Studies using ambulatory monitoring in smokers not assessed for psychiatric disorders, however, have also supported the relationship between negative affect and relapse (Shiffman et al., 1996). In addition to important roles of self-efficacy AZD-2281 and affective states, physiological factors could lead to increased smoking lapse in PTSD. The hypothalamic-pituitary-adrenal (HPA) axis has been implicated in models of smoking onset and maintenance in PTSD (Rasmusson, 2006). Smoking behavior appears to be associated with changes in dehydroepiandrosterone (DHEA) and its sulfated metabolite DHEA(S), which are neuroendrocrine hormones on the HPA axis. Smoking a cigarette results in a significant increase in DHEA/DHEA(S) (Mendelson, Sholar, Goletiani, Siegel, & Mello, 2005), and regular smokers exhibit increased baseline DHEA/DHEA(S) levels (Baron, Comi, Cryns, Brinck-Johnsen, & Mercer, 1995).

Physiological models of resilience suggest that DHEA/DHEA(S) has important protective effects against stress (Kroboth, Salek, Pittenger, Fabian, & Frye, 1999). This proposal is supported by the positive effects of DHEA/DHEA(S) on coping in individuals with PTSD (Rasmusson et al., 2004; Yehuda, Brand, Golier, & Yang, 2006) and on decreased negative affect in individuals with depressive disorders (Wolkowitz et al., 1999). The contributions of self-efficacy, affective states, and physiological disruption to smoking lapse are illustrated in Figure 1. Figure 1. Model of posttraumatic stress disorder (PTSD) and smoking onset and maintenance.

Further research is needed to characterize the smoking lapse process and investigate lapse occasions using real-time ecological momentary assessment (EMA) methods to minimize retrospective recall bias in psychiatric and situational lapse antecedents. In this study, we hypothesized that (a) the presence of PTSD, lower self-efficacy, and quit date decrease in DHEA/DHEA(S) would be related to shorter time to lapse, (b) smokers with PTSD would be more likely than those without PTSD to cite negative affect and trauma reminders as causes of a smoking lapse, and (c) relative to baseline levels, DHEA/DHEA(S) would decrease on the quit date and would interact with PTSD, such that the decrease in DHEA/DHEA(S) would be larger in the PTSD group. METHODS Participants Participants were smokers with PTSD (n = 52) and a group with no current Axis I psychiatric disorders (n = 55).

Eligibility criteria included smoking at least 10 cigarettes daily for the past year, willingness to make a smoking cessation attempt, and age between 18�C65. Participants meeting criteria for current alcohol or other substance abuse or dependence, current psychotic Cilengitide disorder (including schizophrenia), or bipolar disorder with active manic symptoms were excluded from both groups.