This week we discuss my favorite topic and personal passion: traumatic stress. There is no way we can discuss traumatic stress without discussing the disorder that may develop after experiencing such stress – Post-Traumatic Stress Disorder (PTSD). PTSD is now listed under the Trauma and Stress-related disorders in the DSM-5. In order for an individual to meet DSM-5 criteria for PTSD, they need to have experienced a traumatic event in which they were exposed to death, threatened death, natural disasters, and other events. Additionally, an individual needs to have experienced a certain amount of symptoms in each of the four symptom clusters. These symptoms clusters include intrusion symptoms, avoidance symptoms, negative alterations in cognitions and mood, and alterations in arousal and reactivity. Lastly, all symptoms must be present for at least one month and cause significant distress or functional impairment (APA, 2013).
Close to 75% of the general population will experience a traumatic event at least once in their lifetime (Breslau and Kessler, 2001). However, only 8% of the general population will go on to develop PTSD after experiencing a traumatic event (Kessler et al., 2005). Much research has been conducted to understand why some people are more susceptible to developing the disorder than others. A review conducted by Yehuda and LeDoux (2007) examined risk factors for developing PTSD, brain structures that are important in the disorder, altered fear processing and regulation, and genetics. In this review, we learn that interpersonal violence as compared to other traumatic events is more potent stressors. Additionally, we learn the neurological mechanisms that underlie the disorder. The hippocampus plays a role in memory processes and contextual fear conditioning (Shin, 2006) and is smaller in individuals with PTSD. Additionally, the amygdala is important in the acquisition and expression of conditioned fear, while the prefrontal cortex is important in inhibiting the amygdala’s response to conditioned fear when appropriate too. In PTSD, it seems there is an inability for the prefrontal cortical structures to inhibit the amygdala from responding to conditioned associations, leading to many of the symptoms associated with the disorder.
While having the disorder alone can be debilitating, many impairments also stem from having the disorder. The general public and veterans with PTSD are more prone to developing health problems such as obesity, hypertension, and heart disease (Kibler et al. 2008; Cohen et al. 2009b). We delve more into this topic in two readings this week. The first, a review (meta-analysis-ish) that discusses physical activity and eating disorders in relation to the disorder written by Hall and colleagues (2014). In this review, we learn that in regard to physical activity, some studies state that there is a decrease of activity in PTSD, while other studies report no differences. Furthermore, there is also mixed findings for inactivity in PTSD. Some studies have found that an increase in PTSD symptoms leads to a decrease in physical activity. This review also examines PTSD and eating behaviors, specifically if PTSD was a predictor of eating disorders. Some studies have shown a higher prevalence of PTSD symptoms in women who engaged in binge eating, those with PTSD are more likely to eat fast food and drink soda and eat fewer servings of fruit in a day. In all, this review provides a large amount of information on the relationship between PTSD and physical activity/eating habits. However, the studies presented show much inconsistency and mixed findings that it is hard to make a conclusion with such data.
A study conducted by Kubzansky and colleagues in 2014 examined if PTSD alters the trajectory of weight gain in a sample of women. To do this, the authors had women who were originally a part of an ongoing prospective study of female registered nurses, complete the Trauma and PTSD Screening Questionnaire (a retrospective measure) was used to determine which women would be eligible to take part in the study and when trauma exposure/PTSD occurred. In order to assess trauma and PTSD, the authors used a variety of retrospective measures. Additionally, they asked women to report their weight biennially. Ultimately, the author’s results showed that symptoms of PTSD were associated with faster weight gain and increased risk of obesity in women.
The way I would like to end this post is with some implications. Schnurr (2015) brings up many important implications in her article that discuss how traumatic exposure can lead to physical health decline. When speaking to research, she stresses the importance of integrating efforts to reduce health risk behaviors with treatment. For example, we can start using exercise in addition to cognitive behavioral treatment in order to reduce obesity rate and PTSD symptoms in the disorder. Additionally, many clinicians need to read the research that is out there on physical health and PTSD in order to shape treatment to the individual patient. Lastly, as a whole, we need to be aware of how traumatic exposure can affect individuals differently. For example, the current events in Las Vegas have left many people in attendance traumatized. We as a society should do everything we can to make sure the individuals who experienced the event are mentally well taken care of. Most people experience a traumatic event and do not talk about the event for months, increasing their likelihood of developing symptoms of the disorder. Clinicians and others should make sure to make themselves available for such publicised traumatic events.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders : DSM-5(5th ed.). Arlington, VA: American Psychiatric Association.
Bresleu, N., and Kessler, R.C. (2001). The stressor criterion in DSM-IV posttraumatic stress disorder: an empirical investigation. Biol. Psychiatry, 50, 699-704.
Cohen, B.E., Marmar, C., Ren, L., Bertenthal, D., and Seal, K.H. (2009b). Association of cardiovascular risk factors with mental health diagnoses in Iraq and Afghanistan war veterans using VA health care. JAMA, 302, 489-491.
Hall, K.S., Hoerster, K.D., and Yancy, W.S. (2015). Post-traumatic stress disorder, physical activity, and eating behaviors. Epidemiologic Reviews, 37, 103-115.
Kessler, R.C., Chiu, W.T., Demier, O., and Walters, E.E. (2005). Prevalence, severity, and comorbidity of twelve-month DSM-IV disorders in the National Comorbidity Survey Replication (NCS-R). Arch. Gen. Psychiatry, 62, 617-627.
Kibler, J.L., Joshi, K., and Ma, M. (2008). Hypertension in relation to posttraumatic stress disorder and depression in the US National Comorbidity SurBehavioralioral Medicine, 34, 125-131.
Kubzansky, L.D., Bordelois, P., Jin Jun, H., Roberts, A.L., Cerda, M., Bluestone, N., Koenen, K.C. (2014). The weight of traumatic stress a prospective study of posttraumtic stress disorder symptoms and weight status in women. JAMA Psychiatry, 71(1), 44-51.
Schnurr, P.P. (2015). Understanding pathways from traumatic exposure to physical health. Evidence Based Treatments for Trauma-Related Psychological Diosrders: A Practical Guide for Clinicians. U. Schnyder, M. Cloitre (eds.).
Shin, L.M., Rauch, S.L., and Pitman, R.K. (2006). Amygdala, medial prefrontal cortex, and hippocampal function in PTSD. Ann. N.Y. Acad. Sci., 1071, 67-79.
Yehuda, R., and Ledoux, J. (2007). Response variation following trauma: A translational neuroscience approach to understanding PTSD. Neuron, 56, 19-32.