Prospective associations between cannabis use, abuse, and dependence and panic attacks and disorder

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Abstract

The present study prospectively evaluated cannabis use, abuse, and dependence in relation to the development of panic attacks and panic disorder. Participants at the start of the study were adolescents (n = 1709) with a mean age of 16.6 years (SD = 1.2; time 1) and were re-assessed 1 year later (time 2) and then again as young adults (time 3; mean age = 24.2 years, SD = 0.6). Results indicated that cannabis use and dependence were significantly prospectively associated with an increased odds for the development of panic attacks and panic disorder. However, cannabis was not incrementally associated with the development of panic after controlling for daily cigarette smoking. The theoretical and clinical implications of these findings are discussed.

Introduction

Cannabis is one of the most commonly used recreational drugs in the United States (US) and beyond (Office of Applied Studies (SAMHSA), 2001, Rey et al., 2002). For example, approximately 4% of adults have used cannabis in the past year and rates of cannabis abuse and dependence are on the rise (Compton et al., 2004). These data are noteworthy given empirical evidence that cannabis use, aside from being linked to negative physical health and social outcomes (Ameri, 1999, Cohen, 1981, Lehman and Simpson, 1992, Lynskey and Hall, 2000), may be related to certain psychological symptoms and conditions (Green and Ritter, 2000, Tunving, 1985).

Panic attacks have historically been linked to cannabis use (Gale and Guenther, 1971). This work was initially stimulated by the observation that cannabis use may acutely promote heightened levels of anxiety symptoms and elicit panic attacks under certain conditions or among certain individuals (Hall et al., 1994, Hollister, 1986, Szuster et al., 1988, Thomas, 1996, Tunving, 1985). Subsequent studies have strengthened confidence that (a) more frequent cannabis use and/or (b) more severe cannabis problems may be related to an increased risk of panic attacks. For example, Hathaway (2003) found that among weekly users of cannabis (n = 104), approximately 40% reported having had at least one panic attack related to such use. These prevalence rates are noteworthy in light of lifetime rates of panic attacks among the general population of approximately 5–8% (Katerndahl and Realini, 1993). Although methodological differences in the assessment of panic attacks may hinder comparisons across studies, the limited study suggests the possibility of a cannabis-panic linkage. Increasing confidence in the generalizability of these types of associations, a recent study involving a representative sample (n = 4745) found that a lifetime history of cannabis dependence, but not use or abuse, was related to an increased risk of panic attacks after covarying the effects of polysubstance use, alcohol abuse, and demographic variables (Zvolensky et al., 2006). This work also is supported by other investigations showing that daily or weekly users of cannabis report greater levels of symptoms of somatic tension and arousal such as feeling dizzy compared to nonusers (Bonn-Miller et al., 2005, Milich et al., 2000, Pickard et al., 2000, Thomas, 1996) and cognitive dyscontrol symptoms (e.g., depersonalization; Dannon et al., 2004, Mathew et al., 1993, Troisi et al., 1998, Zvolensky et al., 2006). The nature of the direction(s) of the putative cannabis-panic association is as of yet unknown from the extant empirical research.

Overall, a growing corpus of evidence collectively suggests that heavier patterns of use or more severe forms of cannabis use problems (e.g., dependence) are related to increased risk of panic attacks. Yet, existing studies on this topic are limited in a number of key respects. Perhaps most notably, the vast majority of investigations evaluating cannabis-panic associations utilized cross-sectional designs. These cross-sectional studies, by definition, cannot explicate temporal order of onset between cannabis and panic attacks, and by extension, it is not possible to differentiate possible risk factor effects from concomitants or consequences. Only prospective studies that test whether putative risk factors predict the subsequent onset of panic attacks can achieve this aim. Unfortunately, of the limited number of prospective tests involving evaluations of cannabis in terms of psychiatric conditions, panic attacks have not been assessed (Block et al., 1991, Fergusson et al., 1996). A second key limitation of past work is that none of the previous studies have tested whether the association between cannabis and panic is not simply attributable to cigarette smoking. This limitation is unfortunate, as there is a strong association between cannabis use and its disorders and cigarette smoking (Degenhardt et al., 2001, Degenhardt et al., 2003). Moreover, daily cigarette smoking is related to an increased risk of panic attacks (Zvolensky and Bernstein, 2005, Zvolensky et al., 2005). A final limitation of past work is that the previously reported association between cannabis dependence and panic attacks may simply be accounted for by a comorbid pattern of more severe non-cannabis drug dependence (Ross et al., 1988). Specifically, because individuals with more severe cannabis use problems (i.e., abuse and dependence) are more likely to have problems with other substances as well as be more prone to psychological problems (Kessler et al., 1997, Regier et al., 1990), it is possible non-cannabis drug dependence could account for the documented association between cannabis dependence and panic attack.

The aim of the present study was to provide a prospective test evaluating cannabis use, abuse, and dependence in relation to the development of panic attacks and panic disorder. Participants at the start of the study were adolescents (n = 1709) with a mean age of 16.6 years (SD = 1.2; time 1 [T1]) and were re-assessed 1 year later (time 2; [T2]) and then again as young adults (time 3 [T3], mean age = 24.2 years, SD = 0.6; see Method section for details). It was hypothesized that cannabis dependence, but not use or abuse, would prospectively predict an increased risk for panic attacks and panic disorder after controlling for non-cannabis drug dependence and daily cigarette smoking. These hypotheses were collectively driven by past work indicating that more severe or problematic forms of cannabis use are particularly associated with panic symptoms and psychopathology (Zvolensky et al., 2006).

Section snippets

Participants

Participants were a subset of individuals from the Oregon adolescent depression project. Participants were originally randomly selected from nine senior high schools in western Oregon. All participants consented to participate in the investigation. A total of 1709 adolescents (ages 14–18; mean age at initial assessment = 16.6 years, SD = 1.2) completed the initial assessment (T1), which consisted of an interview and questionnaires, between 1987 and 1989. Approximately 1 year later (T2), 1,507

Results

See Table 1 for prospectively measured lifetime base-rates of the studied predictor and dependent variables. In terms of the covariates, 20.9% (n = 315) of the sample met criteria for lifetime history of daily cigarette smoking at T2. 1.9% (n = 29) of the sample met criteria for a lifetime history of non-cannabis drug dependency on one or more substances at T2. In terms of the cannabis use variables, 43.4% (n = 695) met criteria for a positive history of cannabis use, 2.3% (n = 34) of the sample met

Discussion

Based on cross-sectional studies, research has suggested an association between cannabis and panic attacks (Thomas, 1996, Zvolensky et al., 2006, Zvolensky et al., 2006). The present study builds from such work and offers novel empirical insight into the nature of cannabis-panic associations from a longitudinal perspective.

Partially consistent with expectation, cannabis use and dependence were prospectively associated with increased odds for the development of panic attacks and panic disorder.

Conflict of interest statement

No author has any conflict of interest to report.

All authors contributed to and have approved the final manuscript.

Role of funding source

This paper was supported by National Institute on Drug Abuse research grants (1 R01 DA018734-01A1, R03 DA16307-01, and 1 R21 DA016227-01) awarded to Dr. Zvolensky. Dr. Bernstein acknowledges that this work was supported in part by VA Office of Academic Affairs and Health Services Research and Development Service Research funds.

Acknowledgements

This paper was supported by National Institute on Drug Abuse research grants (1 R01 DA018734-01A1, R03 DA16307-01, and 1 R21 DA016227-01) awarded to Dr. Zvolensky. Dr. Bernstein acknowledges that this work was supported in part by VA Office of Academic Affairs and Health Services Research and Development Service Research funds.

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