Consistent with prior research (e.g., Dierker et al., 2001
), we found that greater family loading of mood and anxiety disorders and substance-related disorders were associated with the subsequent development of greater posttraumatic stress symptoms, extending previous findings with our use of a prospective design. A novel contribution of this study is that peritraumatic distress to the officers’ worst critical incident experienced during the first year of police service was an important mediator of these relationships. This is consistent with the model that vulnerability for PTSD is expressed via increased peritraumatic arousal responses, leading to greater fear conditioning and overconsolidation of traumatic memories (Koenen et al., 2002
; Pitman, Shalev, & Orr, 2000
). We also found that general symptoms of emotional distress during training were another significant mediator between family history of mood and anxiety disorders and posttraumatic stress symptoms. This finding is not surprising given that problems in prior adjustment have been found to predict PTSD in other research (Ozer et al., 2003
). Interestingly, peritraumatic responses accounted for significant variability even after considering prior symptomatology in the model.
Our findings emphasize the important role of emotional regulation at the time of a traumatic stressor, in the prevention of subsequent distress. Emotional dysregulation may be transmitted among members of a family in a number of ways. While our use of the family history method did not include genotyping, several genetic markers for PTSD (e.g., polymorphisms in FKBP5 (Binder et al., 2008
; Koenen et al., 2005
)) and for associated brain abnormalities (e.g., serotonin transporter gene (Hariri et al., 2002
; Pezawas et al., 2005
)) have been proposed. Further, family dynamics and relationships may be impacted by the turning of attention, either positive or negative, to the affected individual. (Bremner, 2002
; Pitman et al., 2001
In addition to biological mechanisms, sociocontextual variables also influence the development of emotional regulation skills. Parents play a particularly important role as they are responsible for the direct care of the child and typically serve as a protector and a role model. Recruits raised by parents who had difficulty regulating emotional responses during stress may have had fewer opportunities to learn effective emotion regulation skills (Cole et al., 1994
). Officers with affected family members may have received inadequate social support, an important stress buffer, from family members during childhood and they may not have learned how to seek out or effectively use other potential sources of support later in their lives. Further, having a sibling with a psychological disorder can impact family dynamics by drawing greater attention, either positive or negative, from parents to the affected sibling, influencing relationships between officers, their parents, and their siblings.
In addition, children of individuals with psychiatric disorders or addictions may be exposed to more traumatic events because of risky or abusive parental behaviors (e.g., Koenen et al., 2007
; Yehuda, Halligan, & Grossman, 2001
). Our results highlight the importance of examining the role of prior cumulative trauma exposure in such models, specifically in association with familial mood, anxiety, and substance-related disorders as well as general distress and PTSD symptoms. Although distress and symptoms were relatively lower than typically seen in other populations, prior cumulative civilian trauma exposure before academy training was associated with more general emotional distress during the academy, perhaps in response to the stress of training, and recruits with greater prior cumulative civilian trauma exposure were more vulnerable when exposed to subsequent critical incidents during the first year of police service. Officers with more prior cumulative civilian trauma exposure who were initially resilient may have had some degree of sensitization by repeated exposure to critical incident stress related to police work. A sensitization hypothesis was supported by a study of emergency service personnel involved in the clean up and recovery of an major airline crash (Dougall, Herberman, Delahanty, Inslicht, & Baum, 2000
). In this study, more prior exposure to trauma that was dissimilar from rescue work was associated with greater distress symptoms and intrusive thoughts at 2, 6, 9 and 12 months after the crash, and greater urinary catecholamine levels at 12 months after the crash. Biological studies conducted in more symptomatic populations have suggested that early life trauma exposure leads to prefrontal cortex damage via stress-related hormonal alterations (De Bellis et al., 1999
; Nelson & Carver, 1998
), resulting in dysregulated stress responsivity to future traumatic events (De Bellis et al., 1999
; Perry, 1995
). Our group has previously found that police recruits with childhood trauma had greater emotion modulated startle reactivity to startling sounds (Pole et al., 2007
) and greater catecholamine responses to a laboratory stressor (Otte et al., 2005
) during academy training. While less symptomatic, it is possible that police recruits who experience repeated trauma and ongoing chronic occupational and familial stress may have similar stress related biological alterations that may influence risk for the development of posttraumatic stress symptoms to later trauma exposure. Future research should consider a finer analysis of prior trauma characteristics that may explain a potential differential impact on peritraumatic reactivity as well as biological underpinnings of increased vulnerability in these police officers.
Another possibility is that prior cumulative civilian trauma exposure may have increased risk for future trauma exposure. We found a trend suggesting a relationship between prior cumulative civilian trauma exposure and greater distress during academy training, greater exposure to life-threatening critical incidents, greater peritraumatic distress, and posttraumatic stress symptoms. Koenen suggested that individuals with an overly reactive amygdala and impairments in emotional processing may also have difficulties with stimulus registration and the assessment of threat (Fox, 1994
; Koenen, 2006
), potentially increasing the likelihood that they are exposed to dangerous situations. Previous research also suggests that impulsivity or sensation-seeking, a potentially inherited trait, could increase risk of exposure to trauma and PTSD (Koenen, 2006
; McLeod et al., 2001
Prior research has also suggested that substance abusers (and potentially those at high risk for substance abuse) have heightened stress reactivity and turn to substances to dampen their reactivity to stress (Jacobsen, Southwick, & Kosten, 2001
). Our findings partially support this possibility since family history of addictions was associated with greater posttraumatic stress symptoms and this was mediated through peritraumatic distress to officers’ worst critical incident over the first year of police work. However, a lack of relationships between alcohol use and family history of drug and alcohol use disorders or posttraumatic stress symptoms, contradicts prior research conducted in other trauma-exposed populations (e.g., McFarlane et al., 2009
; Prescott & Kendler, 1999
; Stewart, 1996
). We may have been unable to detect these relationships due to minimal alcohol use during academy training and at 12 months, which suggest that alcohol use does not play an important role in this sample at this time. Low rates of alcohol use may be a result of self-selection into law enforcement, underreporting, and rigorous police academy screening and continual monitoring of alcohol and substance use.
Our study was limited in that the family history method did not allow us to determine whether family effects were due to genetics versus shared environmental influences. It also relies on recruit reports of their relatives functioning. While a more ideal method would be to personally interview family members about their symptoms, we interviewed largely asymptomatic recruits prior to critical incident exposure, which would have likely mitigated potential recall biases associated with current distress (Milne et al., 2008
It is notable that even though most officers experienced life-threatening exposure to critical incident stressors, PTSD symptoms scores were positively skewed. Despite a restricted range in symptomatology, we had adequate variability in posttraumatic symptomatology to detect significant relationships after only one year of police service. There are several reasons that symptom reports were relatively low and only 3% of the sample had full or subsyndromal PTSD at the 12-month assessment, based on the PCL-S. Because police officers are a self-selected group, carefully screened by the police academies, and trained to manage life threat exposure, it is a particularly resilient population, and as a result the generalizability of our findings to other trauma-exposed populations may be limited. In addition, emergency services personnel have been noted to underreport symptoms (Wagner et al., 1998), perhaps due to bravado, concerns about confidentiality and potential impact on job security and advancement. Further, it is possible that individuals with higher levels of symptomatology may have dropped out of the study or police service. While our sample is seemingly resilient, they are early in their careers. Research in officers at later stages in their careers suggest that police are at heightened risk for posttraumatic distress symptoms, chronic stress, burnout and stress-related health problems due to the nature of their repeated exposure to stress and violence extended over their careers (Pole, 2008
). Police officers assessed at mid-career had rates approximating 5% for full PTSD and an additional 2% for subthreshold PTSD; full criteria for PTSD were found in 15% of retired police officers (Pole, 2008
). In addition, we acknowledge that our measure of PTSD (i.e., PCL-S) was designed to capture symptoms related to a single focal event and is not a cumulative measure; thus, it may not capture symptoms related to other critical incidents or traumatic experiences that may have occurred in civilian life.
Despite these potential limitations, to our knowledge, this is one of the first studies to examine the impact of family history on posttraumatic stress symptoms using a prospective design, while considering historical variables systematically measured prior to exposure to a focal trauma, trauma characteristics, and peritraumatic emotional reactivity. These data provide initial support for a model in which peritraumatic reactivity mediates the relationship between pre-exposure family history risk factors and the development of critical incident related posttraumatic stress symptoms. Given that those with family disorders are at heightened risk for peritraumatic distress which in turn increases risk for developing posttraumatic stress symptoms, interventions to reduce peritraumatic distress including stress inoculation during training and as soon as possible after critical incident exposure will likely benefit at risk police officers. It will be important to evaluate the possibility that familial factors may increase risk for peritraumatic reactivity and posttraumatic stress symptomatology in other trauma-exposed populations. Given the critical function that police serve in our society, it is of great importance to better understand the early processes that lead to the development of symptoms that may incubate over time and could result in psychiatric distress and dysfunction at later stages in their careers.