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. Author manuscript; available in PMC: 2020 Oct 5.
Published in final edited form as: Cogn Behav Ther. 2019 Apr 5;49(2):137–148. doi: 10.1080/16506073.2019.1583277

Anxiety Sensitivity and Daily Cigarette Smoking in Relation to Sleep Disturbances in Treatment-Seeking Smokers

Samantha G Farris a, Stephen V Matsko b, Lisa Uebelacker b,c, Richard A Brown b,d, Lawrence H Price b,c, Ana M Abrantes b,c
PMCID: PMC6778490  NIHMSID: NIHMS1522035  PMID: 30947621

Abstract

Although the association between anxiety and sleep disturbance is well-documented, the underlying mechanisms are less clear. Anxiety sensitivity (AS), the fear of physiological arousal and bodily sensations, is a risk factor for anxiety and poor sleep. Smoking also contributes to poor sleep and may compound the effects of AS on sleep quality. This study evaluated the main and interactive effects of AS and cigarettes/day on sleep quality among smokers. Participants (n=190) were adult treatment-seeking daily smokers who completed a baseline assessment as part of a larger smoking cessation trial. Sleep quality was self-reported. Results indicated that AS was significantly correlated with greater disturbance in sleep duration, subjective sleep quality, sleep onset latency, sleep disturbance, daytime dysfunction, and sleep medication use. There was a significant interaction between AS and cigarettes/day in terms of sleep onset latency, but not other sleep quality indices. AS was associated with significantly longer sleep onset latency minutes among heavier smokers, but not lighter smokers. Specifically, the association between AS and sleep onset latency was significant for those who smoked ≥ 33 cigarettes/day. AS is a psychological factor that may contribute to poor sleep quality, especially in heavy smokers, and thus may be a promising intervention target.

Keywords: sleep, nicotine, anxiety psychopathology, transdiagnostic

1. Introduction

Sleep disturbances, including insomnia, circadian rhythm sleep-wake disorders, sleep related breathing disorders, parasomnias, and sleep-movement disorders, impact 10-18% of the general population (Colten et al., 2006) and have a significant negative impact on cognitive, social, and adaptive functioning (Soehner and Harvey, 2012). The prevalence of sleep disturbances is especially high among individuals with psychopathology (Chokroverty, 2010), particularly anxiety disorders (Cox and Olatunji, 2016; McMakin and Alfano, 2015; Staner, 2003). Indeed, there is a well-documented bidirectional association between sleep disturbances and anxiety, such that sleep problems can serve as a risk factor for the development of anxiety disorders (Alvaro et al., 2013; Gregory et al., 2005; Neckelmann et al., 2007) and, conversely, anxiety disorders can contribute to problematic sleep (Benca et al., 1992; Johnson et al., 2006). Several cognitive and neurobiological processes associated with disrupted anxiety and sleep (e.g., impaired executive functioning, cortisol dysregulation) are thought to maintain problematic symptoms via allostatic overload (Cox and Olatunji, 2016).

Emerging research indicates that certain psychological processes contribute to the anxiety-sleep association (Bei et al., 2015). Anxiety sensitivity (AS), defined as the fear of fear of the physical, mental, and social consequences of anxiety-related bodily sensations (Reiss et al., 1986; Reiss and McNally, 1985), is a trait-like cognitive vulnerability that is implicated in the development of anxiety disorders (Olatunji and Wolitzky-Taylor, 2009). AS is a difficult fear to have because of the ubiquity of bodily sensations. AS is associated with problematic sleep (Otto et al., 2016), including poor sleep quality, delayed sleep onset latency, and poor subjective sleep (Babson et al., 2013, 2008; Hoge et al., 2011; Raines et al., 2015). Individuals with higher levels of AS may be particularly attuned to bodily arousal and bodily sensations, which can heighten the subjective experience of such sensations. When an individual is trying to go to sleep, there are fewer things to distract from attention to bodily sensations, which may contribute to poor sleep initiation and maintenance.

Cigarette smoking is highly comorbid with anxiety disorders (Grant et al., 2004; Lasser et al., 2000; Lawrence et al., 2010; Piper et al., 2011), and is an identified explanatory factor related to the link between anxiety and sleep disturbance (Babson, Feldner, Sachs-Ericsson, Schmidt, & Zvolensky, 2008). Frequent cigarette consumption throughout the day contributes to recurrent bouts of nicotine-induced physiological activation (e.g., increase heart rate; Gajewska, Worth, Urani, Briesen, & Schramm, 2014) and acute withdrawal characterized by anger/irritability, anxiety, restlessness, dysphoria, craving, difficulty concentrating, and increased appetite, which can onset within 30 minutes post-smoking (Hendricks, Ditre, Drobes, & Brandon, 2006). Nicotine withdrawal contributes to the severity of anxious responding to bodily sensations (e.g., Feldner, Vujanovic, Gibson, & Zvolenksy, 2008; Zvolensky et al., 2005) and severity of sleep disturbances (e.g., Jaehne et al., 2015; Zhang, Samet, Caffo, & Punjabi, 2006; Zhang, Samet, Caffo, Bankman, & Punjabi, 2008). Moreover, nicotine-induced arousal and withdrawal produces physiological sensations to which people with elevated AS may be very attentive. In fact, AS amplifies the subjective experience of nicotine withdrawal (Zvolensky, Farris, Guillot, & Leventhal, 2014), which may be one explanation as to why AS is linked to the comorbidity of anxiety and sleep disorders in substance users (Dixon et al., 2018).

We are aware of only one study that examined the association between AS and sleep in the context of cigarette smoking. Among adolescents with varying levels of cigarette use (Mean cigarettes/day = 3.9), AS was associated with poorer self-reported sleep quality across sleep domains, and there was a significant interaction between AS and smoking level (cigarette/day) for sleep onset latency, but not other sleep domains (Bilsky et al., 2016). Among adolescents with elevated AS, those who smoked more (≥9 cigarettes/day) had significantly longer delayed sleep onset relative to lighter/non-daily smokers. Thus, higher levels of daily cigarette use may heighten arousal and contribute to sleep onset difficulty, especially for individuals with elevated AS who may be particularly focused on internal states while attempting to initiate sleep.

The current study was designed to extend the abovementioned line of work to adult daily smokers with higher average daily smoking levels (≥10 cigarettes/day). The primary aim was to evaluate the main and interactive effects of AS and smoking rate on sleep disturbances in adult daily smokers. We hypothesized that AS would be positively associated with sleep disturbances. Additionally, we hypothesized that there would be a significant interaction between AS and smoking levels on sleep disturbance, such that the combination of elevated AS and heavier smoking levels would be associated with greater sleep disturbance (e.g., poorest sleep onset latency).

2. Material and Methods

2.1. Participants

Participants were adult daily smokers with at least mild depressive symptoms who were seeking smoking cessation treatment (clinicaltrials.gov #: NCT02086149) who enrolled in a randomized control trial testing the efficacy of cognitive-behavioral smoking cessation treatment and nicotine replacement therapy, with one of two adjunctive interventions: (a) 12-session, group aerobic exercise (AE) intervention or (b) 12-session, group health-education control (HEC) intervention. Participants were included on the basis of being between ages 18-65, low active (i.e., not engaging in more than 90 minutes of weekly moderate-to-vigorous physical activity in the last 12 weeks), smoking 10 or more cigarettes per day, and at least mild depressive symptoms (≥6 on the Center for Epidemiological Studies Depression Scale; CES-D) (Radloff, 1977). Secondary data analyses were conducted using of data collected at baseline, prior to randomization, from cases with complete data on the variables of interest for the current study (n = 190). Informed consent was obtained from all participants. All protocol procedures were approved by the Institutional Review Board where the study took place.

2.2. Measures

The Anxiety Sensitivity Index-3 (ASI-3;Taylor et al., 2007) is an 18-item self-report assessment of fears about the possible negative effects of anxiety and related bodily sensations (e.g., “It scares me when my heart beats rapidly”; “When my thoughts seem to speed up, I worry that I might be going crazy”). Items are rated on a five-point Likert scale ranging from 0 (very little) to 4 (very much) and summed to create a total score (possible range 0-72). The ASI-3 items have strong and improved psychometric properties relative to previously measured items of the construct (Taylor et al., 2007), and have strong documented psychometric properties in treatment-seeking smokers (Farris et al., 2015).

The Smoking History Questionnaire (Brown et al., 2002) was used to document average cigarettes per day in the past week. Positive smoking status was biochemically verified at baseline via expired carbon monoxide breath samples ≥10 parts per million, which is an optimal cut-off for distinguishing between tobacco use versus non-use (SRNT Subcommittee on Biochemical Verification, 2002). The Fagerström Test for Cigarette Dependence (Fagerström, 2012) is a 6-item self-report assessment of tobacco dependence severity. Higher scores reflect greater physiological dependence on tobacco (possible range 0-10).

The Positive and Negative Affect Schedule (PANAS; Watson, Clark, & Tellegen, 1988) is a 20-item self-report measure in which respondents rate the extent to which they experience different feelings and emotions (e.g., nervous, interested) in the past 2 weeks. Each item is on a Likert scale that ranges from 1 (“Very slightly or not at all”) to 5 (“Extremely”). The measure yields two factors, negative and positive affect. The negative affectivity subscale was used in the present study.

The Pittsburg Sleep Quality Questionnaire (PSQI; Buysse, Reynolds, Monk, Berman, & Kupfer, 1989) measures seven domains of sleep including subjective sleep quality, sleep latency (i.e., time to fall asleep), sleep duration (i.e., time asleep), habitual sleep efficiency (hours slept relative to hours in bed), sleep disturbances (e.g., frequent waking, snoring), use of sleep medication, and daytime dysfunction (i.e., trouble during the day due to poor sleep), over the last month. Item scoring is based on a 0-3 scale, which can was used to calculate subscales in the domains listed above as well as a global score. A global score of 5 of greater indicates a “poor” sleeper, with a possible range of 0-21.

2.3. Data Analytic Strategy

Zero order bivariate associations were examined between AS and sleep indices. Next, we examined the interaction between anxiety sensitivity and cigarettes per day in terms of sleep indices, consistent with prior work (Bilsky et al., 2016). Interaction analyses were conducted using PROCESS, a conditional process modeling program that utilizes an ordinary least squares-based analytical framework (Hayes, 2013). Based on prior work, age and sex were included as model covariates (Bilsky et al., 2016). Negative affect, a core feature that underlies depression and anxiety disorders (Norton and Mehta, 2007), was also included as covariate in light of the clinical characteristics of the sample (i.e., smokers with at least mild depression symptoms) and to test the specificity of AS as a model predictor relative to negative affect more broadly. The Johnson–Neyman (J–N) technique (Johnson and Fay, 1950; Johnson and Neyman, 1936) was utilized to evaluate the association between AS and sleep across the range of cigarettes/day to identify where the association transitioned from being statistically significant to non-significant. The J-N technique identifies the value of the third variable for which the ratio of the conditional effect to its standard error is equal to the critical t score.

3. Results

3.1. Descriptive Overview

Participants (n = 190, Mage = 43.7, SD = 12.0) were primarily female (68.9%), smoked on average 18.6 (SD = 8.0) cigarettes per day and had moderate levels of tobacco dependence (M = 5.41, SD = 2.08). AS was elevated in the sample, with an average ASI-3 score of 14.4 (SD = 13.6). Approximately one-third (34.2%) of the sample had ASI-3 scores ≥17, reflecting moderately elevated level anxiety sensitivity. On average, the sample had low sleep quality, as evidenced by average scores ≥5 (M = 8.44, SD = 4.31). See Table 1 for descriptive summary and bivariate associations between study variables.

Table 1.

Bivariate associations between study variables

Variable 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.
1. Sex (female) - .185* −.010 −.039 .130 .149* .097 .020 .055 .166* .136 .099 .112
2. Age - −.085 −.034 −.014 −.108 −.216** −.239** −.022 −.035 .077 .004 −.025
3. Negative affect - .180* .476** .267** .218** .179* .142 .111 .137 .138 .314**
4. Cigarettes/day - .127 .173* .172* .146* .153* .057 .190** −.011 .141
5. Anxiety sensitivity - .326** .301** .151* .139 .138 .206** .188** .409**
6. PSQI Global score - .784** .725** .650** .688** .596** .500** .573**
7. PSQI Subjective sleep quality - .555** .598** .490** .444** .147* .399**
8. PSQI Sleep onset latency - .320** .372** .359** .245** .392**
9. PSQI Sleep duration - .537** .367** .012 .143*
10. PSQI Sleep efficiency - .289** .172* .181*
11. PSQI Sleep disturbance - .153* .328**
12. PSQI Sleep medication use - .285**
13. PSQI Daytime dysfunction -
Mean or N 131 43.7 18.8 18.6 14.4 8.4 1.4 1.5 1.4 0.8 1.5 0.8 1.1
SD or % 68.9% 12.0 6.9 8.0 12.8 4.3 0.9 1.1 1.0 1.0 0.7 1.2 0.8
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*

p < .05,

**

p < .01

3.2. Anxiety Sensitivity and Sleep Quality

As presented in Table 1, AS was significantly correlated with higher scores on the PSQI, reflecting lower sleep quality. Specifically, AS was positively correlated with the PSQI subscales reflecting problems due to subjective sleep quality, sleep onset latency, sleep medication use, sleep disturbance, and daytime dysfunction. AS was not significantly associated with sleep duration or efficiency.

3.3. Interaction between AS and Cigarettes/Day on Sleep Quality

Results from regression models revealed a non-significant interaction between AS and cigarettes/day in terms of sleep quality, with the exception of sleep onset latency. See Table 2 for model results for (a) sleep onset latency minutes and (b) frequency of delayed sleep onset.

Table 2.

Regression results of interaction between AS, Cigarette/Day and Sleep Latency

Sleep Onset Latency Minutes
b se t p
Sex 4.34 5.27 0.82 .411
Age −0.59 0.20 −2.92 .004
Negative Affectivity 0.72 0.40 1.81 .073
Anxiety Sensitivity (AS) 1.86 0.84 2.23 .027
Cigarettes/Day (CPD) 0.42 0.30 1.40 .164
AS × CPD 0.03 0.02 2.29 .023
Delayed Sleep Onset Frequency
b se t p
Sex 0.09 0.19 0.48 .634
Age −0.03 0.01 −2.77 .006
Negative Affectivity 0.01 0.01 0.03 .975
Anxiety Sensitivity (AS) 0.03 0.01 0.82 .411
Cigarettes/Day (CPD) 0.03 0.01 2.27 .024
AS × CPD 0.01 0.01 0.33 .742
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3.3.1. Sleep onset latency.

With regard to sleep onset in minutes, participants reported an average sleep onset latency of 35.48 (SD = 33.07) minutes in the past month. The model predicting sleep onset latency minutes was significant (F[5,184] = 4.42, p < .001, R2 = .107). There was a significant main effect of younger age in terms of greater sleep onset delay, although no other significant effects of model covariates. There was a significant main effect of anxiety sensitivity, such that every 1-point increase in AS was associated with a 1.86 minute increase in sleep onset latency. There was a non-significant main effect of cigarettes/day in terms of sleep onset latency minutes, however the interaction between AS and cigarettes/day was associated with significant incremental variance in sleep onset latency minutes (R2 = .06, p = .023). Figure 1 illustrates the form of the interaction. The J-N technique revealed that the conditional effect of AS on sleep onset latency minutes was significant for those who smoked ≥ 33 cigarettes per day. Thus, as smoking rate increased, the association between AS and sleep onset latency minutes became stronger, whereas in smokers using fewer than 33 cigarettes per day, the association between AS and sleep onset latency was non-significant.

Figure 1.

Figure 1.

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Interaction between anxiety sensitivity and smoking rate on sleep onset latency in minutes

3.3.2. Frequency of delayed sleep onset.

Delayed sleep onset of 30 or more minutes in the past month was reported as never occurring (33.3%), occurring less than once per week (21.2%), occurring one or twice per week (15.3%), and occurring three or more times per week (30.5%). The model with the interaction term predicting frequency of delayed sleep onset was significant (F[4,185] = 3.48, p = .003, R2 = .103). There was a non-significant main effect of AS, however cigarettes per day was significantly positively associated with more frequent delayed sleep onset in the past month. The interaction between AS and cigarettes per day did not account for significant incremental variance in the frequency of delayed sleep onset (R2 = .001, p = .742).

4. Discussion

Findings indicate that evidence of an association between AS and sleep disturbance among adult daily cigarette smokers. AS was associated with subjective indices of sleep, including poorer subjective sleep quality, longer sleep onset latency, greater sleep disturbance and daytime dysfunction, and more sleep medication use. The current set of findings are generally consistent with prior work documenting the link between AS and sleep disturbance among adults with anxiety symptoms and disorders (Babson et al., 2013, 2008; Hoge et al., 2011; Raines et al., 2015), adults with comorbid anxiety and substance use disorders (Dixon et al., 2018), and adolescent smokers (Bilsky et al., 2016). Individuals with higher levels of AS may be more likely to selectively attend to, and then be distressed by, internal sensations, making sleep initiation more difficult (Cox and Olatunji, 2016). AS is also characterized by cognitive biases to negative psychological and physiological states. As a result, AS may (a) heighten attention to sleep-related changes in mental or physical functioning in the morning after waking, (b) contribute to the perception that such changes are evidence of poor sleep (poor sleep quality, greater sleep disturbance), (c) influence biased interpretations of the potential impact of such changes (e.g., overestimate the impact), which (d) could lead to the use of sleep medication out of concern that sleep may not be sufficient otherwise.

AS was not related to sleep duration or sleep efficiency, which are evaluated based on concrete events (i.e., sleep time, wake time) relative to subjective evaluations of sleep. Subjective experience of sleep is commonly reported as worse relative to objectively-measured sleep (Kaplan et al., 2017), especially in individuals with anxiety (Klumpp et al., 2017; McMakin and Alfano, 2015). Thus, AS appears to be most strongly related to subjective (perceived) sleep disturbances, which is consistent with cognitive models of sleep disturbance (Bei et al., 2015).

The present findings indicated that the combination of elevated AS and heavier smoking (≥33 cigarettes/day) contributed to longest sleep onset latency, which extend prior findings in adolescents (Bilsky et al., 2016). Heavier smokers (relative to lighter) likely have higher plasma levels of nicotine throughout the day, including before bedtime, which can heighten nicotine-induced physiological arousal and subsequent periods of acute withdrawal when attempting to fall asleep (e.g., sensations such as restlessness, anxiety, and difficulty concentrating). , Heavier smoking among individuals with elevated AS may heighten awareness to nicotine-related arousal and subsequent worry about the symptoms, as well as the inability to fall asleep. Notably, findings were unique to the duration of sleep onset latency but not frequency of delayed sleep onset. This pattering of findings might suggest that AS and heavier smoking may contribute to contribute to same-day delayed sleep, rather than producing a cumulative effect on delayed sleep over time. Future laboratory-based examinations of within-day cigarette consumption and objectively-measured sleep onset latency in the context of AS over time would provide a more fine-grained understanding of the AS-smoking-sleep associations.

There are several notable limitations worth consideration. First, the data were cross-sectional in nature, so the directionality of the associations between smoking, AS, and sleep disturbances are unknown. Future experimental work designed to isolate the specific influence of smoking and nicotine on the AS-sleep association is needed. A prospective test would also be important to understand temporal relations between AS and daily sleep disturbances, in the context of same-day cigarette use. Second, we relied exclusively on self-reported sleep disturbance per the PSQI. Future work in this area should include objective indices of sleep disturbance (e.g., polysomnography, actigraphy), in conjunction with self-reported sleep quality, to isolate the influence of AS on objective and subjective aspects of sleep. Third, there may be additional, unmeasured factors that could contribute to sleep disturbances. For example, alcohol and substance use contribute to poor sleep quality (Dixon et al., 2018), although were not evaluated in the current study. Fourth, the clinical characteristics of the sample are important to consider in terms of their potential effect on external validity (i.e., generalizability): the sample comprised primarily of female smokers (68.9%), with at least mild depression who were all low active. Importantly though, females are twice as likely to have anxiety and depressive psychopathology (Kessler et al., 1993; McLean and Anderson, 2009) and are more sensitive to the rewarding effects of smoking (e.g., Isaksson et al., 2014) compared to males; thus, female smokers may be a particularly important group of individuals to consider when evaluating the interplay between AS, tobacco use, and sleep disturbances.

Overall, the present findings add to the understanding of AS and sleep disturbance, and the influence of cigarette smoking. AS is a transdiagnostic cognitive vulnerability that is implicated in anxiety disorders (Olatunji and Wolitzky-Taylor, 2009), comorbidity of anxiety and sleep disturbances (Hoge et al., 2011), and persistence of smoking (Leventhal and Zvolensky, 2015), and thus may be a promising treatment target for these clinical conditions individually or as they co-occur with one another. AS is malleable through cognitive-behavioral interventions (Smits et al., 2008), including brief interventions requiring minimal therapist involvement (Keough and Schmidt, 2012; Schmidt et al., 2016, 2014, 2007). AS interventions that address fearful appraisal and responses to arousal, produced through sleep or nicotine deprivation, might have promising effects for anxiety management. For example, a cognitive-behavioral smoking cessation intervention that targets AS (Zvolensky et al., 2018) could be used help decrease nicotine-related arousal and reactivity to such arousal, which in turn might have positive effects on sleep and result in improved mental health outcomes (Schmidt et al., 2016).

Highlights.

  • AS is positively associated with self-reported sleep disturbance in adult smokers

  • AS is most strongly associated with poorer perceived sleep disturbance

  • Elevated AS was associated with longer delayed sleep onset latency in heavy smokers

Acknowledgments

Role of Funding Sources: This work was supported by a grant (R01CA173551) funded by the National Cancer Institute. The first author was supported by a grant (T32-HL076134-11) funded by the National Heart, Lung, and Blood Institute. The funding sources had no involvement in the research other than financial support.

Footnotes

Conflict of Interest: Drs. Farris, Matsko, Uebelacker, Price, and Abrantes have no disclosures to report. Dr. Brown has equity ownership in Health Behavior Solutions, Inc., which is developing products for tobacco cessation although not products directly related to this publication. The terms of this arrangement have been reviewed and approved by the University of Texas at Austin in accordance with its policy on objectivity in research.

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