Brief reportBasal and suppressed salivary cortisol in female Vietnam nurse veterans with and without PTSD
Introduction
As a unifying concept, post-traumatic stress disorder (PTSD) was intended to capture a universal response to any life-threatening event. Consequently, studies examining biological alterations in PTSD have not typically included subgroup analyses addressing whether the type of trauma exposure, chronicity of the PTSD, or other individual difference factors might explain heterogeneous biological findings (Yehuda, 2002, Yehuda, 2006). And, yet, the type of event to which the person has been exposed is (among other things) a potential source of individual variability that might explain different biological phenotypes in this disorder.
The earliest biological investigations in PTSD were performed in combat veterans, who seemed to be a prototypic PTSD group in that their symptom manifestations appeared to generalize to survivors of other types of traumatic exposures. The first published neuroendocrine study demonstrated significantly lower 24-h mean urinary cortisol excretion in Vietnam combat veterans with PTSD compared with veterans with other psychiatric disorders (Mason et al., 1986). To determine whether low cortisol levels reflected altered regulation of the hypothalamic-pituitary-adrenal axis, studies using the low dose dexamethasone suppression test (DST) were performed. Most found evidence for an exaggerated suppression of cortisol following 0.50 mg dexamethasone (DEX), reflecting a greater negative feedback inhibition in PTSD (reviewed in Yehuda, 2002).
With subsequent studies, discrepant observations about cortisol levels and, to a lesser degree, the cortisol response to DEX administration, emerged. Generally, evidence for lower basal urinary and plasma cortisol, and increased plasma cortisol suppression on the DST, has come from studies that compared relatively homogeneous PTSD and trauma-exposed groups (e.g., combat veterans, Holocaust survivors, victims of domestic violence, adult survivors of childhood sexual abuse, and children exposed to earthquakes) (e.g., Yehuda, 2002, Yehuda, 2005, Yehuda, 2006, Bremner et al., 2007, Heim et al., 2001, Griffin et al., 2005), whereas negative findings were more likely in studies in which more heterogeneous or epidemiological samples have been compared with a control group consisting of non-trauma-exposed persons without PTSD (Wessa et al., 2006, Young and Breslau, 2004a, Young and Breslau, 2004b, de Kloet et al., 2007). It may be that in the latter studies the “noise” associated with individual differences in gender, PTSD duration, type of exposure, and/or age overwhelms the neuroendocrine “signal” associated with PTSD. Alternatively, previously reported neuroendocrine correlates of PTSD might actually reflect specific PTSD risk factors. Consequently, the reliability and generality of cortisol findings is difficult to ascertain due to the sometimes substantive sample differences between studies that produce differing results.
Gender, in particular, is a potentially important mediator/moderator of basal cortisol levels and hyper-suppression of cortisol. There is some evidence suggesting that gender may be an important variable in differentiating different cortisol-related phenotypes. For example, Gill et al. (2005) observed that studies of male veterans have more consistently supported lower cortisol in PTSD than studies of females. However, studies of men have typically involved more chronic PTSD, thereby confounding gender and chronicity. The confounding of gender, trauma heterogeneity and PTSD chronicity makes it difficult to test which of these variables, or their combinations, contribute to cortisol alterations in PTSD.
The present study examined basal cortisol and cortisol suppression in a unique, homogeneous sample of female nurse veterans who served in Vietnam. This group closely paralleled previously studied male Vietnam combat veterans with respect to age at time of trauma (early adulthood), exposure to the culture of the Vietnam War experience, time elapsed since trauma, and duration of PTSD (30 + years). We hypothesized that female nurse Vietnam veterans with PTSD would show lower basal cortisol and higher cortisol suppression compared with nurse veterans without PTSD.
Section snippets
Participants
Mailings about the study were sent out to women all across the United States whose names appeared on the Women's Vietnam War Memorial database. Interested persons completed the Women's Wartime Stressor Scale (WWSS; Wolfe et al., 1993) for screening purposes (see Carson et al., 2000) and were flown to the Manchester, VA Medical Center if they met initial inclusion/exclusion criteria. Women were not invited to participate if it was determined during screening that they had current or past
Results
Participants were classified into current PTSD (Current, N = 40) vs. never-had PTSD (Never, N = 43) based on the CAPS results. Current co-morbid Axis I disorders for nurses with current PTSD included 14 major depressive, 4 dysthymic, 5 panic, 2 agoraphobic, 5 social phobic, 6 specific phobic, 1 obsessive compulsive, 1 undifferentiated somatoform, and 2 binge eating. Current disorders for nurses who never met criteria for PTSD included 1 major depressive, 1 dysthymic, 1 social phobic, and 3 specific
Discussion
The present study found no significant differences in cortisol levels as measured in morning and afternoon samples in nurses with current PTSD compared with those without any (current or lifetime) PTSD, and no cortisol hyper-suppression following administration of 0.50 DEX. The inclusion of depression as a covariate in the statistical model eliminated the trend for elevated baseline cortisol levels in the PTSD group when the two cortisol samples were considered together. These findings differ
Acknowledgements
This research was supported by a Department of Veterans Affairs Health Services Research and Development Service Award (Dr. Carson), a Department of Veterans Affairs Medical Research Service Award (Dr. Orr), and National Institute of Mental Health Grant #RO3MH57386 (Dr. Metzger).
The authors thank Heike Croteau, Karen Sheldon, and Pauline Simard for assistance in the implementation of this project. Finally, appreciation is owed to the Vietnam Women's Memorial Project, Inc., for support, and to
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Dr. Metzger died February 9, 2008.