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Published in final edited form as: Addict Behav. 2017 Jun 20;75:1–6. doi: 10.1016/j.addbeh.2017.06.014

Visceral sensitivity, anxiety, and smoking among treatment-seeking smokers

Michael J Zvolensky a,b,*, Jafar Bakhshaie a, Peter J Norton c, Jasper AJ Smits d, Julia D Buckner e, Lorra Garey a, Kara Manning a
PMCID: PMC10062190  NIHMSID: NIHMS1854105  PMID: 28654824

Abstract

It is widely recognized that smoking is related to abdominal pain and discomfort, as well as gastrointestinal disorders. Research has shown that visceral sensitivity, experiencing anxiety around gastrointestinal sensations, is associated with poorer gastrointestinal health and related health outcomes. Visceral sensitivity also increases anxiety symptoms and mediates the relation with other risk factors, including gastrointestinal distress. No work to date, however, has evaluated visceral sensitivity in the context of smoking despite the strong association between smoking and poor physical and mental health. The current study sought to examine visceral sensitivity as a unique predictor of cigarette dependence, threat-related smoking abstinence expectancies (somatic symptoms and harmful consequences), and perceived barriers for cessation via anxiety symptoms. Eighty-four treatment seeking adult daily smokers (Mage = 45.1 years [SD = 10.4]; 71.6% male) participated in this study. There was a statistically significant indirect effect of visceral sensitivity via general anxiety symptoms on cigarette dependence (b = 0.02, SE = 0.01, Bootstrapped 95% CI [0.006, 0.05]), smoking abstinence somatic expectancies (b = 0.10, SE = 0.03, Bootstrapped 95% CI [0.03, 0.19]), smoking abstinence harmful experiences (b = 0.13, SE = 0.05, Bootstrapped 95% CI [0.03, 0.25]), and barriers to cessation (b = 0.05, SE = 0.06, Bootstrapped 95% CI [0.01, 0.13]). Overall, the present study serves as an initial investigation into the nature of the associations between visceral sensitivity, anxiety symptoms, and clinically significant smoking processes among treatment-seeking smokers. Future work is needed to explore the extent to which anxiety accounts for relations between visceral sensitivity and other smoking processes (e.g., withdrawal, cessation outcome).

Keywords: Visceral sensitivity, Anxiety, Smoking, Gastrointestinal distress

1. Introduction

There is wide recognition that smoking is related to abdominal pain and discomfort, including Irritable Bowel Syndrome (IBS) and other functional gastrointestinal (GI) disorders (Lakatos, 2009). In fact, research has illustrated that smoking is related to heart burn (Lakatos, 2009), stomach ulcers (Lakatos, 2009), chronic inflammation in the bowels (USDHHS, 2004), stomach and colon cancer (Hannan, Jacobs, & Thun, 2009), among other GI-related problems (e.g., gallstones; Tolstrup, Kristiansen, Becker, & Grønbæk, 2009). The prevalence of smoking among persons with GI disturbances and clinical conditions is estimated to be at least twice the rate observed in the general population (Garrow & Delegge, 2010; Sandler, 1990).

Given the heterogeneity of GI-related symptoms and disorders, scholars have sought to identify common processes that may undergird such clinical complex and varied presentations (Leventhal & Zvolensky, 2015). One such construct is visceral sensitivity (Labus et al., 2004). Visceral sensitivity reflects anxiety about GI sensations and the context that may occasion them (Labus, Mayer, Chang, Bolus, & Naliboff, 2007). Research suggests visceral sensitivity is related to, but unique from, anxiety symptoms and associated with poorer GI and related health outcomes among persons with and without IBS (Drossman et al., 1988). Other work has documented the clinically significant role of visceral sensitivity in the treatment of GI disorders (Hazlett-Stevens, Craske, Mayer, Chang, & Naliboff, 2003); reductions in visceral sensitivity, rather than anxiety in general, contribute to improvements in GI clinical outcome. For example, visceral sensitivity is an active element of change in the treatment of IBS (Craske et al., 2011).

Despite the substantive co-occurrence of smoking and GI symptoms and disorders, there is presently no empirical understanding of visceral sensitivity in the context of smoking. Several smoking-related factors that have consistently been shown to predict poorer cessation outcomes include greater cigarette dependence (Heatherton, Kozlowski, Frecker, & Fagerström, 1991) and stronger expectancies for negative outcomes associated with quitting and abstinence (Abrams, Zvolensky, Dorman, Gonzalez, & Mayer, 2011; Farris, Langdon, DiBello, & Zvolensky, 2015). Yet, this work has not yet been extended to the study of visceral sensitivity. Numerous studies suggest that visceral sensitivity increases anxiety symptom severity and mediates the relation between other risk factors (e.g., neuroticism) and GI symptom distress (Hazlett-Stevens et al., 2003). Drawing from such (indirect) work, greater visceral sensitivity among smokers may be associated with greater anxiety symptom severity, which in turn, would be expected to be related to more severe smoking behavior and threat-based smoking cognition. Indeed, heightened anxiety may contribute to a threat-based emotional state(s) wherein smokers are more apt to smoke because it may offer perceived or objective relief from such aversive interoceptive states.

Together, the current study sought to test the hypothesis that, among treatment-seeking smokers, visceral sensitivity would be related to cigarette dependence, threat-related smoking abstinence expectancies (somatic symptoms and harmful consequences), and perceived barriers for cessation via anxiety symptoms. All effects were expected to be evident above and beyond the variance accounted for by gender, psychopathology, and perceived health status.

2. Method

2.1. Participants

Participants were 84 adult daily smokers (Mage = 45.1 years [SD = 10.4]; 71.6% male) seeking smoking cessation treatment. On average, the sample reported 5.3 (SD = 8.3) serious quit attempts in their lifetime. Age of onset for regular smoking was 17.5 years (SD = 5.3). Most of the sample (78.5%) had at least one Axis I diagnosis. Please find the detailed demographic characteristics of the participants in Table 1.

Table 1.

Sample characteristics.

Variable Mean(SD) or % (n)
Race/ethnicity
 Black/African American 65.1% (55)
 White 29.1% (24)
 “Other” 4.7% (4)
 Asian 1.2% (1)
Marital status
 Single/never married 62.5% (52)
 Divorced 11.4% (9)
 Married 9.1% (8)
 Live with partner 8.0% (7)
 Separated 5.7% (5)
 Widowed 3.4% (3)
Education status
 < 7 years formal education 1.1% (1)
 Junior high school 5.7% (5)
 Partial high school 11.4% (10)
 High school/GED 34.1% (29)
 Partial college 31.8% (27)
 College degree 8.0% (6)
 Graduate school 8.0% (6)
Resident status
 Urban area 65.9% (55)
 Suburban AREA 22.7% (19)
 Rural area 11.4% (10)
Employment status
 Full-time 17.2% (14)
 Part-time 26.4% (22)
 Public or private assistance 20.7% (17)
 Dependence on spouse or student status 5.7% (6)
 Unemployment 29.9% (25)
Income
 Less than $5000 a year 39.2% (33)
 $5000–$9999 16.6% (14)
 $10,000–$14,999 15.4% (13)
 $15,000–$24,999 7.1% (6)
 $25,000–$34,999 11.9% (10)
 More than $34,999 a year 9.5% (8)
Axis I diagnosis
 Major depressive disorder 17.8% (15)
 Substance use disorder 15.9% (12)
 Posttraumatic stress disorder 12.3% (10)
 Bipolar I/II 12.3% (10)
 Social anxiety disorder 10.8% (9)
 Alcohol use disorder 10.7% (9)
 Generalized anxiety disorder 7.4% (6)
 Dysthymia 3.2% (3)
 Specific phobia 1.9% (2)
 Panic disorder 1.8% (2)
 Agoraphobia 1.8% (2)
 Anxiety not otherwise specified 1.8% (2)
 Obsessive-compulsive disorder 1.8% (2)
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2.2. Measures

2.2.1. Demographics questionnaire

Demographic information collected included gender, age, race/ethnicity, income, marital status, education, resident status, and employment status.

2.2.2. Structured clinical interview for DSM-IV disorders (SCID-I; First, Spitzer, Gibbon, & Williams, 2002)

The SCID-I is a clinician-administered diagnostic assessment used to assess the presence of psychopathology. In the current study, the SCID-I was administered by trained doctoral students under the supervision of a clinical psychologist. It was used to index current (past month) Axis I diagnoses. The SCID-I has demonstrated good reliability (Zanarini et al., 2000) and excellent validity (Basco et al., 2000) in past work. All assessments were reviewed by an independent for between-rater agreement; no cases of disagreement were noted.

2.2.3. The short-form health survey (SF-36; Ware & Sherbourne, 1992)

The short-form health survey (SF-36) is a 36-item survey that assesses physical and mental health-related quality of life and functional impairment. The SF-36 has demonstrated good psychometric properties (Ware & Sherbourne, 1992). In the current study, the response to the question “In general, would you say your health is: excellent, very good, good, fair, poor” was included as a covariate.

2.2.4. Mood anxiety symptom questionnaire short form (MASQ; Watson & Clark, 1991)

The MASQ is a 62-item self-report measure of affective symptoms. Participants rate each item (e.g., “felt dizzy”) on a Likert scale from 1 (not at all) to 5 (extremely). The MASQ short form contains two scales assessing symptoms of anxiety and two scales measuring symptoms of depression. The scales were created rationally using the tripartite model as a conceptual guide (Watson et al., 1995). The MASQ has demonstrated convergent validity with other measures of anxiety and depression (Watson et al., 1995). The general distress anxious symptoms scale (MASQ-General Anxiety; MASQ-GA; 11 items) was used in the current study. This sub-scale includes indicators of anxious mood (e.g., inability to relax, upset stomach); (Schalet, Cook, Choi, & Cella, 2014). Internal consistency for the MASQ-GA was excellent (Cronbach’s alpha = 0.92).

2.2.5. Visceral sensitivity index (VSI; Labus et al., 2004)

The VSI is a 15-item self-report questionnaire measuring fear, worry, hypervigilance, and avoidance of visceral sensations and discomfort. An example item is: “I experience abdominal discomfort as frightening.” The VSI employs a six-point response scale yielding a range of possible scores from 0 (no) to 75 (severe). The VSI utilizes a global single score (Labus et al., 2004). The VSI has excellent psychometric properties, including concurrent, divergent, and discriminant validity (Labus et al., 2004). The VIS is related to, but distinct from, anxiety symptoms (Labus et al., 2004). The internal consistency for the VSI in the current sample was excellent (Cronbach’s alpha = 0.90).

2.2.6. Smoking history questionnaire (SHQ; Brown, Lejuez, Kahler, & Strong, 2002)

The SHQ is a self-report questionnaire used to assess history of smoking (e.g., smoking quantity, age of smoking onset). It was employed as a descriptive measure in the current investigation.

2.2.7. Fagerström test for cigarette dependence (FTCD)

The FTCD is a 6-item scale that assesses gradations in tobacco dependence (Fagerström, 2012; Heatherton et al., 1991). The FTCD has adequate internal consistency, positive relations with key smoking variables (e.g., saliva cotinine), and high test-retest reliability (Heatherton et al., 1991; Pomerleau, Carton, Lutzke, Flessland, & Pomerleau, 1994). In the current study (Cronbach’s alpha = 0.64).

2.2.8. Smoking abstinence expectancies questionnaire (SAEQ; Abrams et al., 2011)

The SAEQ is a 28-item self-report measure that assesses expected consequences form smoking abstinence. Items are rated in terms of expected likelihood on a scale from 0 (very unlikely) to 6 (very likely). The SAEQ yields four subscales: somatic symptoms (e.g., “I would feel short of breath”), harmful consequences (e.g., “I would feel like I’m dying”), negative mood consequences (e.g., “I would feel tense”), and positive consequences (e.g., “I would find it easy to conentrate”; Abrams et al., 2011). The SAEQ has demonstrated excellent psychometric properties across independent samples (Svicher, Zvolensky, & Cosci, 2017). In the current study, the somatic symptoms and harmful consequences subscales for the SAEQ were used (Cronbach’s alpha’s = 0.88 and 0.90, respectively).

2.2.9. The Barriers to cessation scale (BCS; Macnee & Talsma, 1995)

The BCS is a 19-item self-report measure assessing the severity of perceived barriers to successfully quitting smoking. Each item (e.g., “No encouragement or help from friends”) is rated on a Likert scale from 0 (not a barrier/not applicable) to 3 (large barrier) and summed. Past work has found good content validity, predictive validity, and internal consistency for the BCS (Garey et al., 2016; Macnee & Talsma, 1995). In the current study, the BCS total score internal consistency was excellent (Cronbach’s alpha = 0.90).

2.3. Procedure

Participants were recruited from Houston, Texas between 2013 and 2016. Following written informed consent, participants completed a diagnostic interview and a computerized assessment protocol. The current investigation is based on secondary analyses of baseline (pre-treatment) data obtained from a larger ongoing smoking cessation trial. Inclusionary criteria for the current study included smoking a minimum of 6 CPD (for at least 1 year) and reporting motivation to quit smoking (i.e., scoring 5 or greater on a 0–10 Likert scale). Participants were excluded if they reported using other tobacco products besides cigarettes, reported suicidality or psychotic symptoms consistent with a current psychotic disorder, were using any pharmacotherapy or enrolled in psychotherapy for smoking cessation, were unwilling to cease use of benzodiazepines or other fast-acting anxiolytics, reported concurrent psychotherapy initiated in the past three months or ongoing anxiety psychotherapy, and reported current or intended participation in a concurrent substance abuse treatment. The study protocol was approved by the Institutional Review Board at the University of Houston. Each participant was paid $20 upon completion of the baseline portion of the study.

2.4. Analytic strategy

Analyses were conducted using the PROCESS macro for SPSS (Hayes & Preacher, 2013), a computational tool for estimating indirect effects of a predictor (X) on a criterion (Y) via one or more mediating variables (Mi). The indirect effect (path ab) is computed as the product of path a (the effect of X on Mi) and path b (the effect of Mi on Y). In the current study, VSI was the predictor with general anxiety (M) as the indirect explanatory variable. Separate analyses were run with each criterion (see Fig. 1). Covariates included gender, presence of axis I disorders, and subjective health status. Both direct and total effects for each model were reported. Further, bootstrapping with 10,000 bootstrap re-samplings was conducted to detect the significance of the indirect effects. Bootstrapping is a non-parametric method that estimates the sampling distribution of an estimator based on re-sampling with replacement from the data set. The indirect effect is computed for each of the re-samples, which results in an empirically generated sampling distribution (Hayes & Preacher, 2013). Bootstrapping has more accurate Type I error rates and power than single sample method that assumes a normal distribution. A bootstrapped confidence interval that does not include zero indicates a statistically significant indirect effect (Preacher & Hayes, 2008).

Fig. 1.

Fig. 1.

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Proposed model. Note: ai = E ect of X on Mi; bi = Effect of Mi on Yi; c = Total effect of X on Yi; c′ = Direct effect of X on Yi controlling for Mi; a * b = Indirect effect of X via Mi. General Anxiety (M) was the mediator in primary analyses. Variables C1–C3 were included as covariates in all models.

Note: ai = Effect of X on Mi; bi = Effect of Mi on Yi; c = Total effect of X on Yi; c’= Direct effect of X on Yi controlling for Mi; a*b = Indirect effect of X via Mi. General Anxiety (M) was the mediator in primary analyses. Variables C1-C3 were included as covariates in all models.

3. Results

3.1. Descriptive statistics

Bivariate correlations and descriptive statistics are presented in Table 2. Visceral sensitivity was positively associated with general anxiety symptoms, but shared only 14% of variance with such (anxiety) symptoms. Visceral sensitivity was significantly related to the studied smoking abstinence expectancies subscales. General anxiety symptoms were significantly positively associated with all dependent variables.

Table 2.

Means, standard deviations, and bivariate correlations.

Variable 1 2 3 4 5 6 7 8 9
1.Gender (male) –
2. Axis I 0.09 –
3. Health 0.03 −0.08 –
4. VSI −0.02 −0.04 0.33** –
5. MASQ-GA 0.21* 0.01 0.32** 0.38** –
6. FTCD 0.25* 0.38** 0.27* 0.16 0.43** –
7. SAEQ-Somatic 0.13 0.01 0.36** 0.25* 0.66** 0.41** –
8. SAEQ-Harmful 0.22 0.12 0.31** 0.24* 0.68** 0.48** 0.79** –
9. BCS 0.15 0.13 0.19 0.13 0.31** 0.55** 0.38** 0.52** –
Mean/N 60 66 3.10 25.80 32.04 9.24 13.60 13.42 27.92
SD/% 71.6 78.5 1.10 21.77 14.70 3.45 9.43 10.63 12.01
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Note: Gender = percent male; Axis I = percent with current Axis I disorder; Health = Subjective report of health per Short Form Health Survey; VSI = visceral sensitivity; MASQ-GA = general anxiety symptoms; FTCD = cigarette dependence; SAEQ = smoking abstinence expectancies; BCS = barriers to cessation. Numbers across header correspond with variables numbered 1–9.

*

p < 0.05.

**

p < 0.01.

3.2. Indirect effect analyses

In predicting cigarette dependence, there was a statistically significant indirect effect of visceral sensitivity via general anxiety (b = 0.02, SE = 0.01, Bootstrapped 95% CI [0.006, 0.05], Completely Standardized Indirect Effect = 0.16). There was no significant total effect of visceral sensitivity (b = 0.01, SE = 0.01, p = 0.51). After accounting for general anxiety, the direct effect of visceral sensitivity was also non-significant (b = −0.01, SE = 0.01, p = 0.64; Table 3). A reverse model was run, examining the indirect effect of general anxiety via visceral sensitivity; the indirect effect was not statistically significant (b = −0.004, SE = 0.01, Bootstrapped 95% CI [−0.03, 0.01]). Additionally, there was no indirect effect of visceral sensitivity on general anxiety symptoms through cigarette dependence (b = 0.02, SE = 0.03, Bootstrapped 95% CI [−0.05, 0.09]).

Table 3.

Mediation models.

Y Model B SE t p LLCI ULCI
1 VSI ➔ MASQ-GA (a) 0.27 0.08 3.11 0.002 0.09 0.44
MASQ-GA ➔ FTCD (b) 0.07 0.03 2.94 0.004 0.02 0.13
VSI ➔ FTCD (c) 0.01 0.01 0.66 0.51 −0.02 0.04
VSI ➔ FTCD (c′) −0.01 0.01 −0.47 0.64 −0.04 0.02
VSI ➔ MASQ-GA ➔ FTCD (a * b) 0.02 0.01 0.006 0.05
2 MASQ-GA ➔ SAEQ-somatic (b) 0.37 0.06 5.56 < 0.001 0.23 0.53
VSI ➔ SAEQ-somatic (c) 0.08 0.05 1.5 0.13 −0.02 0.19
VSI ➔ SAEQ-somatic (c′) −0.04 0.04 −0.42 0.67 −0.11 0.07
VSI ➔ MASQ-GA ➔ SAEQ-somatic (a * b) 0.10 0.03 0.03 0.19
3 MASQ-GA ➔ SAEQ-harmful (b) 0.49 0.07 6.64 < 0.001 0.33 0.62
VSI ➔ SAEQ-harmful (c) 0.08 0.06 1.31 0.19 −0.04 0.24
VSI ➔ SAEQ-harmful (c′) −0.04 0.05 −0.98 0.35 −0.13 0.06
VSI ➔ MASQ-GA ➔ SAEQ-harmful (a * b) 0.13 0.05 0.03 0.25
4 MASQ-GA ➔ BCS (b) 0.21 0.13 1.93 0.05 −0.005 0.42
VSI ➔ BCS (c) 0.05 0.06 0.80 0.39 −0.07 0.19
VSI ➔ BCS (c′) 0.01 0.07 0.08 0.93 −0.13 0.15
VSI ➔ MASQ-GA ➔ BCS (a * b) 0.05 0.06 0.01 0.13
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Note.

a = Effect of X on Mi; b = Effect of Mi on Yi; c = Total effect of X on Yi; c′ = Direct effect of X on Yi controlling for Mi; Path a is equal across all models; therefore, it presented only in the model with Y1 to avoid redundancies. VSI (Visceral sensitivity index) is the predictor; MASQ-GA (Mood and anxiety symptoms scale-general anxiety sub-scale) is the explanatory variable; FTCD (Fargestrom test of cigarette dependence), SAEQ (Smoking abstinence expectancies questionnaire), and BCS (Barriers to cessation scale) are the outcome variables in models 1–4, respectively. LLCI = lower bound of a 95% confidence interval; ULCI = upper bound; ➔ = affects. The indirect effect (a * b) is the product of path a and b. Gender, presence of axis I disorder, and subjective health status were covariates.

Regarding smoking abstinence somatic expectancies, there was a statistically significant indirect effect of visceral sensitivity via general anxiety symptoms (b = 0.10, SE = 0.03, Bootstrapped 95% CI [0.03, 0.19], Completely Standardized Indirect Effect = 0.24). The total effect of visceral sensitivity was non-significant (b = 0.08, SE = 0.05, p = 0.13). However, after accounting for general anxiety, the direct effect of visceral sensitivity was also not significant (b = −0.04, SE = 0.04, p = 0.67; Table 3). The reverse model yielded a non-significant indirect effect of general anxiety via visceral sensitivity (b = −0.01, SE = 0.01, Bootstrapped 95% CI [−0.06, 0.03]). Smoking abstinence somatic expectancies was also not the mediator of the relation between visceral sensitivity and general anxiety symptoms (b = 0.07, SE = 0.05, Bootstrapped 95% CI [−0.01, 0.20]).

In terms of smoking abstinence harmful expectancies, there was a statistically significant indirect effect of visceral sensitivity via general anxiety symptoms (b = 0.13, SE = 0.05, Bootstrapped 95% CI [0.03, 0.25], Completely Standardized Indirect Effect = 0.27). The total effect of visceral sensitivity was nonsignificant (b = 0.08, SE = 0.06, p = 0.19). After accounting for general anxiety, the direct effect of visceral sensitivity was not significant (b = −0.04, SE = 0.05, p = 0.35; Table 3). The reverse model yielded a non-significant indirect effect of general anxiety via visceral sensitivity (b = −0.02, SE = 0.02, Bootstrapped 95% CI [−0.10, 0.01]), and a nonsignificant indirect effect of visceral sensitivity on general anxiety symptoms via smoking abstinence harmful expectancies (b = 0.07, SE = 0.06, Bootstrapped 95% CI [−0.03, 0.23]).

For barriers to cessation, there was a statistically significant indirect effect of visceral sensitivity via general anxiety symptoms (b = 0.05, SE = 0.06, Bootstrapped 95% CI [0.01, 0.13], Completely Standardized Indirect Effect = 0.09). There was no statistically significant total effect of visceral sensitivity (b = 0.05, SE = 0.06, p = 0. 39). After accounting for general anxiety, the direct effect of visceral sensitivity was not significant (b = 0.01, SE = 0.07, p = 0.93; Table 3). The indirect effect of general anxiety via visceral sensitivity was not significant (b = 0.03, SE = 0.04, Bootstrapped 95% CI [−0.07, 0.11]). Also, there was no significant indirect effect for visceral sensitivity on general anxiety symptoms through barriers to cessation (b = 0.01, SE = 0.02, Bootstrapped 95% CI [−0.01, 0.08]).

4. Discussion

The present study examined whether anxiety explains, in part, the relation between visceral sensitivity and an array of clinically-relevant smoking processes among treatment-seeking smokers. Results indicated that visceral sensitivity exerted a significant indirect effect on cigarette dependence, threat-related smoking abstinence expectancies (somatic symptoms and harmful consequences), and perceived barriers for cessation through anxiety symptom severity. Notably, the indirect effects were of medium to large size for all four dependent variables (Completely Standardized Indirect Effects = 0.09–0.27). These results are consistent with the hypothesis that visceral sensitivity is related to anxiety (the ‘a’ path), which is related to a variety of smoking maintenance processes (the ‘b’ path). The observed indirect effects were evident after adjusting for the influence of factors known to correlate with the severity of smoking behavior and anxiety-somatic states, including gender, psychopathology, and perceived health status. Moreover, results from the comparative models examining the indirect effect of general anxiety via visceral sensitivity and the indirect effect of visceral sensitivity on general anxiety symptoms through the dependent variables were rejected. Still, to more fully explore the nature of relations among these variables over time, future prospective modeling of the temporal ordering of visceral sensitivity, anxiety symptom severity, and smoking processes is warranted.

Theoretically, the current results suggest that visceral sensitivity may impact anxiety symptom severity. Visceral sensitivity may foster a threat-based emotional stance wherein smokers are more apt to smoke because it may offer perceived or objective relief from aversive GI-related interoceptive states. For example, smokers with heightened visceral sensitivity may experience greater anxiety symptom severity and such heightened anxiety may increase the chance that they expect smoking abstinence to be personally threatening (e.g., fluctuations in bodily symptoms, fears of losing control). Such smokers could therefore be more apt to smoke, resulting in elevated rates of cigarette dependence. Future work is needed to explore other facets of this working model, including coping-oriented smoking and how these processes relate to smoking behavior and withdrawal patterns during quit attempts.

Although not a primary aim of the current study, it is noteworthy that visceral sensitivity and anxiety symptom severity shared only 14% of variance with one another at the bi-variate level. These data are to the empirical literature that visceral sensitivity is empirically and theoretically distinguishable from anxiety symptoms (Labus et al., 2007). Notably, the current study extends past work to a smoking sample, which is frequently related to a wide array of GI symptoms and disorders (Lakatos, 2009).

The findings from the present investigation may serve to conceptually inform the development of specialized intervention strategies for smokers with elevated visceral sensitivity. Specifically, among smokers with elevated visceral sensitivity, it may be advisable to understand and clinically address visceral sensitivity directly and anxiety more broadly to enhance psychological flexibility related to maladaptive smoking cognitions (e.g., “I need a cigarette to feel better”) and facilitate change in smoking behavior. For example, cognitive-behavioral strategies and pharmacotherapies have shown promise in reducing irritable bowel symptoms among those with and without IBS (Blanchard, 2001; Toner, Segal, Emmott, & Myran, 2000). It is possible that integrating such therapeutic programing into smoking cessation treatment may promote greater rates of abstinence. As such, it is possible that tailoring these treatments to smokers with elevated visceral sensitivity would offer a novel and more personalized approach to improve health and change smoking behavior.

There are several interpretive caveats to the present study. First, given the cross-sectional nature of these data, causal relations cannot be explicated. The present tests were based on a theoretical framework supported by extant empirical data, but did not allow for testing of temporal sequencing. Based upon the present results, future prospective studies are necessary to determine the directional effects of these relations. Second, our sample was relatively small in overall size and consisted of community-recruited, treatment-seeking low-income daily cigarette smokers. Future studies may benefit by sampling a larger pool of smokers and from lighter and heavier smoking populations to ensure the generalizability of the results to the general smoking population. Likewise, sampling smokers who fall in a greater range of socio-economic status would be useful from a generalizability perspective. Third, as the key variables were assessed via self-report, there is the possibility that the observed relations were in part a function of shared method variance. Future research would benefit by employing a multimethod assessment approach to cross-index the nature of the relations observed in the current report.

5. Conclusion

Overall, the present study serves as an initial investigation into the nature of the associations between visceral sensitivity, anxiety symptoms, and clinically significant smoking processes among treatment-seeking smokers. Future work is needed to explore the extent to which anxiety accounts for relations between visceral sensitivity and other smoking processes (e.g., withdrawal, cessation outcome).

HIGHLIGHT.

  • Visceral sensitivity via anxiety symptoms on cigarette dependence was significant.

  • Visceral sensitivity via anxiety symptoms on somatic expectancies was significant.

  • Visceral sensitivity via anxiety symptoms on harmful consequences was significant.

  • Visceral sensitivity via anxiety symptoms on barriers to cessation was significant.

Funding

This work was supported by the National Institute on Drug Abuse (1R34DA031313-01A1).

Role of funding source

This work was supported by the National Institute on Drug Abuse (1R34DA031313-01A1). NIDA had no role in the study design, collection, analysis or interpretation of the data, writing the manuscript, or the decision to submit the paper for publication.

Footnotes

Conflict of interest

All authors declare that they have no conflicts of interest.

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