پاسخ عاطفی به چالش بیولوژیکی به عنوان یک تابع از اختلال پانیک و سیگار کشیدن
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31605||2004||13 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Anxiety Disorders, Volume 18, Issue 1, 2004, Pages 19–32
The present investigation evaluated anxious and fearful responding to bodily sensations as a function of panic disorder (PD) and smoking status. Participants completed a voluntary hyperventilation procedure that elicits panic-relevant bodily sensations. Psychophysiological data were collected throughout the study procedures. Assessments of anxiety and bodily distress were conducted pre-challenge baseline, post-hyperventilation, and during a recovery period following the challenge. Results indicated that smokers with PD reported greater levels of anxiety and bodily distress than smokers without PD and than nonsmokers with PD at the post-challenge assessment and recovery period. No differences in autonomic responding were evident during the challenge or in the recovery phase. In terms of rate of recovery, the linear decrease in anxiety, but not bodily distress, was significantly more steep for nonsmokers with PD than for smokers with PD. These findings are discussed in relation to better understanding the potential role that smoking may play in terms of anxious and fearful responding to bodily sensations.
There has been a long-standing recognition that rates of cigarette smoking are greater among persons with psychopathology compared to rates of smoking in persons with no history of psychopathology. To date, most of the investigations in this domain have focused on individuals with schizophrenia, alcohol and drug dependencies, and depressive disorders (e.g., Black, Zimmerman, & Coryell, 1999; Burling & Zift, 1988, Hall et al., 1995 and Merikangas et al., 1998). More recently, researchers have found a strong association between cigarette smoking and a history of panic attacks (Amering et al., 1999; Degenhardt, Hall, & Lynskey, 2001; McCabe et al., this issue; Pohl, Yeragani, Balon, Lycaki, & McBride, 1992). In a recent epidemiologic study (>4000 respondents), for example, Lasser and colleagues (2000) found that smokers were significantly more apt to have a history of panic attacks compared to nonsmokers. These findings are consistent with other epidemiologic data (Breslau, Kilbey, & Andreski, 1991; De Graaf, Bijl, Smit, Vollebergh, & Spijker, 2002) and studies using samples from treatment clinics (Hayward, Killen, & Taylor, 1989; Himle, Thyer, & Fischer, 1988; Norton, Cox, & Malan, 1992). The observed associations between smoking and panic attacks do not appear to be due to sociodemographic characteristics, comorbid psychiatric conditions (e.g., major depressive disorder, alcohol dependence), or symptom overlap in diagnostic criteria for panic attacks and nicotine dependence (see Zvolensky et al., 2003, Zvolensky et al., 2003 and Zvolensky et al., 2003). Recent studies suggest that cigarette smoking is associated with increased risk for developing panic psychopathology (Breslau & Klein, 1999, Goodwin & Hamilton, 2002 and Kandel et al., 1997). For instance, Johnson et al. (2000) investigated the longitudinal association between cigarette smoking and anxiety disorders among adolescents and young adults using a community-based sample (n=688). Heavy smoking (≥20 cigarettes per day) during adolescence was associated with higher risk of developing agoraphobia and panic disorder (PD) during early adulthood even after controlling for a variety of theoretically-relevant factors (e.g., alcohol and other drug use, parental history of psychopathology, childhood temperament). In this same investigation, there was no evidence that anxiety disorders during adolescence were associated with an increased risk of chronic cigarette use in young adulthood. These findings support earlier reports that the direction of the smoking-panic association is most likely to be from smoking to panic ( Amering et al., 1999, Breslau & Klein, 1999 and Pohl et al., 1992), although other alternative hypotheses (e.g., a third factor—negative affect—contributes to both; see Goodwin & Hamilton, 2002) still need to be ruled out. Zvolensky et al., 2003, Zvolensky et al., 2003 and Zvolensky et al., 2003 recently examined the extent to which smoking is associated with prototypical panic-related processes in an epidemiologically-defined sample of smokers from Russia. Results indicated that smoking status (cigarettes per day) significantly predicted indices of panic-specific distress (e.g., level of agoraphobic avoidance), but not general anxiety symptoms. These findings are consistent with past research that suggests smoking is most strongly related to panic-like symptoms (e.g., bodily vigilance; Zvolensky et al., 2003, Zvolensky et al., 2003 and Zvolensky et al., 2003; Zvolensky, Forsyth, Fuse, Feldner, & Leen-Feldner, 2002; Zvolensky, Schmidt, & McCreary, 2003), and to a relatively lesser extent, generalized anxiety symptoms (Breslau & Klein, 1999, Goodwin & Hamilton, 2002 and Johnson et al., 2000; McCabe et al., this issue). Moreover, the combination of high levels of anxiety sensitivity and smoking predicted agoraphobic avoidance even after controlling for problem alcohol use and negative affect. These findings suggest anxiety sensitivity may moderate the relation between level of smoking and certain panic psychopathology processes. The extant literature on smoking and panic has thus far relied exclusively on studies conducted in naturalistic settings. Although the findings across such investigations have been generally consistent (see Zvolensky et al., 2003, Zvolensky et al., 2003 and Zvolensky et al., 2003, for a review), laboratory-based tests are a useful next research step for several reasons. First, a laboratory approach provides a controlled environment whereby extraneous sources of variance can be removed or held constant. Second, such a laboratory approach has the distinct advantage of using concurrent as opposed to retrospective observational tactics, and in so doing, helps remove the concern that the findings are due to a variety of reporting errors common to emotional processesing (e.g., recall biases; see McNally, 1994, pp. 105–136). Third, laboratory preparations that reliably induce psychophysiological responses and symptoms that closely mirror the experience of panic allow investigators to link smoking to the phenomenon of panic. Finally, the laboratory provides an opportunity for a multi-modal, “on-line” observation of emotional responding, thereby reducing concerns about method variance. A critical and heretofore unaddressed question is to what extent smoking is associated with emotional reactivity to, and recovery from, bodily perturbation among individuals with PD. If smoking is a factor that is associated with heightened emotional vulnerability to bodily sensations, then it may be a relevant variable to target in the treatment and relapse prevention of PD. Research suggests that regular smoking may increase the likelihood of emotional reactivity to bodily sensations (Breslau & Klein, 1999). We therefore hypothesized that persons with PD who smoke compared to persons with PD alone and to smokers with no psychiatric history would respond with greater levels of anxiety and bodily distress during laboratory-induced physical stress. Given that smoking also can be associated with impaired recovery from physical stress, we hypothesized that persons with PD who smoke, as compared to persons with PD alone and to smokers with no psychiatric history, would demonstrate retarded recovery from somatic distress following laboratory-induced bodily sensations.