The purpose of this paper was to review and to integrate research that has examined associations between the affective dimensions of Watson and Clark's tripartite model of anxiety and depression and smoking variables. Generally, univariate studies suggested that all three of the tripartite dimensions consistently associated with smoking status. By contrast, the relationship of tripartite dimensions to nicotine dependence and smoking heaviness and chronicity among daily smokers was mixed, but more commonly showed modest or no relationship. This pattern could be interpreted as evidence that any type of affective disturbance may be a risk factor or consequence of smoking, regardless of the severity of smoking behavior. However, once daily tobacco use is established, individual differences in affective disturbance (of any type) may not be an influential factor on the severity of smoking behavior. Low PA and anhedonia evidenced consistent univariate relationships with difficulty maintaining abstinence and stronger craving in tobacco deprived and nondeprived smokers. More research is needed to clarify whether AA and NA are linked with cessation and craving.
Multivariate analyses suggest that the tripartite affective dimensions may have multiplicative (amplifying) effects on smoking behaviors, such that having emotional disturbance on multiple dimensions (i.e., high NA and low PA, Wills et al., 1999
; high NA and high AA, McLeish et al., 2009
) may result in disproportionate increases in smoking risk. Analyses of the unique versus overlapping effects of multiple affective dimensions tend to indicate that low PA and anhedonia are unique and robust risk factors for smoking status, relapse, and craving above and beyond other affective dimensions, whereas NA and AA were not consistently associated with smoking status or relapse after accounting for the influence of PA or anhedonia. Accordingly, low-PA or anhedonic individuals (especially those with concurrent NA or AA) should perhaps be targeted as a high-risk group in prevention and cessation interventions. Furthermore, given findings suggesting a unique relationship between low PA, anhedonia, and relapse, interventions which successfully raise PA and hedonic capacity following cessation may potentially be most effective at buffering relapse during cessation.
It is important to note that although low PA and anhedonia have overlapping features and are both specific to depression, these constructs also have distinct characteristics. Accordingly, anhedonia and PA may perhaps have a multifaceted impact on smoking involving both shared and discrete effects. Both anhedonic and low-PA smokers may share the tendency to smoke in order to increase global PA and counteract withdrawal-related reductions in PA (Leventhal et al., 2008
; Leventhal, Waters, et al., 2009
; Cook et al., 2007
). By contrast, the propensity to use nicotine in order to enhance one's ability to respond more pleasurably to environmental rewards may be specific to anhedonic smokers (Cook et al., 2007
) and potentially not present among low-PA smokers who are normally hedonic. These possible distinctions may be important for the development of prevention and cessation interventions as treatments may have to target slightly different areas (i.e., reduced global PA vs. inability to respond pleasurably to rewards) to be effective for the anhedonic individual versus the normally hedonic individual with low PA. However, future research is required to elucidate the types of interventions that could be deployed to target these underlying appetitive mechanisms.
Applying the tripartite model to understand the comorbidity of emotional disorders and smoking can shed light on the reasons why certain mental health disorders are associated with smoking. The documented pattern of univariate and multivariate findings in this review suggests that depressive disorders are related to certain aspects of smoking because of: (a) common variance shared by NA, low PA, and anhedonia (e.g., Leventhal et al., 2008
); (b) specific variance in PA and anhedonia that is unique from NA (e.g., Leventhal et al., 2008
; Zvolensky, Stewart, et al., 2009
; Leventhal, Waters, et al., 2009
); and (c) concomitant high NA and low PA, which multiplicatively increases smoking vulnerability (Wills et al., 1999
). Thus, low PA and anhedonia (either alone or in combination with high NA) may perhaps underlie a significant portion of the link between depression and aspects of smoking behavior. Drawing conclusions about the reasons why anxiety disorders are associated with smoking is perhaps more difficult because of the heterogeneity of anxiety disorders (e.g., panic disorder vs. generalized anxiety disorder) and the lack of multivariate studies in the smoking literature that have explored the concomitant influence of AA and NA. Nonetheless, preliminary evidence suggests that individuals who experience symptoms or fear of AA and also have high NA may account for a significant portion of the relationship between anxiety and aspects of smoking behavior (McLeish et al., 2009
; Zvolensky et al., 2006
; Zvolensky, Bernstein, et al., 2007
There are some limitations in the literature exploring the role of tripartite affective dimensions in smoking and the scope of this review. While studies of the univariate relations of affective dimensions to smoking are becoming more common, research examining relations to certain clinically relevant aspects of smoking behavior (e.g., craving, relapse) is limited and should be targeted in future research. Similarly, studies exploring the concomitant and interactive effects of multiple tripartite dimensions is rare but is nonetheless needed to tease apart the complex interplay of affective disturbance factors in smoking vulnerability. Furthermore, a large number of studies in this review were cross-sectional, which precludes definitive conclusions regarding the temporal features of these relationships and highlights the need for additional research using prospective designs. Additionally, the tripartite model is based on underlying traits that account for heterogeneity in affective disturbance. However, several of the studies included in the review used state measures collected at only one time point and thus may not be reflective of trait disturbances. Finally, although identifying which affective dimensions are linked with specific aspects of the tobacco dependence syndrome will shed light on the underpinnings of smoking behavior, exploration of biobehavioral mechanisms that mediate the influence of affect on smoking will ultimately be of greatest value. Such data are critical for advancing theory regarding the affective basis of tobacco dependence and guiding the development of more refined and effective interventions for smokers with affective disturbance.