has been linked to decreased volume of the hippocampus, which negatively affects its function in the negative feedback mechanism and may lead to continued hyperactivity of the HPA-axis (Hamilton et al., 2008; Treadway et al., 2015; Zhu et al., 2014). MDD and GAD have both been linked to decreased connectivity between the PFC and the amygdala which negatively affects the top-down control (Lui et al., 2011; Qiao et al., 2017). Increased functional connectivity within the SN, including the amygdala and insula, is exhibited in individuals with GAD. Lastly, enhanced connectivity within the DMN is present in both MDD and GAD (Li et al., 2018; Sheline et al., 2010; Qiao et al., 2017).
There were some limitations to the current study that must be mentioned and taken into consideration. Unfortunately, due to COVID-19 the data collection had to be cut short, which meant that the data could not be collected from the intended number of participants. As Sapolsky (2015) argues, a big sample size is necessary when investigating the vulnerability and resilience to stress because of the variation in the individuals’ perception and
interpretation of stressors. Due to the sample being relatively small and a convenience
sample, these results cannot be generalized, although they are interesting and can be explored further.
The second limitation has to do with the questionnaires. Due to COVID-19 the data collection had to be performed earlier than planned, and the time was not enough to finish the back-translation of the questionnaire package before the departure for the data collection in Siraha. As a result, the correctness of the translation could not be controlled for as planned. Despite all the precautions and steps that were taken in order to guarantee a correct
questionable internal consistency of the PHQ-9 scale. It is also important to note that these scales are created in a Western cultural context, which can create a lack of understanding of some questions when using them in an Asian cultural context. Answering and understanding the questions regarding mental health can be problematic in a Nepalese sample. In the current sample, half of the participants were illiterate, therefore possibly making it harder for these respondents to answer the question with numbers on a scale properly. Also, there is a higher degree of stigma to “illnesses of the mind” that has been seen to be closely linked to a lack of awareness about mental illness and symptoms (Brenman, Luitel, Mall, & Jordans, 2014). In addition, the questionnaire was conducted via an interview and this could affect the answers since it is not entirely anonymous, like an online survey would be. Therefore, the answers could be biased because the respondents were possibly not comfortable enough to be honest in the interview.
Another limitation is that there was an eight-month gap between the occurrence of the flood and the participants answering the questionnaire regarding their experiences. As mentioned previously, distorted memories from the traumatic event can occur since both amygdala and hippocampus can exhibit maladaptive functioning in the encoding of memories during the trauma (Bremner, 2006; Gonzalez & Martinez, 2014; Sapolsky, 2015; Stevens et al., 2017). This could have impacted the way in which the respondents answered to the TESS scale in this study.
11. Conclusion
The aim of this study was to investigate how trauma severity and CSE are associated with symptoms of PTSD, depression, and anxiety in Nepalese villagers who had experienced the traumatic event of a flash flood. Key findings from this study showed that individuals with higher CSE experienced fewer depressive symptoms. Given the high rates of depression in the current sample and in Nepal in general, this implies that CSE may prove to be a
protective factor for depression. Future studies should directly investigate this and also investigate possible interventions aimed at enhancing CSE and whether such interventions can reduce symptoms of depression. Lastly, exploratory analyses showed associations between repeated flood experiences and more depressive symptoms. It would therefore be important for the country of Nepal to conduct longitudinal studies to understand whether and how natural disasters, including floods, make it more likely for individuals to report
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