- Email: [email protected]
abuse and anxiety sensitivity
Addictive Behaviors 26 (2001) 935 – 946
Substance use/abuse and anxiety sensitivity What are the relationships? G. Ron Norton Department of Psychology, University of Winnipeg, Winnipeg, Manitoba, Canada
Abstract The eight articles in this special issue on anxiety sensitivity (AS) and substance abuse provide provocative new information on the relationships, or lack of relationships, between AS and several types of substance use and abuse. The eight articles provide data that extend our understanding of the role of AS in substance abuse with younger people, people who use substances other than alcohol, people who have disorders comorbid with substance use disorders, and people who experience chronic headaches. In addition, one of the articles attempts to determine how AS develops in relationship to parental substance abuse. Finally, several of the studies show that the three Anxiety Sensitivity Index (ASI) subscales (physical concerns, social concerns, and psychological concerns) are uniquely associated with different aspects of substance use/abuse. Each of the articles is discussed as to its merits and potential domains that may require additional research. Finally, several general suggestions are provided for new directions that research on the relations of AS and substance use/abuse should take. D 2001 Elsevier Science Ltd. All rights reserved. Keywords: Anxiety sensitivity; Anxiety sensitivity index
Anxiety sensitivity (AS), as measured by the Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986) consists of three lower-order factors: fear of bodily sensations (physical concerns), fear of publicly observable behaviors (social concerns), and fear of loss of cognitive control (psychological concerns). As assessed with the 16-item ASI (Peterson & Reiss, 1992), AS tends to be stable over time (Peterson & Plehn, 1999). AS has also been shown to be a robust and reliable predictor of anxiety (e.g., Taylor, Koch, & McNally, 1992), panic attacks (e.g., Schmidt, Lerew, & Jackson, 1997), problems associated with low-back pain (Asmundson & Norton, 1995), and alcohol/drug use (Stewart, Samoluk, & MacDonald, 1999), amongst other problematic behaviors (see Taylor, 1999). 0306-4603/01/$ – see front matter D 2001 Elsevier Science Ltd. All rights reserved. PII: S 0 3 0 6 - 4 6 0 3 ( 0 1 ) 0 0 2 4 4 - 1
936
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
The eight papers in this series address relationships between AS and various aspects of substance use and abuse. These studies add to an already large corpus of research showing that many aspects of substance use are associated with high scores on the ASI (see review by Stewart et al., 1999). Although the relationship between AS and alcohol abuse, especially in the context of negative coping styles, has been generally well validated (e.g., Stewart et al., 1999), far less is known about how AS relates to the use of other substances. The eight studies in this series address relations with several drugs in addition to alcohol, including the role of AS in the use and abuse of marijuana, pain medication, and cigarettes. A greater understanding of the mechanisms leading to initial substance use, inappropriate substance use, and effective treatment models are necessary. Martin (2001) cited a recent study by the Lewin Group, a health policy research and management consulting firm in the US, in which it was estimated that the annual economic cost of alcohol and drug abuse is more than US$240 billion. About US$97 billion is due to drug abuse. This estimate includes abuse treatment, prevention costs, health care, costs due to reduced job productivity, or lost earnings, crime, and welfare. In spite of these alarming costs, a recent report from the Center for Substance Abuse Treatment showed that two-thirds of Americans with serious substance abuse treatment needs are not being treated (Martin, 2001). Even though alcohol and other substances have been used and abused for thousands of years, it is obvious that we still lack in our understanding of the factors influencing substance use and why some people misuse substances. Research, including the current set of studies on the relationships between AS and substance use/abuse, may greatly increase our understanding of why at least some people misuse substances. A better understanding of factors influencing maladaptive substance use will greatly improve our ability to treat and prevent substance abuse. This would markedly decrease the horrible personal and social costs of substance abuse. The articles in the present series suggests that we unfortunately still have much to learn about how personality dimensions, reasons for using substances, and other factors, such as negative affectivity, influence substance use. If AS and related constructs can be reliably shown to predict heavy substance use or substance use for inappropriate reasons (e.g., coping with distress), it is likely that we can begin to develop more effective models of substance use and abuse and, possibly, interventions for treating people who are abusing. Even more importantly, this knowledge may help us prevent substance use from escalating into abuse or dependence. I will review each of the eight papers in this special issue with the purpose of describing important contributions made by each study. I will also attempt to identify areas that may require further clarification. Finally, I will address several general issues related to the relationships between AS and substance use/abuse and provide some general guidelines for future research in the area. DeHaas, Calamari, Bair, and Martin (2001, this volume) address several important questions. First, what is the relationship between AS and reasons for using substances, when reasons are defined in terms of the types of situations in which the person most often uses substances? Second, is the relationship between AS and substance abuse the same with people only diagnosed with a substance abuse disorder compared to those who have an additional anxiety or mood disorder, as well? Finally, is the relationship between AS and substance use merely secondary to the relation of AS to trait anxiety?
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
937
Because of the very high comorbidity between substance abuse and anxiety disorders (Cox, Norton, Swinson, & Endler, 1990), and because AS is elevated in people with almost all anxiety disorders (Taylor et al., 1992), it is possible that the association between AS and substance abuse is spurious. It is possible that the relationship between AS and substance abuse may be, in reality, a relationship between AS and anxiety disorders. This seems unlikely, however, in light of the findings of DeHaas et al. (2001, this volume). First, they confirmed that ASI scores were significantly correlated with substance use in negative situations (e.g., unpleasant emotions) but not in positive situations (e.g., pleasant times with others) as measured by the Inventory of Drug Taking Situations (Annis, Graham, & Davis, 1987). They also found that there were no differences in the relationships between AS and drinking in negative situations for participants with a dual diagnosis of substance abuse/ dependence and an anxiety disorder and those with a diagnosis of only substance abuse/ dependence. This suggests that the relationship between AS and negative situations substance use is not simply secondary to having a comorbid anxiety disorder. Nonetheless, DeHaas et al. found that there was a difference between those substance-disordered patients with a comorbid anxiety disorder and those with a comorbid mood disorder: the relationship between AS and negative situation substance use was observed only among those with a comorbid anxiety disorder. This pattern of findings makes the conclusion of a lack of involvement of comorbid anxiety disorders in explaining the relationship of AS to negative situation substance use much more tentative. Other findings by DeHaas et al. (2001) suggest that the relationship between AS and substance use is not secondary to relations of AS to trait anxiety. They found, using hierarchical regression analyses, that AS contributed additional variance to drinking in negative situations when the Trait subscale of the State Trait Anxiety Inventory (Spielberger, Gorsuch, Luchene, Vagg, & Jacobs, 1983) was entered first. Since there is some evidence that AS may be a lower-order factor of trait anxiety (Taylor, 1995), this finding suggests that the specificity achieved by measuring this lower-order component of trait anxiety results in statistically increased precision in predicting negative situation substance use. The paper by Comeau, Stewart, and Loba (2001, this volume) evaluated the relationship of AS, trait anxiety, and sensation seeking to adolescents’ motives for using alcohol, cigarettes, and marijuana. This paper nicely extended earlier work on motives for alcohol use to a younger group of participants. In addition, Comeau et al. assessed whether the same motives for using alcohol applied to high AS adolescents’ use of cigarettes and marijuana. Motives for drinking alcohol were measured with the Drinking Motives Questionnaire-Revised (DMQ-R; Cooper, 1994). Motives for using marijuana and cigarettes were measured with the Teen Marijuana Motives Questionnaire and the Teen Smoking Motives Questionnaire—measures developed by the authors (Comeau, Stewart, & Loba, 2000), and based on the DMQ-R. The authors found that several substance use motives were correlated with the ASI. However, when they used hierarchical regression analyses (as opposed to simple bivariate correlations) the relationship between AS and motives became less clear. For example, they found coping motives for both alcohol and cigarettes were predicted by trait anxiety, but not AS. However, using alcohol and marijuana for conformity motives was predicted by AS. These findings suggest both that there may be motives common to why high AS people use different
938
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
substances, and different substances may be used for very different motivations among anxious individuals. The paper by Comeau et al. also raises the question of developmental changes in the relationships between AS and motives for using various substances. Are these relationships the same for teens as they are for adults? Longitudinal research may provide a more definitive answer to this question. Asmundson, Wright, Norton, and Veloso (2001, this volume) compared high, medium, and low AS people with chronic headaches on a variety of mood-, personality-, and pain-related measures. Asmundson and Norton (1995) had shown that high AS patients with unexplained back pain were more likely to use pain medications than were those scoring in a medium or low range on the ASI. In their present study, Asmundson et al. (2001) did not replicate these findings for use of either over-the-counter or prescription pain medications in chronic headache patients. In fact, when they used hierarchical regression analyses, they found that only the cognitive anxiety scale of the Pain Anxiety Symptoms Scale (PASS; McCracken, Zayfert, & Gross, 1993) predicted use of over-the-counter pain medications. The dimensions measured by this instrument are similar in concept to AS in that they measure fearful appraisals, but the scales of the PASS are focused on the experience of pain (as opposed to the experience of arousal-related bodily sensations which are tapped on the ASI). When Asmundson et al. looked at use of prescription medications they found that the physiological anxiety scale of the PASS and the physical concerns scale of the ASI predicted use of prescription medications. However, unexpectedly, it was people with low ASI physical concerns who were more likely to use prescription pain medications. Unfortunately, as Asmundson et al. (2001, this volume) pointed out, they measured only whether people used over-the-counter or prescription headache medication, but not how often or how much medication they used. It is possible that there is a positive relationship between AS and pain medication use frequency or amount of medication taken. This certainly appears to be so for alcohol use (see review by Stewart et al., 1999) which has central nervous system depressant effects similar to many pain medications (Arana & Rosenbaum, 2000). Finally, it would be interesting to assess the motivations for taking headache medications and relations of these motives to negative affectivity factors such as AS. It may be that people who are taking analgesic medications for negative reinforcement reasons (e.g., to escape physiological sensations of pain) may differ from those who are taking such medications for positive reinforcement reasons (e.g., to allow them to pursue pleasurable activities with which pain otherwise interferes). However, it is also possible that analgesic use in response to headache pain may be related to factors that are dissimilar to those motivating alcohol use, and dissimilar to those motivating analgesic use in response to unexplained low back pain for that matter. Future research is needed to clarify the various reasons people take medications for headaches, and whether different motivations for analgesic medication use are associated with AS. MacDonald, Stewart, Hutson, Rhyno, and Loughlin (2001, this volume) assessed the effects of alcohol and alcohol expectancies in dampening cognitive, affective, and somatic distress due a hyperventilation challenge. Some of their participants received a dose of alcohol equivalent to 4–5 drinks (‘‘alcohol’’ group), and others were falsely led to believe they received an equivalent amount of alcohol (‘‘placebo’’ group). Finally, a third group was
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
939
not led to believe they were consuming alcohol; they consumed only a control beverage (‘‘control’’ group). The participants in both the alcohol and placebo groups rated themselves as more intoxicated than did the participants in the control group. All participants were then subjected to a hyperventilation challenge where they were asked to breathe 30 times per minute for 3 min. MacDonald et al. found that during hyperventilation, affective and somatic distress as measured by the Hyperventilation Questionnaire (HVQ; Rapee & Medoro, 1994) increased less for those high AS participants who consumed alcohol compared to high AS participants in the placebo or control groups. These results suggest that the alcohol dampening effects observed among high AS participants in their previous research (MacDonald, Baker, Stewart, & Skinner, 2000) were likely due to the pharmacological effects of alcohol rather than the expectancy that alcohol would reduce distress. This dampening effect could make alcohol a powerful negative reinforcer and increase the likelihood that high AS people may drink more and more frequently to reduce distress due to bodily symptoms of anxiety and/or withdrawal symptoms (i.e., symptoms that are mimicked during hyperventilation). Two issues related to the dampening effects of alcohol on high AS participants should be explored in future studies. First, are the dampening effects specific to high AS or are they due to a more general effect of negative affectivity? To investigate this issue, future research should include, and control for, alternative negative affectivity constructs when examining the contribution of AS to sensitivity to alcohol dampening of responses to arousal-induction challenges. Secondly, the items on the HVQ may tap domains that are similar to those tapped by the ASI. To control for this potential confound, future studies may wish to obtain psychophysiological and behavioral measures of arousal and distress as well as self-report measures following challenges designed to evaluate dampening effects associated with alcohol. These additional measures may help clarify whether alcohol does, indeed, dampen somatic and/or emotional responses in high AS people during physical and emotional challenges, and whether high AS people are indeed more sensitive to such alcohol dampening effects. Kushner, Thuras, Abrams, Brekke, and Stritar (2001, this volume) address the issue of whether AS is directly or indirectly associated with alcohol use in negative situations (i.e., drinking to cope). They suggest that AS may act to accelerate anxiety, which in turn leads to alcohol use to dampen feelings of anxiety. To test for this possibility, they used mediator analysis to determine if anxiety acts as a mediator between AS and coping-motivated drinking. Mediator analysis involves a series of regressions between predictor and outcome variables. Kushner et al. assessed coping drinking motives with two instruments, Drinking for Anxiety Management (DAM; Bibb & Chambless, 1986) and Reasons for DrinkingNegative Affect (RFD-NA; Sher, Walitzer, Wood, & Brent, 1991). The two outcome measures, although both assessing drinking for coping purposes (cf. Comeau et al., 2001, this volume), differ in that the DAM focuses specifically on coping with symptoms of anxiety whereas the RFD-NA focuses on coping with negative affect symptoms, more generally. Their results partially confirm that anxiety mediates the relationship between AS and drinking for coping reasons. Specifically, Kushner et al. found that social anxiety, and to a lesser extent worry and trait anxiety, were significant mediators of the relationship of AS levels to RFD-NA scores. State anxiety, withdrawal symptoms and symptoms of other
940
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
anxiety disorders did not meet criteria as mediators. Somewhat different results were found when the authors looked at whether anxiety was a mediator between AS and DAM scores. Here, all measures of anxiety except state anxiety and withdrawal symptoms mediated between AS levels and DAM scores. The authors suggest that this discrepancy may be due to the different ways in which the two outcome instruments conceptualize and measure copingmotivated drinking. They suggest that the RFD-NA may be assessing drinking to cope with negative affect defined more broadly than with the DAM (where coping is defined as drinking to manage anxiety in particular). Although theoretically interesting, the difference in the degree to which anxiety mediates between AS and the RFD-NA vs. AS and the DAM may be less important at a practical level. Results with either outcome measure show that anxiety mediates between AS and coping-motivated drinking suggests that anxiety is an important construct in describing why high AS people misuse alcohol. As suggested by the authors (Kushner et al., 2001, this volume), this set of results suggests that we should be treating symptoms of anxiety in high AS alcoholics in order to minimize their motivation to use alcohol to cope with negative affect. Future research needs to identify potential mechanisms other than heightened anxiety that may mediate the relationship between AS and drinking to manage negative affect. If AS amplifies negative affect in coping-related drinking situations, as Kushner et al. (2001, this volume) suggest, how does it do so? And which particular lower-order AS components are most involved in this anxiety or negative affect amplification? Do AS psychological concerns (e.g., fear of losing control) increase anxiety or other negative affect? Or do AS physical concerns (i.e., fears of physical symptoms)? Future research should attempt to determine more precisely how and why AS amplifies anxiety and other negative affect in various coping-related drinking situations. Brown, Kahler, Zvolensky, Lejuez, and Ramsey (2001, this volume) evaluated the relationship between several smoking related variables, and relapse following a smoking cessation program. They hypothesized that the ASI would show positive correlations with expectations and motivations for smoking involving negative reinforcement (e.g., coping with negative affect), but not positive reinforcement reasons (e.g., pleasure and stimulation). Smoking expectancies and motives were measured with the Smoking Effects Questionnaire (SEQ; Rohsenow et al., 1992) and the Reasons for Smoking test (RFS; Ikard, Green, & Horn, 1969), respectively. Their results showed that the ASI was not correlated with either smoking rate or level of nicotine dependence as measured by Fagerstrom’s (1978) scale. However, Brown et al. (2001, this volume) showed positive correlations between the ASI and the Negative Psychological and Negative Physical Effects of the SEQ. These correlations were not expected, but are of interest as they indicate that high AS smokers may experience more of the negative psychological and physical effects of smoking, as suggested by the authors, or that they may be more sensitive to these effects when they occur. They also found positive correlations between the ASI and the Crutch subscale of the RFS and the Reduce Negative Affect subscale of the SEQ. Finally, they found that correlations between the ASI and the Beck Depression Inventory (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961) or a history of recurrent depression were not significant. This suggests that the relationship between the ASI
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
941
and negative reinforcement smoking measures was not secondary to the relation of AS to general negative affectivity. Brown et al. (2001, this volume) also evaluated the relationship between the ASI and rate of relapse following a cessation program. Their results showed that, although the ASI did not predict relapse rates after 1-week smoking cessation, it did predict relapse in the first week after treatment for people with a history of major depressive disorder. Overall, the results of the Brown et al. (2001, this volume) study show that the ASI is predictive of smoking for negative reinforcement reasons and of expectations for negative affect reduction from smoking, and that these relationships are independent of levels of addiction and depression. Their intriguing finding that ASI was also predictive of negative psychological and physical smoking expectancies should be viewed with some caution. The R2 values for the relationship of ASI to negative psychological and negative physical expectancies were only in the range of 6–8% shared variance. However, it is still possible, as Brown et al. point out, that high ASI smokers may find the psychological and physical consequences intolerable and may smoke more to reduce these feelings. This study importantly shows that smoking may have a similar relationship to AS as that seen for alcohol use, in that high AS people may smoke to reduce unpleasant affective states. Future research on the relationship between AS and smoking may benefit from a more detailed analysis of the social, psychological, and physical concern subscales of the ASI. It is possible that one or more of the subscales would be more sensitive to smoking in response to negative internal states. In addition, it would be interesting to see if affective states other than depression (e.g., anger, anxiety) mediate the relationship between ASI and measures of smoking for coping-related motives (cf. Kushner et al., 2001, this volume). Zvolensky, Feldner, Eifert, and Brown (2001, this volume) used a C02 challenge with heavy smokers ( > 20 cigarettes per day) who had, in the past, quit smoking for less than 7 days or more than 7 days. They hypothesized that participants who had not been able to quit smoking for 1 week would have higher ASI scores, show greater intolerance of physical discomfort during a preexperimental breath holding task, and display greater emotional reactivity during a C02 challenge. Their results showed that that, indeed, those who had been unable to quit smoking for at least 1 week did show greater cognitive–affective reactivity to the C02 challenge compared to those with longer periods of smoking abstinence. However, the two groups did not differ on measures of heart rate produced during the challenge, breathholding duration, or on levels of AS. The authors suggest that the ASI might not be specific enough to identify those who are intolerant of withdrawal-related bodily sensations and thus at risk for early relapse to smoking during a quit attempt, and suggest the development of a withdrawal symptom sensitivity assessment instrument for use in future research. However, because those who had greater difficulty abstaining from smoking did show greater emotional reactivity to the challenge in the Zvolensky et al. study, future research should consider including measures of negative affectivity other than AS as predictors of length of abstinence. Zvolensky et al.’s failure to find that scores on the ASI distinguish those with shorter versus longer prior successful quit attempts is particularly interesting in light of Brown et al.’s (2001, this volume) findings regarding the relations of AS and success in smoking cessation. Brown et al. showed that those who had the greatest difficulty stopping smoking during the first
942
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
week of a quitting attempt were more likely to have high ASI scores. More research is needed to explain this discrepancy in results regarding the predictive utility of ASI scores in identifying difficulties abstaining during the early stages of a smoking cessation attempt. Finally, MacPherson, Stewart, and McWilliams (2001, this volume) attempted to determine if parental problem drinking was associated with the development of high AS in their children. Their young adults participants completed several questionnaires including the ASI, Children of Alcoholics Screening Test (CAST; Jones, 1983), and the parental forms of the short form of the Michigan Alcoholism Screening Test (F-SMAST and M-SMAST; Sher & Descutner, 1986). Although both of the latter questionnaires are designed to assess aspects of parental drinking behavior, the CAST taps into a variety of factors associated with parental excessive drinking that cause distress for the child (e.g., marital discord). The F-SMAST and the M-SMAST tap more specifically into the parent’s experience with problems with alcohol use. The authors argue that if CAST scores were predictive of ASI scores, after controlling for SMAST scores, this would indicate that childhood exposure to distressing parental problem drinking behavior might contribute to the development of increased AS levels in the child. Controlling for SMAST scores controls for the possibility that AS might be transmitted genetically as part of the familial transmission of alcoholism. MacPherson et al. (2001, this volume) used hierarchical regression analyses to predict ASI subscale scores. Their results showed that when CAST scores were entered in Stage two, following SMAST and gender in Stage one, CAST scores accounted for an additional 6% of the explained variance of the psychological concerns subscale. Similarly, CAST scores accounted for an additional 3% of the explained variance of the physical concerns subscale, over-and-above that explained by SMAST scores and participant gender. When this two-step analysis was applied to the social concerns subscale of the ASI, none of the predictor variables accounted for a significant amount of variance. MacPherson et al. also evaluated whether scores on any of the three ASI subscales were mediators of the association between CAST scores and the development of anxiety disorder symptoms in the participants. Their findings suggest that the psychological concerns subscale of the ASI may serve as a modest mediator of the association between childhood exposure to distressing parental problem drinking behaviors and the development of elevated anxiety symptoms in the offspring. In sum, the results of the MacPherson et al. (2001, this volume) study suggest that increases in AS (especially AS psychological concerns) are more likely due to observing distressing behaviors associated with a parent’s excessive alcohol use, rather than being a direct (genetically mediated) result of parental alcoholism. Further, there appears to be some evidence that the ASI-psychological concerns subscale may mediate the relationship between exposure to parental problem drinking behaviors and anxiety symptoms in the adult child, including trait anxiety and uncued panic. Future research should try to identify other parental behaviors that might predispose children to developing high AS. Several areas that might be worth investigating would be parental overprotection, inconsistencies in methods of parental discipline, and marital conflict. These domains have been suggested as contributing to anxiety disorders such as obsessive–compulsive disorder (Steketee & Pruysn, 1998).
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
943
1. Conclusions The studies presented in this special issue evaluated the role of AS in the use and abuse of alcohol, cigarettes, marijuana, and analgesic medications. The results obtained in the eight studies suggest that AS likely plays a role in the use of some substances (cigarettes and alcohol) at least when motivated by a desire to control negative affective states (i.e., coping motives). Unfortunately, the evidence is mixed with some studies showing a positive correlation between AS and substance use (e.g., Brown et al., 2001, this volume) whereas other studies did not find this relationship (e.g., Asmundson et al., 2001, this volume). Interestingly, one study (i.e., Kushner et al., 2001, this volume) provided evidence that elevated anxiety might act as a mediator in explaining the relations between AS and copingrelated substance use. It appears that the strongest relationships between AS and substance use are for alcohol and, to a lesser extent, cigarette smoking. However, even here the magnitude of associations are not large, suggesting that factors other than those measured by the ASI may be important alternative or additional determinants of substance use. Researchers interested in the relationship of AS and substance use should consider three important issues in planning their future research. First, several studies (e.g., MacPherson et al., 2001, this volume) in this special issue suggest that the subscales of the ASI may be differentially predictive of various aspects of substance use behavior and the motives for using different substances. This suggests that future researchers use the subscales of the ASI rather than relying solely on the total score. It is possible that using the total score may diminish specific relationships between AS and substance use. Secondly, the study by Asmundson et al. (2001, this volume) found that the PASS (McCracken et al., 1993) was a better predictor than AS of pain medication usage in chronic headache patients. The ASI and the PASS share many similarities in that both are designed to measure fear of symptoms. The ASI has been shown to be a good measure of fear of anxiety symptoms (Reiss et al., 1986) whereas the PASS was specifically designed to measure fear of pain symptoms. It is possible that we need to consider developing a new instrument that is more specifically designed to measure fear of symptoms that may lead to substance abuse. We have good evidence from the studies in this special issue that ASI is most closely related to substance use motivated by a desire to cope with anxiety and other negative affect. We also know that negative affectivity is associated with inappropriate substance use. These findings might help direct researchers in designing an instrument that taps the personality and individual difference domains that best predict substance use and abuse. The studies in this special issue have shown that the AS construct, as measured by the ASI, demonstrates an inconsistent relationship with substance use. It would be interesting to determine if there may be more consistent relations of AS with substance use if we consider motive by substance type relationships. This type of analysis may direct our efforts to better assess the relationship between fear variables (e.g., fear of anxiety symptoms; fear of pain) and substance use. It may be that AS is the best predictor of use of some substances (e.g., arousal dampening drugs) as a result of some use motives (e.g., coping or conformity motives). Other domains may require measurement of fears more specific to substance use driven by other use motives. For example, fear of pain (as opposed to AS) may turn out to be
944
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
the best predictor of use of analgesic drugs (as opposed to anxiolytic drugs) for the purposes of coping with pain (as opposed to arousal) experiences. A third question that demands further attention is this: What causes people to have high AS? The study by MacPherson et al. (2001, this volume) is an excellent example of research directed towards identifying the determinants of AS. In a recent twin study, Stein, Jang, and Livesley (1999) estimated that approximately 45% of the variance in AS could be accounted for by genetic factors. What accounts for the additional 55%? The evidence that we do have is consistent with recent findings for anxiety which appears to result from a combination of genetic factors and early childhood experiences (Andrews, 1996). This also appears to be true of AS. Two recent studies are consistent with the MacPherson et al. results in showing that early childhood experiences are positively related to the development of high AS. Watt, Stewart, and Cox (1998) have shown that AS levels are positively related to instrumental and vicarious conditioning experiences during childhood. They also found that exposure to uncontrolled parental behaviors due to drunkenness and anger was related to the development of high AS. Similarly, Scher and Stein (1999) found that children exposed to parental threatening, hostile and rejecting behaviors were more likely to have high AS compared to children not exposed to these parental behaviors. If AS truly is an important factor in motivating at least some types of substance misuse, then research on the origins of this personality risk factor may be helpful in identifying ways of ultimately preventing substance abuse and dependence. Considering the high personal and social costs of substance abuse, it is necessary that we become more effective in determining the factors that lead to and maintain substance misuse. Research on the relationship between AS and substance use provides a good model for other types of research on the etiological and maintenance factors involved in substance use and abuse.
References Andrews, G. (1996). Comorbidity in neurotic disorders: the similarities are more important than the differences. In: R. M. Rapee (Ed.), Current controversies in the anxiety disorders ( pp. 3 – 20). New York: Guilford. Annis, H. M., Graham, J., & Davis (1987). Inventory of drinking situations. Toronto, ON: Addictions Research Foundation. Arana, G., & Rosenbaum, J. (2000). Handbook of psychiatric drug therapy. Philadelphia, PA: Williams & Wilkin. Asmundson, G. J. G., & Norton, G. R. (1995). Anxiety sensitivity in patients with physically unexplained chronic back pain. Behaviour Research and Therapy, 33, 771 – 777. Asmundson, G. J. G., Wright, K. D., Norton, P. J., & Veloso, F. (2001). Anxiety sensitivity and other emotional traits in predicting headache medication use in patients with recurring headaches: implications for abuse and dependency. Addictive Behaviors (this volume). Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for measuring depression. Archives of General Psychiatry, 4, 561 – 571. Bibb, J. L., & Chambless, D. L. (1986). Alcohol use and abuse among diagnosed agoraphobics. Behaviour Research and Therapy, 24, 49 – 58. Brown, R. A., Kahler, C. W., Zvolensky, M. J., Lejuez, C. W., & Ramsey, S. E. (2001). Anxiety sensitivity: relationship to negative affect smoking and smoking cessation in smokers with past major depressive disorder. Addictive Behaviors (this volume).
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
945
Comeau N., Stewart, S. H., & Loba, P. (2000). Adolescents’ motives for smoking and marijuana use: factor structure and relations to motives for alcohol use. In Stewart, S. H. (Chair), New research on human motivations for alcohol use. Symposium conducted at the 3rd Joint Meeting of the British Experimental Psychology Society and the Canadian Society for Brain, Behaviour, and Cognitive Sciences, Cambridge, UK, June. Comeau, N., Stewart, S. H., & Loba, P. (2001). The relations of trait anxiety, anxiety sensitivity, and sensation seeking to adolescents’ motivations for alcohol, cigarette, and marijuana use. Addictive Behaviors (this volume). Cooper, M. L. (1994). Motivation for alcohol use among adolescents. Psychological Assessment, 6, 117 – 128. Cox, B. J., Norton, G. R., Swinson, R. P., & Endler, N. S. (1990). Substance abuse and panic-related anxiety: a critical review. Behaviour Research and Therapy, 28, 385 – 393. DeHaas, R. A., Calamari, J. E., Bair, J. P., & Martin, E. D. (2001). Anxiety sensitivity and drug or alcohol use in individuals with anxiety and substance use disorders. Addictive Behaviors (this volume). Fagerstrom, K. O. (1978). Measuring the degree of physical dependence to tobacco smoking with reference to individualization of treatment. Addictive Behaviors, 3, 235 – 241. Ikard, F. F., Green, D. E., & Horn, D. (1969). A scale to differentiate between types of smoking related to the management of affect. International Journal of the Addictions, 4, 649 – 659. Jones, J. W. (1983). The Children of Alcoholics Screening Test (CAST). Chicago, IL: Camelot Unlimited. Kushner, M. G., Thuras, P., Abrams, K., Brekke, M., & Stritar, L. (2001). Anxiety mediates the association between anxiety sensitivity and coping-related drinking motives in alcoholism treatment patients. Addictive Behaviors (this volume). MacDonald, A. B., Baker, J. M., Stewart, S. H., & Skinner, M. (2000). The effects of alcohol on the response to hyperventilation of participants high and low in anxiety sensitivity. Alcoholism: Clinical and Experimental Research, 24, 1656 – 1665. MacDonald, A. B., Stewart, S. H., Hutson, R., Rhyno, E., & Louglin, H. L. (2001). The roles of alcohol and alcohol expectancy in the dampening of responses to hyperventilation among high anxiety sensitivity young adults. Addictive Behaviors (this volume). MacPherson, P. S. R., Stewart, S. H., & McWilliams, L. A. (2001). Parental problem drinking and anxiety disorder symptoms in adult offspring: examining the mediating role of anxiety sensitivity components. Addictive Behaviors (this volume). Martin, S. (2001). Most substance abusers aren’t getting treatment. Monitor on Psychology, 32, 11. McCracken, L. M., Zayfert, C., & Gross, R. T. (1993). The pain anxiety symptom scale: development and validation of a scale to measure fear of anxiety. Pain, 50, 67 – 73. Peterson, R. A., & Plehn, K. (1999). Measuring anxiety sensitivity. In: S. Taylor (Ed.), Anxiety sensitivity: theory, research and treatment of the fear of anxiety ( pp. 61 – 81). Mahwah, NJ: Erlbaum. Peterson, R. A., & Reiss, S. (1992). Anxiety sensitivity manual (2nd ed.). Worthington, OH: International Diagnostics Systems. Rapee, R. M., & Medoro, L. (1994). Fear of physical sensations and trait anxiety as mediators of the response to hyperventilation in nonclinical subjects. Journal of Abnormal Psychology, 103, 693 – 699. Reiss, S., Peterson, R. A., Gursky, D. M., & McNally, R. J. (1986). Anxiety sensitivity, anxiety frequency and the prediction of fearfulness. Behaviour Research and Therapy, 24, 1 – 8. Rohsenow, D. J., Abrams, D. B., Colby, S. M., Gulliver, S. B., Niaura, R. S., & Monti, P. M. (1992). Smoking Effects Questionnaire: development and psychometric properties. Poster presented at the annual meeting of the Association for Advancement of Behavior Therapy, Boston, MA, November. Scher, C. D., & Stein, M. B. (1999). Developmental antecedents of anxiety sensitivity. (Summary) In: Program and abstracts of the 19th National Conference of the Anxiety Disorders Association of America ( pp. 86 – 87). Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1997). Prospective evaluation of anxiety sensitivity in the pathogenesis of panic: replication and extension. Journal of Abnormal Psychology, 106, 532 – 538. Sher, K. J., & Descutner, C. (1986). Reports of parental alcoholism: reliability across siblings. Addictive Behaviors, 11, 25 – 30. Sher, K. J., Walitzer, K. S., Wood, P. K., & Brent, E. E. (1991). Characteristics of children of alcoholics: putative risk factors, substance use and abuse, and psychopathology. Journal of Abnormal Psychology, 100, 427 – 448.
946
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
Spielberger, C. D., Gorsuch, R. K., Luchene, R., Vagg, D. R., & Jacobs, G. A. (1983). Manual for the State – Trait Anxiety Inventory (Form Y). Palo Alto, CA: Consulting Psychologists Press. Stein, M. B., Jang, K. L., & Livesley, W. J. (1999). Heritability of anxiety sensitivity: a twin study. American Journal of Psychiatry, 156, 246 – 251. Steketee, G., & Pruysn, N. A. (1998). Families of individuals with obsessive – compulsive disorder. In: R. P. Swinson, M. M. Antony, S. Rachman, & M. A. Richter (Eds.), Obsessive – compulsive disorder: theory, research and treatment. New York, NY: Guilford. Stewart, S. H., Samoluk, S. B., & MacDonald, R. B. (1999). Anxiety sensitivity and substance abuse. In: S. Taylor (Ed.), Anxiety sensitivity: theory, research and treatment of the fear of anxiety ( pp. 287 – 319). Mahwah, NJ: Erlbaum. Taylor, S. (1995). Anxiety sensitivity: theoretical perspectives of recent findings. Behaviour Research and Therapy, 33, 243 – 258. Taylor, S. (Ed.) (1999). Anxiety sensitivity: theory, research and treatment of the fear of anxiety. Mahwah, NJ: Erlbaum. Taylor, S., Koch, W. J., & McNally, R. J. (1992). How does anxiety sensitivity vary across the anxiety disorders? Journal of Anxiety Disorders, 6, 249 – 259. Watt, M., Stewart, S. H., & Cox, B. J. (1998). A retrospective study of the origins of anxiety sensitivity. Behaviour Research and Therapy, 36, 505 – 525. Zvolensky, M. J., Feldner, M. T., Eifert, G. H., & Brown, R. A. (2001). Affective style among smokers: understanding anxiety sensitivity, emotional reactivity, and distress tolerance using biological challenge. Addictive Behaviors (this volume).
Substance use/abuse and anxiety sensitivity What are the relationships? G. Ron Norton Department of Psychology, University of Winnipeg, Winnipeg, Manitoba, Canada
Abstract The eight articles in this special issue on anxiety sensitivity (AS) and substance abuse provide provocative new information on the relationships, or lack of relationships, between AS and several types of substance use and abuse. The eight articles provide data that extend our understanding of the role of AS in substance abuse with younger people, people who use substances other than alcohol, people who have disorders comorbid with substance use disorders, and people who experience chronic headaches. In addition, one of the articles attempts to determine how AS develops in relationship to parental substance abuse. Finally, several of the studies show that the three Anxiety Sensitivity Index (ASI) subscales (physical concerns, social concerns, and psychological concerns) are uniquely associated with different aspects of substance use/abuse. Each of the articles is discussed as to its merits and potential domains that may require additional research. Finally, several general suggestions are provided for new directions that research on the relations of AS and substance use/abuse should take. D 2001 Elsevier Science Ltd. All rights reserved. Keywords: Anxiety sensitivity; Anxiety sensitivity index
Anxiety sensitivity (AS), as measured by the Anxiety Sensitivity Index (ASI; Reiss, Peterson, Gursky, & McNally, 1986) consists of three lower-order factors: fear of bodily sensations (physical concerns), fear of publicly observable behaviors (social concerns), and fear of loss of cognitive control (psychological concerns). As assessed with the 16-item ASI (Peterson & Reiss, 1992), AS tends to be stable over time (Peterson & Plehn, 1999). AS has also been shown to be a robust and reliable predictor of anxiety (e.g., Taylor, Koch, & McNally, 1992), panic attacks (e.g., Schmidt, Lerew, & Jackson, 1997), problems associated with low-back pain (Asmundson & Norton, 1995), and alcohol/drug use (Stewart, Samoluk, & MacDonald, 1999), amongst other problematic behaviors (see Taylor, 1999). 0306-4603/01/$ – see front matter D 2001 Elsevier Science Ltd. All rights reserved. PII: S 0 3 0 6 - 4 6 0 3 ( 0 1 ) 0 0 2 4 4 - 1
936
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
The eight papers in this series address relationships between AS and various aspects of substance use and abuse. These studies add to an already large corpus of research showing that many aspects of substance use are associated with high scores on the ASI (see review by Stewart et al., 1999). Although the relationship between AS and alcohol abuse, especially in the context of negative coping styles, has been generally well validated (e.g., Stewart et al., 1999), far less is known about how AS relates to the use of other substances. The eight studies in this series address relations with several drugs in addition to alcohol, including the role of AS in the use and abuse of marijuana, pain medication, and cigarettes. A greater understanding of the mechanisms leading to initial substance use, inappropriate substance use, and effective treatment models are necessary. Martin (2001) cited a recent study by the Lewin Group, a health policy research and management consulting firm in the US, in which it was estimated that the annual economic cost of alcohol and drug abuse is more than US$240 billion. About US$97 billion is due to drug abuse. This estimate includes abuse treatment, prevention costs, health care, costs due to reduced job productivity, or lost earnings, crime, and welfare. In spite of these alarming costs, a recent report from the Center for Substance Abuse Treatment showed that two-thirds of Americans with serious substance abuse treatment needs are not being treated (Martin, 2001). Even though alcohol and other substances have been used and abused for thousands of years, it is obvious that we still lack in our understanding of the factors influencing substance use and why some people misuse substances. Research, including the current set of studies on the relationships between AS and substance use/abuse, may greatly increase our understanding of why at least some people misuse substances. A better understanding of factors influencing maladaptive substance use will greatly improve our ability to treat and prevent substance abuse. This would markedly decrease the horrible personal and social costs of substance abuse. The articles in the present series suggests that we unfortunately still have much to learn about how personality dimensions, reasons for using substances, and other factors, such as negative affectivity, influence substance use. If AS and related constructs can be reliably shown to predict heavy substance use or substance use for inappropriate reasons (e.g., coping with distress), it is likely that we can begin to develop more effective models of substance use and abuse and, possibly, interventions for treating people who are abusing. Even more importantly, this knowledge may help us prevent substance use from escalating into abuse or dependence. I will review each of the eight papers in this special issue with the purpose of describing important contributions made by each study. I will also attempt to identify areas that may require further clarification. Finally, I will address several general issues related to the relationships between AS and substance use/abuse and provide some general guidelines for future research in the area. DeHaas, Calamari, Bair, and Martin (2001, this volume) address several important questions. First, what is the relationship between AS and reasons for using substances, when reasons are defined in terms of the types of situations in which the person most often uses substances? Second, is the relationship between AS and substance abuse the same with people only diagnosed with a substance abuse disorder compared to those who have an additional anxiety or mood disorder, as well? Finally, is the relationship between AS and substance use merely secondary to the relation of AS to trait anxiety?
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
937
Because of the very high comorbidity between substance abuse and anxiety disorders (Cox, Norton, Swinson, & Endler, 1990), and because AS is elevated in people with almost all anxiety disorders (Taylor et al., 1992), it is possible that the association between AS and substance abuse is spurious. It is possible that the relationship between AS and substance abuse may be, in reality, a relationship between AS and anxiety disorders. This seems unlikely, however, in light of the findings of DeHaas et al. (2001, this volume). First, they confirmed that ASI scores were significantly correlated with substance use in negative situations (e.g., unpleasant emotions) but not in positive situations (e.g., pleasant times with others) as measured by the Inventory of Drug Taking Situations (Annis, Graham, & Davis, 1987). They also found that there were no differences in the relationships between AS and drinking in negative situations for participants with a dual diagnosis of substance abuse/ dependence and an anxiety disorder and those with a diagnosis of only substance abuse/ dependence. This suggests that the relationship between AS and negative situations substance use is not simply secondary to having a comorbid anxiety disorder. Nonetheless, DeHaas et al. found that there was a difference between those substance-disordered patients with a comorbid anxiety disorder and those with a comorbid mood disorder: the relationship between AS and negative situation substance use was observed only among those with a comorbid anxiety disorder. This pattern of findings makes the conclusion of a lack of involvement of comorbid anxiety disorders in explaining the relationship of AS to negative situation substance use much more tentative. Other findings by DeHaas et al. (2001) suggest that the relationship between AS and substance use is not secondary to relations of AS to trait anxiety. They found, using hierarchical regression analyses, that AS contributed additional variance to drinking in negative situations when the Trait subscale of the State Trait Anxiety Inventory (Spielberger, Gorsuch, Luchene, Vagg, & Jacobs, 1983) was entered first. Since there is some evidence that AS may be a lower-order factor of trait anxiety (Taylor, 1995), this finding suggests that the specificity achieved by measuring this lower-order component of trait anxiety results in statistically increased precision in predicting negative situation substance use. The paper by Comeau, Stewart, and Loba (2001, this volume) evaluated the relationship of AS, trait anxiety, and sensation seeking to adolescents’ motives for using alcohol, cigarettes, and marijuana. This paper nicely extended earlier work on motives for alcohol use to a younger group of participants. In addition, Comeau et al. assessed whether the same motives for using alcohol applied to high AS adolescents’ use of cigarettes and marijuana. Motives for drinking alcohol were measured with the Drinking Motives Questionnaire-Revised (DMQ-R; Cooper, 1994). Motives for using marijuana and cigarettes were measured with the Teen Marijuana Motives Questionnaire and the Teen Smoking Motives Questionnaire—measures developed by the authors (Comeau, Stewart, & Loba, 2000), and based on the DMQ-R. The authors found that several substance use motives were correlated with the ASI. However, when they used hierarchical regression analyses (as opposed to simple bivariate correlations) the relationship between AS and motives became less clear. For example, they found coping motives for both alcohol and cigarettes were predicted by trait anxiety, but not AS. However, using alcohol and marijuana for conformity motives was predicted by AS. These findings suggest both that there may be motives common to why high AS people use different
938
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
substances, and different substances may be used for very different motivations among anxious individuals. The paper by Comeau et al. also raises the question of developmental changes in the relationships between AS and motives for using various substances. Are these relationships the same for teens as they are for adults? Longitudinal research may provide a more definitive answer to this question. Asmundson, Wright, Norton, and Veloso (2001, this volume) compared high, medium, and low AS people with chronic headaches on a variety of mood-, personality-, and pain-related measures. Asmundson and Norton (1995) had shown that high AS patients with unexplained back pain were more likely to use pain medications than were those scoring in a medium or low range on the ASI. In their present study, Asmundson et al. (2001) did not replicate these findings for use of either over-the-counter or prescription pain medications in chronic headache patients. In fact, when they used hierarchical regression analyses, they found that only the cognitive anxiety scale of the Pain Anxiety Symptoms Scale (PASS; McCracken, Zayfert, & Gross, 1993) predicted use of over-the-counter pain medications. The dimensions measured by this instrument are similar in concept to AS in that they measure fearful appraisals, but the scales of the PASS are focused on the experience of pain (as opposed to the experience of arousal-related bodily sensations which are tapped on the ASI). When Asmundson et al. looked at use of prescription medications they found that the physiological anxiety scale of the PASS and the physical concerns scale of the ASI predicted use of prescription medications. However, unexpectedly, it was people with low ASI physical concerns who were more likely to use prescription pain medications. Unfortunately, as Asmundson et al. (2001, this volume) pointed out, they measured only whether people used over-the-counter or prescription headache medication, but not how often or how much medication they used. It is possible that there is a positive relationship between AS and pain medication use frequency or amount of medication taken. This certainly appears to be so for alcohol use (see review by Stewart et al., 1999) which has central nervous system depressant effects similar to many pain medications (Arana & Rosenbaum, 2000). Finally, it would be interesting to assess the motivations for taking headache medications and relations of these motives to negative affectivity factors such as AS. It may be that people who are taking analgesic medications for negative reinforcement reasons (e.g., to escape physiological sensations of pain) may differ from those who are taking such medications for positive reinforcement reasons (e.g., to allow them to pursue pleasurable activities with which pain otherwise interferes). However, it is also possible that analgesic use in response to headache pain may be related to factors that are dissimilar to those motivating alcohol use, and dissimilar to those motivating analgesic use in response to unexplained low back pain for that matter. Future research is needed to clarify the various reasons people take medications for headaches, and whether different motivations for analgesic medication use are associated with AS. MacDonald, Stewart, Hutson, Rhyno, and Loughlin (2001, this volume) assessed the effects of alcohol and alcohol expectancies in dampening cognitive, affective, and somatic distress due a hyperventilation challenge. Some of their participants received a dose of alcohol equivalent to 4–5 drinks (‘‘alcohol’’ group), and others were falsely led to believe they received an equivalent amount of alcohol (‘‘placebo’’ group). Finally, a third group was
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
939
not led to believe they were consuming alcohol; they consumed only a control beverage (‘‘control’’ group). The participants in both the alcohol and placebo groups rated themselves as more intoxicated than did the participants in the control group. All participants were then subjected to a hyperventilation challenge where they were asked to breathe 30 times per minute for 3 min. MacDonald et al. found that during hyperventilation, affective and somatic distress as measured by the Hyperventilation Questionnaire (HVQ; Rapee & Medoro, 1994) increased less for those high AS participants who consumed alcohol compared to high AS participants in the placebo or control groups. These results suggest that the alcohol dampening effects observed among high AS participants in their previous research (MacDonald, Baker, Stewart, & Skinner, 2000) were likely due to the pharmacological effects of alcohol rather than the expectancy that alcohol would reduce distress. This dampening effect could make alcohol a powerful negative reinforcer and increase the likelihood that high AS people may drink more and more frequently to reduce distress due to bodily symptoms of anxiety and/or withdrawal symptoms (i.e., symptoms that are mimicked during hyperventilation). Two issues related to the dampening effects of alcohol on high AS participants should be explored in future studies. First, are the dampening effects specific to high AS or are they due to a more general effect of negative affectivity? To investigate this issue, future research should include, and control for, alternative negative affectivity constructs when examining the contribution of AS to sensitivity to alcohol dampening of responses to arousal-induction challenges. Secondly, the items on the HVQ may tap domains that are similar to those tapped by the ASI. To control for this potential confound, future studies may wish to obtain psychophysiological and behavioral measures of arousal and distress as well as self-report measures following challenges designed to evaluate dampening effects associated with alcohol. These additional measures may help clarify whether alcohol does, indeed, dampen somatic and/or emotional responses in high AS people during physical and emotional challenges, and whether high AS people are indeed more sensitive to such alcohol dampening effects. Kushner, Thuras, Abrams, Brekke, and Stritar (2001, this volume) address the issue of whether AS is directly or indirectly associated with alcohol use in negative situations (i.e., drinking to cope). They suggest that AS may act to accelerate anxiety, which in turn leads to alcohol use to dampen feelings of anxiety. To test for this possibility, they used mediator analysis to determine if anxiety acts as a mediator between AS and coping-motivated drinking. Mediator analysis involves a series of regressions between predictor and outcome variables. Kushner et al. assessed coping drinking motives with two instruments, Drinking for Anxiety Management (DAM; Bibb & Chambless, 1986) and Reasons for DrinkingNegative Affect (RFD-NA; Sher, Walitzer, Wood, & Brent, 1991). The two outcome measures, although both assessing drinking for coping purposes (cf. Comeau et al., 2001, this volume), differ in that the DAM focuses specifically on coping with symptoms of anxiety whereas the RFD-NA focuses on coping with negative affect symptoms, more generally. Their results partially confirm that anxiety mediates the relationship between AS and drinking for coping reasons. Specifically, Kushner et al. found that social anxiety, and to a lesser extent worry and trait anxiety, were significant mediators of the relationship of AS levels to RFD-NA scores. State anxiety, withdrawal symptoms and symptoms of other
940
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
anxiety disorders did not meet criteria as mediators. Somewhat different results were found when the authors looked at whether anxiety was a mediator between AS and DAM scores. Here, all measures of anxiety except state anxiety and withdrawal symptoms mediated between AS levels and DAM scores. The authors suggest that this discrepancy may be due to the different ways in which the two outcome instruments conceptualize and measure copingmotivated drinking. They suggest that the RFD-NA may be assessing drinking to cope with negative affect defined more broadly than with the DAM (where coping is defined as drinking to manage anxiety in particular). Although theoretically interesting, the difference in the degree to which anxiety mediates between AS and the RFD-NA vs. AS and the DAM may be less important at a practical level. Results with either outcome measure show that anxiety mediates between AS and coping-motivated drinking suggests that anxiety is an important construct in describing why high AS people misuse alcohol. As suggested by the authors (Kushner et al., 2001, this volume), this set of results suggests that we should be treating symptoms of anxiety in high AS alcoholics in order to minimize their motivation to use alcohol to cope with negative affect. Future research needs to identify potential mechanisms other than heightened anxiety that may mediate the relationship between AS and drinking to manage negative affect. If AS amplifies negative affect in coping-related drinking situations, as Kushner et al. (2001, this volume) suggest, how does it do so? And which particular lower-order AS components are most involved in this anxiety or negative affect amplification? Do AS psychological concerns (e.g., fear of losing control) increase anxiety or other negative affect? Or do AS physical concerns (i.e., fears of physical symptoms)? Future research should attempt to determine more precisely how and why AS amplifies anxiety and other negative affect in various coping-related drinking situations. Brown, Kahler, Zvolensky, Lejuez, and Ramsey (2001, this volume) evaluated the relationship between several smoking related variables, and relapse following a smoking cessation program. They hypothesized that the ASI would show positive correlations with expectations and motivations for smoking involving negative reinforcement (e.g., coping with negative affect), but not positive reinforcement reasons (e.g., pleasure and stimulation). Smoking expectancies and motives were measured with the Smoking Effects Questionnaire (SEQ; Rohsenow et al., 1992) and the Reasons for Smoking test (RFS; Ikard, Green, & Horn, 1969), respectively. Their results showed that the ASI was not correlated with either smoking rate or level of nicotine dependence as measured by Fagerstrom’s (1978) scale. However, Brown et al. (2001, this volume) showed positive correlations between the ASI and the Negative Psychological and Negative Physical Effects of the SEQ. These correlations were not expected, but are of interest as they indicate that high AS smokers may experience more of the negative psychological and physical effects of smoking, as suggested by the authors, or that they may be more sensitive to these effects when they occur. They also found positive correlations between the ASI and the Crutch subscale of the RFS and the Reduce Negative Affect subscale of the SEQ. Finally, they found that correlations between the ASI and the Beck Depression Inventory (Beck, Ward, Mendelson, Mock, & Erbaugh, 1961) or a history of recurrent depression were not significant. This suggests that the relationship between the ASI
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
941
and negative reinforcement smoking measures was not secondary to the relation of AS to general negative affectivity. Brown et al. (2001, this volume) also evaluated the relationship between the ASI and rate of relapse following a cessation program. Their results showed that, although the ASI did not predict relapse rates after 1-week smoking cessation, it did predict relapse in the first week after treatment for people with a history of major depressive disorder. Overall, the results of the Brown et al. (2001, this volume) study show that the ASI is predictive of smoking for negative reinforcement reasons and of expectations for negative affect reduction from smoking, and that these relationships are independent of levels of addiction and depression. Their intriguing finding that ASI was also predictive of negative psychological and physical smoking expectancies should be viewed with some caution. The R2 values for the relationship of ASI to negative psychological and negative physical expectancies were only in the range of 6–8% shared variance. However, it is still possible, as Brown et al. point out, that high ASI smokers may find the psychological and physical consequences intolerable and may smoke more to reduce these feelings. This study importantly shows that smoking may have a similar relationship to AS as that seen for alcohol use, in that high AS people may smoke to reduce unpleasant affective states. Future research on the relationship between AS and smoking may benefit from a more detailed analysis of the social, psychological, and physical concern subscales of the ASI. It is possible that one or more of the subscales would be more sensitive to smoking in response to negative internal states. In addition, it would be interesting to see if affective states other than depression (e.g., anger, anxiety) mediate the relationship between ASI and measures of smoking for coping-related motives (cf. Kushner et al., 2001, this volume). Zvolensky, Feldner, Eifert, and Brown (2001, this volume) used a C02 challenge with heavy smokers ( > 20 cigarettes per day) who had, in the past, quit smoking for less than 7 days or more than 7 days. They hypothesized that participants who had not been able to quit smoking for 1 week would have higher ASI scores, show greater intolerance of physical discomfort during a preexperimental breath holding task, and display greater emotional reactivity during a C02 challenge. Their results showed that that, indeed, those who had been unable to quit smoking for at least 1 week did show greater cognitive–affective reactivity to the C02 challenge compared to those with longer periods of smoking abstinence. However, the two groups did not differ on measures of heart rate produced during the challenge, breathholding duration, or on levels of AS. The authors suggest that the ASI might not be specific enough to identify those who are intolerant of withdrawal-related bodily sensations and thus at risk for early relapse to smoking during a quit attempt, and suggest the development of a withdrawal symptom sensitivity assessment instrument for use in future research. However, because those who had greater difficulty abstaining from smoking did show greater emotional reactivity to the challenge in the Zvolensky et al. study, future research should consider including measures of negative affectivity other than AS as predictors of length of abstinence. Zvolensky et al.’s failure to find that scores on the ASI distinguish those with shorter versus longer prior successful quit attempts is particularly interesting in light of Brown et al.’s (2001, this volume) findings regarding the relations of AS and success in smoking cessation. Brown et al. showed that those who had the greatest difficulty stopping smoking during the first
942
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
week of a quitting attempt were more likely to have high ASI scores. More research is needed to explain this discrepancy in results regarding the predictive utility of ASI scores in identifying difficulties abstaining during the early stages of a smoking cessation attempt. Finally, MacPherson, Stewart, and McWilliams (2001, this volume) attempted to determine if parental problem drinking was associated with the development of high AS in their children. Their young adults participants completed several questionnaires including the ASI, Children of Alcoholics Screening Test (CAST; Jones, 1983), and the parental forms of the short form of the Michigan Alcoholism Screening Test (F-SMAST and M-SMAST; Sher & Descutner, 1986). Although both of the latter questionnaires are designed to assess aspects of parental drinking behavior, the CAST taps into a variety of factors associated with parental excessive drinking that cause distress for the child (e.g., marital discord). The F-SMAST and the M-SMAST tap more specifically into the parent’s experience with problems with alcohol use. The authors argue that if CAST scores were predictive of ASI scores, after controlling for SMAST scores, this would indicate that childhood exposure to distressing parental problem drinking behavior might contribute to the development of increased AS levels in the child. Controlling for SMAST scores controls for the possibility that AS might be transmitted genetically as part of the familial transmission of alcoholism. MacPherson et al. (2001, this volume) used hierarchical regression analyses to predict ASI subscale scores. Their results showed that when CAST scores were entered in Stage two, following SMAST and gender in Stage one, CAST scores accounted for an additional 6% of the explained variance of the psychological concerns subscale. Similarly, CAST scores accounted for an additional 3% of the explained variance of the physical concerns subscale, over-and-above that explained by SMAST scores and participant gender. When this two-step analysis was applied to the social concerns subscale of the ASI, none of the predictor variables accounted for a significant amount of variance. MacPherson et al. also evaluated whether scores on any of the three ASI subscales were mediators of the association between CAST scores and the development of anxiety disorder symptoms in the participants. Their findings suggest that the psychological concerns subscale of the ASI may serve as a modest mediator of the association between childhood exposure to distressing parental problem drinking behaviors and the development of elevated anxiety symptoms in the offspring. In sum, the results of the MacPherson et al. (2001, this volume) study suggest that increases in AS (especially AS psychological concerns) are more likely due to observing distressing behaviors associated with a parent’s excessive alcohol use, rather than being a direct (genetically mediated) result of parental alcoholism. Further, there appears to be some evidence that the ASI-psychological concerns subscale may mediate the relationship between exposure to parental problem drinking behaviors and anxiety symptoms in the adult child, including trait anxiety and uncued panic. Future research should try to identify other parental behaviors that might predispose children to developing high AS. Several areas that might be worth investigating would be parental overprotection, inconsistencies in methods of parental discipline, and marital conflict. These domains have been suggested as contributing to anxiety disorders such as obsessive–compulsive disorder (Steketee & Pruysn, 1998).
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
943
1. Conclusions The studies presented in this special issue evaluated the role of AS in the use and abuse of alcohol, cigarettes, marijuana, and analgesic medications. The results obtained in the eight studies suggest that AS likely plays a role in the use of some substances (cigarettes and alcohol) at least when motivated by a desire to control negative affective states (i.e., coping motives). Unfortunately, the evidence is mixed with some studies showing a positive correlation between AS and substance use (e.g., Brown et al., 2001, this volume) whereas other studies did not find this relationship (e.g., Asmundson et al., 2001, this volume). Interestingly, one study (i.e., Kushner et al., 2001, this volume) provided evidence that elevated anxiety might act as a mediator in explaining the relations between AS and copingrelated substance use. It appears that the strongest relationships between AS and substance use are for alcohol and, to a lesser extent, cigarette smoking. However, even here the magnitude of associations are not large, suggesting that factors other than those measured by the ASI may be important alternative or additional determinants of substance use. Researchers interested in the relationship of AS and substance use should consider three important issues in planning their future research. First, several studies (e.g., MacPherson et al., 2001, this volume) in this special issue suggest that the subscales of the ASI may be differentially predictive of various aspects of substance use behavior and the motives for using different substances. This suggests that future researchers use the subscales of the ASI rather than relying solely on the total score. It is possible that using the total score may diminish specific relationships between AS and substance use. Secondly, the study by Asmundson et al. (2001, this volume) found that the PASS (McCracken et al., 1993) was a better predictor than AS of pain medication usage in chronic headache patients. The ASI and the PASS share many similarities in that both are designed to measure fear of symptoms. The ASI has been shown to be a good measure of fear of anxiety symptoms (Reiss et al., 1986) whereas the PASS was specifically designed to measure fear of pain symptoms. It is possible that we need to consider developing a new instrument that is more specifically designed to measure fear of symptoms that may lead to substance abuse. We have good evidence from the studies in this special issue that ASI is most closely related to substance use motivated by a desire to cope with anxiety and other negative affect. We also know that negative affectivity is associated with inappropriate substance use. These findings might help direct researchers in designing an instrument that taps the personality and individual difference domains that best predict substance use and abuse. The studies in this special issue have shown that the AS construct, as measured by the ASI, demonstrates an inconsistent relationship with substance use. It would be interesting to determine if there may be more consistent relations of AS with substance use if we consider motive by substance type relationships. This type of analysis may direct our efforts to better assess the relationship between fear variables (e.g., fear of anxiety symptoms; fear of pain) and substance use. It may be that AS is the best predictor of use of some substances (e.g., arousal dampening drugs) as a result of some use motives (e.g., coping or conformity motives). Other domains may require measurement of fears more specific to substance use driven by other use motives. For example, fear of pain (as opposed to AS) may turn out to be
944
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
the best predictor of use of analgesic drugs (as opposed to anxiolytic drugs) for the purposes of coping with pain (as opposed to arousal) experiences. A third question that demands further attention is this: What causes people to have high AS? The study by MacPherson et al. (2001, this volume) is an excellent example of research directed towards identifying the determinants of AS. In a recent twin study, Stein, Jang, and Livesley (1999) estimated that approximately 45% of the variance in AS could be accounted for by genetic factors. What accounts for the additional 55%? The evidence that we do have is consistent with recent findings for anxiety which appears to result from a combination of genetic factors and early childhood experiences (Andrews, 1996). This also appears to be true of AS. Two recent studies are consistent with the MacPherson et al. results in showing that early childhood experiences are positively related to the development of high AS. Watt, Stewart, and Cox (1998) have shown that AS levels are positively related to instrumental and vicarious conditioning experiences during childhood. They also found that exposure to uncontrolled parental behaviors due to drunkenness and anger was related to the development of high AS. Similarly, Scher and Stein (1999) found that children exposed to parental threatening, hostile and rejecting behaviors were more likely to have high AS compared to children not exposed to these parental behaviors. If AS truly is an important factor in motivating at least some types of substance misuse, then research on the origins of this personality risk factor may be helpful in identifying ways of ultimately preventing substance abuse and dependence. Considering the high personal and social costs of substance abuse, it is necessary that we become more effective in determining the factors that lead to and maintain substance misuse. Research on the relationship between AS and substance use provides a good model for other types of research on the etiological and maintenance factors involved in substance use and abuse.
References Andrews, G. (1996). Comorbidity in neurotic disorders: the similarities are more important than the differences. In: R. M. Rapee (Ed.), Current controversies in the anxiety disorders ( pp. 3 – 20). New York: Guilford. Annis, H. M., Graham, J., & Davis (1987). Inventory of drinking situations. Toronto, ON: Addictions Research Foundation. Arana, G., & Rosenbaum, J. (2000). Handbook of psychiatric drug therapy. Philadelphia, PA: Williams & Wilkin. Asmundson, G. J. G., & Norton, G. R. (1995). Anxiety sensitivity in patients with physically unexplained chronic back pain. Behaviour Research and Therapy, 33, 771 – 777. Asmundson, G. J. G., Wright, K. D., Norton, P. J., & Veloso, F. (2001). Anxiety sensitivity and other emotional traits in predicting headache medication use in patients with recurring headaches: implications for abuse and dependency. Addictive Behaviors (this volume). Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for measuring depression. Archives of General Psychiatry, 4, 561 – 571. Bibb, J. L., & Chambless, D. L. (1986). Alcohol use and abuse among diagnosed agoraphobics. Behaviour Research and Therapy, 24, 49 – 58. Brown, R. A., Kahler, C. W., Zvolensky, M. J., Lejuez, C. W., & Ramsey, S. E. (2001). Anxiety sensitivity: relationship to negative affect smoking and smoking cessation in smokers with past major depressive disorder. Addictive Behaviors (this volume).
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
945
Comeau N., Stewart, S. H., & Loba, P. (2000). Adolescents’ motives for smoking and marijuana use: factor structure and relations to motives for alcohol use. In Stewart, S. H. (Chair), New research on human motivations for alcohol use. Symposium conducted at the 3rd Joint Meeting of the British Experimental Psychology Society and the Canadian Society for Brain, Behaviour, and Cognitive Sciences, Cambridge, UK, June. Comeau, N., Stewart, S. H., & Loba, P. (2001). The relations of trait anxiety, anxiety sensitivity, and sensation seeking to adolescents’ motivations for alcohol, cigarette, and marijuana use. Addictive Behaviors (this volume). Cooper, M. L. (1994). Motivation for alcohol use among adolescents. Psychological Assessment, 6, 117 – 128. Cox, B. J., Norton, G. R., Swinson, R. P., & Endler, N. S. (1990). Substance abuse and panic-related anxiety: a critical review. Behaviour Research and Therapy, 28, 385 – 393. DeHaas, R. A., Calamari, J. E., Bair, J. P., & Martin, E. D. (2001). Anxiety sensitivity and drug or alcohol use in individuals with anxiety and substance use disorders. Addictive Behaviors (this volume). Fagerstrom, K. O. (1978). Measuring the degree of physical dependence to tobacco smoking with reference to individualization of treatment. Addictive Behaviors, 3, 235 – 241. Ikard, F. F., Green, D. E., & Horn, D. (1969). A scale to differentiate between types of smoking related to the management of affect. International Journal of the Addictions, 4, 649 – 659. Jones, J. W. (1983). The Children of Alcoholics Screening Test (CAST). Chicago, IL: Camelot Unlimited. Kushner, M. G., Thuras, P., Abrams, K., Brekke, M., & Stritar, L. (2001). Anxiety mediates the association between anxiety sensitivity and coping-related drinking motives in alcoholism treatment patients. Addictive Behaviors (this volume). MacDonald, A. B., Baker, J. M., Stewart, S. H., & Skinner, M. (2000). The effects of alcohol on the response to hyperventilation of participants high and low in anxiety sensitivity. Alcoholism: Clinical and Experimental Research, 24, 1656 – 1665. MacDonald, A. B., Stewart, S. H., Hutson, R., Rhyno, E., & Louglin, H. L. (2001). The roles of alcohol and alcohol expectancy in the dampening of responses to hyperventilation among high anxiety sensitivity young adults. Addictive Behaviors (this volume). MacPherson, P. S. R., Stewart, S. H., & McWilliams, L. A. (2001). Parental problem drinking and anxiety disorder symptoms in adult offspring: examining the mediating role of anxiety sensitivity components. Addictive Behaviors (this volume). Martin, S. (2001). Most substance abusers aren’t getting treatment. Monitor on Psychology, 32, 11. McCracken, L. M., Zayfert, C., & Gross, R. T. (1993). The pain anxiety symptom scale: development and validation of a scale to measure fear of anxiety. Pain, 50, 67 – 73. Peterson, R. A., & Plehn, K. (1999). Measuring anxiety sensitivity. In: S. Taylor (Ed.), Anxiety sensitivity: theory, research and treatment of the fear of anxiety ( pp. 61 – 81). Mahwah, NJ: Erlbaum. Peterson, R. A., & Reiss, S. (1992). Anxiety sensitivity manual (2nd ed.). Worthington, OH: International Diagnostics Systems. Rapee, R. M., & Medoro, L. (1994). Fear of physical sensations and trait anxiety as mediators of the response to hyperventilation in nonclinical subjects. Journal of Abnormal Psychology, 103, 693 – 699. Reiss, S., Peterson, R. A., Gursky, D. M., & McNally, R. J. (1986). Anxiety sensitivity, anxiety frequency and the prediction of fearfulness. Behaviour Research and Therapy, 24, 1 – 8. Rohsenow, D. J., Abrams, D. B., Colby, S. M., Gulliver, S. B., Niaura, R. S., & Monti, P. M. (1992). Smoking Effects Questionnaire: development and psychometric properties. Poster presented at the annual meeting of the Association for Advancement of Behavior Therapy, Boston, MA, November. Scher, C. D., & Stein, M. B. (1999). Developmental antecedents of anxiety sensitivity. (Summary) In: Program and abstracts of the 19th National Conference of the Anxiety Disorders Association of America ( pp. 86 – 87). Schmidt, N. B., Lerew, D. R., & Jackson, R. J. (1997). Prospective evaluation of anxiety sensitivity in the pathogenesis of panic: replication and extension. Journal of Abnormal Psychology, 106, 532 – 538. Sher, K. J., & Descutner, C. (1986). Reports of parental alcoholism: reliability across siblings. Addictive Behaviors, 11, 25 – 30. Sher, K. J., Walitzer, K. S., Wood, P. K., & Brent, E. E. (1991). Characteristics of children of alcoholics: putative risk factors, substance use and abuse, and psychopathology. Journal of Abnormal Psychology, 100, 427 – 448.
946
G.R. Norton / Addictive Behaviors 26 (2001) 935–946
Spielberger, C. D., Gorsuch, R. K., Luchene, R., Vagg, D. R., & Jacobs, G. A. (1983). Manual for the State – Trait Anxiety Inventory (Form Y). Palo Alto, CA: Consulting Psychologists Press. Stein, M. B., Jang, K. L., & Livesley, W. J. (1999). Heritability of anxiety sensitivity: a twin study. American Journal of Psychiatry, 156, 246 – 251. Steketee, G., & Pruysn, N. A. (1998). Families of individuals with obsessive – compulsive disorder. In: R. P. Swinson, M. M. Antony, S. Rachman, & M. A. Richter (Eds.), Obsessive – compulsive disorder: theory, research and treatment. New York, NY: Guilford. Stewart, S. H., Samoluk, S. B., & MacDonald, R. B. (1999). Anxiety sensitivity and substance abuse. In: S. Taylor (Ed.), Anxiety sensitivity: theory, research and treatment of the fear of anxiety ( pp. 287 – 319). Mahwah, NJ: Erlbaum. Taylor, S. (1995). Anxiety sensitivity: theoretical perspectives of recent findings. Behaviour Research and Therapy, 33, 243 – 258. Taylor, S. (Ed.) (1999). Anxiety sensitivity: theory, research and treatment of the fear of anxiety. Mahwah, NJ: Erlbaum. Taylor, S., Koch, W. J., & McNally, R. J. (1992). How does anxiety sensitivity vary across the anxiety disorders? Journal of Anxiety Disorders, 6, 249 – 259. Watt, M., Stewart, S. H., & Cox, B. J. (1998). A retrospective study of the origins of anxiety sensitivity. Behaviour Research and Therapy, 36, 505 – 525. Zvolensky, M. J., Feldner, M. T., Eifert, G. H., & Brown, R. A. (2001). Affective style among smokers: understanding anxiety sensitivity, emotional reactivity, and distress tolerance using biological challenge. Addictive Behaviors (this volume).