Mind–body practices: An alternative, drug-free treatment for smoking cessation? A systematic review of the literature

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Nicotine & Tobacco Research, 2015, 1–10
doi:10.1093/ntr/ntv210
Original investigation
© The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved.
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1
Original investigation
Impulsivity and Stress Response in
Nondependent Smokers (Tobacco Chippers) in
Comparison to Heavy Smokers and Nonsmokers
LauraCarim-Todd PhD1,2, Suzanne H.Mitchell PhD3,4,
Barry S.Oken MD, MS1,2,3
1Department of Neurology, Oregon Health & Science University (OHSU), Portland, OR; 2Oregon Center for
Complementary and Alternative Medicine in Neurological Disorders (ORCCAMIND), Oregon Health & Science
University, Portland, OR; 3Department of Behavioral Neuroscience, Oregon Health & Science University, Portland,
OR; 4Department of Psychiatry, Oregon Health & Science University, Portland, OR
Corresponding Author: Laura Carim-Todd, PhD, Department of Neurology, Oregon Health & Science University (OHSU),
Mail Code CR120, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA. Telephone: 503-494-7219; Fax: 503-494-9520;
E-mail: carimtod@ohsu.edu
Abstract
Introduction: Tobacco chippers are light smokers with stable patterns of smoking that exhibit lower
nicotine dependence severity than heavy smokers. Chippers may provide valuable information
about the factors influencing drug dependence. Impulsivity and stress are two factors known to
influence smoking. By comparing nondependent smokers (tobacco chippers, n=25) to dependent
smokers (heavy smokers, n =23) and nonsmokers (n=25), this study examines the relationship
between nicotine dependence, impulsivity, chronic stress, and stress reactivity.
Methods: A total of 73 adult participants completed a study visit that included questionnaires
to measure nicotine dependence, chronic stress, personality, affect, withdrawal, and craving.
Impulsivity was measured with the delay discounting task and the flanker task. Stress reactivity
was assessed by monitoring respiration, heart rate, and salivary cortisol during performance of a
titrated Stroop task. Effects of acute stress on affect and craving were examined.
Results: Tobacco chippers were as impulsive as heavy smokers on the delay discounting task but
no different from nonsmokers on the flanker task. Heavy smokers reported higher perceived stress
than chippers and nonsmokers. Perceived stress was a significant predictor of discounting only in
heavy smokers. Acute stress induced changes in respiration, heart rate, and heart rate variability.
Craving and negative affect increased after stress in both smoking groups, but craving was associ-
ated with affect only in chippers.
Conclusions: Tobacco chippers do not differ from heavy smokers in impulsivity, but do differ in per-
ceived stress. One’s perception and experience of stress might be associated to nicotine depend-
ence resistance and could inform smoking cessation treatments.
Implications: By examining impulsivity, chronic stress, and stress reactivity in nondependent
smokers (tobacco chippers) compared to dependent smokers and nonsmokers, this study contrib-
utes to the understanding of nicotine addiction and informs smoking cessation programs.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 002
Introduction
Occasional tobacco smoking often progresses to heavy regular
smoking and nicotine dependence. However, a fraction of smok-
ers remain as occasional smokers with stable patterns of daily or
nondaily light smoking and lower nicotine dependence severity than
heavy smokers.1 These smokers, also known as tobacco chippers, do
not differ in nicotine absorption or metabolism from regular heavy
smokers.2 Identifying physiological and/or psychological differences
between chippers and heavy smokers might provide information
about the factors that inuence drug dependence, and hence, inform
and improve smoking cessation treatments.2
Impulsivity and stress are two factors known to inuence smok-
ing behavior.3–5 The stress-vulnerability model hypothesizes that
stress increases risk for addiction by decreasing behavioral control
(increasing impulsivity).6 Impulsivity is a multidimensional con-
cept that has been dened as an inability to wait, a tendency to act
without forethought, insensitivity to consequences, and an inability
to inhibit inappropriate behaviors.7 Studies suggest that impulsive
decision-making (ie, choosing small immediate rewards over delayed
larger ones) and impulsive disinhibition (ie, responding prematurely
or failing to inhibit responding) are distinct facets of impulsivity.8–10
A high level of impulsivity has been equated with preferences for
immediate gratication, risky activities, novel sensations, and easier
routes to self-gratication, as well as inability to persist at a task
and shorter reaction times.9,11–13 Regular smokers have been found
to be more impulsive than nonsmokers.9,14 However, there is limited
knowledge about impulsivity in nondependent smokers.15–17 Studies
are needed to determine if chippers are less impulsive than heavy
smokers and, as a result, less dependent and more able to “choose”
when and how much tosmoke.
In contrast to the trait-like inuence of impulsivity on smoking,
stress is a state-like condition known to affect smoking maintenance
and failure to quit.18,19 Physiologically, a stress response involves the
activation of the hypothalamic-pituitary-adrenal axis (HPA) and
consequent secretion of cortisol, as well as the stimulation of the
sympathetic branch of the autonomic nervous system which results,
amongst others, in an increase in cardiovascular load and breath
rate.20,21 As with other psychoactive drugs, most smokers report
smoking as a coping mechanism during stressful situations. In regu-
lar smokers stress triggers increases in craving, smoking amount,
and smoking intensity.22–24 In addition, an individual’s smoking
behavior is inuenced by their subjective arousal state, presmoking
baseline stress level/tolerance and the environment and nature of
the stressor.25,26 However, the role of stress in maintaining a pattern
of light smoking is still unclear. The lower dependence on nicotine
exhibited by tobacco chippers might be in part explained by differ-
ences in the experience, perception, and/or response to stress. More
research is needed to examine this hypothesis and better understand
the relationship between stress and nicotine dependence.
Accordingly, to help understand drug dependence and identify
potential factors of resistance to dependence progression, this article
characterizes nondependent smokers in terms of impulsivity, stress
perception, and acute stress reactivity, and investigates if they dif-
fer and how from dependent smokers and nonsmokers. In addition,
we examine if facets of personality such as neuroticism, previously
associated with chronic stress,27 and sensation-seeking,28 which has
been predictive of drug use, are associated differentially in our study
groups. Furthermore, following previous observations in our labora-
tory suggesting that the nonjudgment factor of the mindfulness trait
scale is inversely associated to stress,27,29 we explore its association
to nicotine dependence. Individual experiences of affect, craving and
withdrawal are also examined.
Methods
Participants
Using online advertising, we recruited participants from the Portland,
Oregon area between 25 and 55years of age. Each one was classied
to one of the following groups:
1. Nonsmokers (NS). No history of regular daily tobacco smoking,
with less than 100 cigarettes smoked in their lifetime, and a cur-
rent breath carbon monoxide concentration under 5 ppm.
2. Nondependent smokers (chippers [CH]). Smoke 1–5 cigarettes/d
at least 2 d/wk for at least 2 years and no history of heavy
smoking.30 Nondependent with a Fagerstrom Test for Nicotine
Dependence score of 4 or less.31
3. Dependent smokers (heavy smokers [HS]). Smoke at least 15
cigarettes/d and breath carbon monoxide over 10 ppm at the
outset of the study.30 Classied as nicotine dependent using the
Fagerstrom Test for Nicotine Dependence (score of 5 or above).31
Exclusion criteria included: (1) unstable signicant medical prob-
lems; (2) evidence suggesting signicant neurologic disease; (3) a his-
tory of substance use disorder (excluding Nicotine Dependence); and
(4) a history of serious psychiatric disorder.
Procedure
All participants provided informed consent. The visits were sched-
uled at 8.30 AM and were approximately 3 hours long. Participants
were asked to smoke as usual preceding their study visit. They were
given the option to smoke once during the visit (60 minutes before
stress induction) to avoid confounding due to withdrawal from
smoking. Among heavy smokers, 82.61% chose to smoke compared
to 16% of chippers. Measures were collected before (baseline) and
after (outcome) performance of a stress-inducing titrated Stroop
task.32 Once outcome measures were completed, participants were
compensated and dismissed.
Measures
A summary of the measures used in this study can be found in
Table1.
Self-Report
Participants completed self-report questionnaires to measure
nicotine dependence (Fagerstrom Test for Nicotine Dependence,
FTND),31 chronic stress (Perceived Stress Scale, PSS),42 personality
traits (Neuroticism Extroversion Openness-Five Factor Inventory,
NEO-FFI43; Sensation-Seeking Scale, SSS44; Five Factor Mindfulness
Questionnaire, Nonjudgment factor, FFMQ-NJ45), affect (Positive
and Negative Affect Scale, PANAS),46 withdrawal symptoms
(Minnesota Nicotine Withdrawal Scale, MNWS),47 and cigarette
craving (Questionnaire on Smoking Urges, QSU).48
Objective Measures
Participants performed two tasks that assessed two different facets
of impulsivity: impulsive decision-making (delay discounting task)
and response inhibition (anker task). To assess stress, we moni-
tored heart rate and respiration, and obtained saliva samples for
cortisolassay.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 00 3
1. Delay discounting task. Impulsivity was assessed based on a self-
paced computerized task.9 Participants chose between a varying
amount of hypothetical money now or a hypothetical $10.00
after a varying delay. The immediate money varied from $0.00
to $10.50 in $0.50 increments. The delayed money was available
after 0, 7, 30, 90, 180, or 365days. Each delayed alternative
was paired with each immediate alternative, and presented in
a random sequence. Two main measures were determined: the
“indifference point,” the amount of immediate money at which
participants are indifferent between the immediate reward or the
delayed amount for each delay period; and the “rate of discount-
ing” using the following hyperbolic equation V=M / (1 + k × D),
where V=subjective value of delayed item, M=value of delayed
item, D=delay length, and k=gradient of discounting function
(rate of discounting).9
2. Flanker task. This task measures a cognitive form of response
inhibition in which participants resolve conicting responses due
to interfering stimulus that, if not inhibited, lead to errors.49,50
Acomputerized version of the Eriksen anker task was used.33
Participants pushed a left or right button depending on the ori-
entation of the central of the 5 chevrons presented at variable
intervals. Stimuli were preceded half the time by a nonspecic
cue. The direction of the 4 anker chevrons was 50% congruent
and 50% incongruent with the central chevron. For each condi-
tion, median reaction time and accuracy were used as outcome
measures. Analysis focused on the incongruent condition, which
required more cognitive inhibition processing. Higher reaction
times and lower accuracy indicated less efcient inhibition.
3. Heart rate and respiration. Heart rate monitoring was per-
formed using ECG electrodes placed bilaterally and subclav-
icular. Respiration was recorded using an elastic piezoelectric
strap (Ambu-Sleepmate, Maryland). ECG and respiration were
recorded during an auditory vigilance task (baseline) and dur-
ing the Stroop task (outcome) using a Biosemi data acquisi-
tion system (Biosemi, Amsterdam, The Netherlands) collected
at 1024 Hz. Data processing used Brain Vision Analyzer 2.0
(Brain Products GmbH, Munich, Germany), Matlab r2007a,
and Kubios HRV v 2.0 (University of Kuopio, Kuopio, Finland).
We computed time-domain measures of HRV because they have
been shown to be more reliable,51 and present data on pNN50
(the proportion of NN50 divided by total number of NNs).
4. Salivary cortisol. Saliva was collected in Sarstedt Salivette tubes
(Sarstedt, Germany) at baseline (10.30 AM to 11.00 AM) and 20
minutes after the end of the stress-inducing task (11.00 AM to
11.30 AM). Due to the circadian rhythm of cortisol concentra-
tion and for consistency across samples, all procedures were per-
formed in the morning.34 Participants chewed on a cotton swab
for 2 minutes. Cortisol values were quantied by the Oregon
Clinical and Translational Research Institute lab in duplicate
with enzyme-linked immunoassay (Salimetrics, State College,
PA).
Stress Induction
A titrated version of the Stroop task was used to induce acute stress.32
Laboratory events that have novelty, unpredictability, threat to one’s
ego, or sense of loss of control (NUTS) such as public speaking, cog-
nitive testing, problem-solving, or emotionally demanding social
interactions, are capable of inducing a stress response.21,35–37,40 When
applied carefully, mental stress testing induces consistent physiological
responses with good test-retest reliability.38,39 Atitrated version of the
Stroop color-word task includes all of the NUTS features and is consid-
ered a nonspecic stressor.35,38 Participants rated how stressed they felt
during performance of the titrated Stroop using a 5-point Likert scale.
Data Analysis
Means, medians, and standard deviations were calculated for each
variable and values examined for outliers and normality of distribu-
tion. Alog transformation was used when necessary for statistical
analysis. To investigate group differences at baseline, variables were
compared between groups using analysis of variance (ANOVA).
Nonparametric analyses (Kruskal-Wallis ANOVA) were performed
for categorical data. To analyze the effect of stress induction on affect,
craving, heart rate, heart rate variability, respiration, and salivary
Table1. Measures Used in the Present Study
Construct Instrument Baseline Outcome Cronbach’s alpha Reference
Nicotine dependence Fagerstrom Test for Nicotine
Dependence (FTND)
x 0.829 Ref.31
Chronic stress Perceived Stress Scale (PSS) x 0.886 Ref.42
Personality traits Neuroticism Extroversion Openness-
Five Factor Inventory (NEO-FFI)
x 0.881 Ref.43
Sensation-Seeking Scale (SSS) x 0.876 Ref.44
Five-facet Mindfulness Questionnaire
(FFMQ), nonjudgment factor
x 0.866 Ref.45
Withdrawal Minnesota Nicotine Withdrawal Scale
(MNWS)
x 0.688 Ref.47
Craving Questionnaire on Smoking Urges (QSU) x x 0.934 Ref.48
Affect Positive and Negative Affect Scale
(PANAS)
x x 0.812 Ref.46
Impulsivity Delay Discounting Task x Ref.9
Flanker task x Ref.33
Physiological measures
of stress
Respiration x x
Heart rate x x
Heart rate variability x x
Salivary cortisol x x
Internal consistency (Cronbach’s alpha) measured in our sample at baseline is shown.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 004
cortisol, a repeated measures ANOVA with group as a between-sub-
jects factor and time as a repeated within-subjects factor was applied.
Bonferroni correction was applied for post hoc testing. To investigate
the relationship between baseline measures and changes in outcome
measures after stress, regression analyses were performed.
Missing data, due to poor signal or technological malfunctions,
were randomly distributed and were handled by excluding partici-
pants from specic analyses. Thus, some analyses had a different n.
All statistical analyses were performed with Stata version 11 (STATA
Corp., Texas)
Results
Baseline Measures
Demographics and PersonalityTraits
After an initial online screening, 178 subjects were eligible. From these,
73 were interested in the study visit, scheduled an appointment, were
conrmed eligible, and after informed consent, completed participa-
tion. Asummary of the demographics of the study sample is shown
in Table 2. The majority of participants were of Caucasian origin
(84.9%). The average age was 33 and there were slightly more females
than males. No signicant differences between groups were found for
age, years of education, race and ethnicity, and marital status. There
were signicant differences in baseline smoking measures and no dif-
ferences in baseline measures of personality (NEO-FFI, the sensation
seeking scale, or the nonjudgment factor of the mindfulness scale).
Impulsivity
Performance of the delay discounting task conrmed that smok-
ers behave more impulsively than nonsmokers (Figure1). ANOVA
with discounting rate (lnk) as dependent variable identied a
signicant effect of group [F(2, 69)=9.11, P < .001; NS= 25,
CH = 24, HS =23]. Bonferroni post hoc analyses showed that
both heavy smokers and chippers discounted signicantly more
than nonsmokers (P < .01). There was no signicant effect of age
or gender in our sample. In contrast, analysis of inhibition (as
another measure of impulsivity) using the anker task revealed
no signicant baseline differences between study groups in
median reaction time [F(2, 64)=1.26, P > .05] or accuracy [F(2,
64)= 0.56, P > .05] during the incongruent condition (NS = 22,
CH=22, HS=23).
Stress
Signicant group differences were detected in baseline self-reported
chronic stress perception [F(2, 68)=4.06, P < .05] with heavy smok-
ers scoring signicantly higher than nonsmokers (NS=24, CH=25,
HS=22). In contrast, tobacco chippers’ perception of chronic stress
did not differ from that of nonsmokers. ANOVA using respiration
rate (breaths/min) revealed no differences in baseline respiration
between study groups [F(2, 66)=1.01, P > .05; NS=24, CH=22,
HS=23]. However, signicant differences were detected in average
heart rate [F(2, 62)=6.50, P<0.01; NS=21, CH= 22, HS=22].
Post hoc analysis identied a signicantly higher baseline average
heart rate in heavy smokers (Table2).
Table2. Baseline Characteristics of the Sample Population
Nonsmokers (NS) Chippers (CH) Heavy smokers (HS) PPost hoc
Sample size (female) 25 (14) 25 (14) 23 (14)
Demographics
Age 33.68 ± 1.61 31.38 ± 1.39 34.75 ± 1.67 .308
Education (%>16years) 40.0 32.0 18.2 .148
Race/ethnicity (%)
African American 4.0 12.5 4.2 .896
Caucasian 92.0 75.0 87.5
Hispanic 0 0 4.2
Other 4.0 16.7 0
Marital status (%)
Never married 73.9 68.0 40.9 .777
Married 17.4 16.0 27.3
Separated/divorced 8.7 16.0 31.8
BMI 27.48 ± 1.41 29.78 ± 1.75 31.69 ± 2.38 .288
Alcohol (drinks/wk) 2.20 ± 0.63 6.04 ± 1.38 2.39 ± 0.63 .008 CH>HS, CH>NS
Smoking measures
Cig/day 0.00 2.61 ± 0.39 17.21 ± 1.00 .000 HS>CH>NS
FTND 0.00 0.63 ± 0.28 5.04 ± 0.36 .000 HS>CH, HS>NS
BCO 0.00 4.27 ± 0.66 18.27 ± 2.25 .000 HS>NS, HS>CH
Cigarette craving 44 ± 2.12 84.08 ± 5.88 137.91 ± 6.05 .000 HS>CH>NS
Withdrawal symptoms 13.36 ± 0.66 15.88 ± 1.11 16.52 ± 0.76 .030 HS>NS
Stress measures
Perceived Stress 14.08 ± 1.25 14.48 ± 1.31 19.04 ± 1.48 .022 HS>NS
Respiration 14.36 ± 0.83 14.97 ± 0.78 15.91 ± 0.63 .237
Heart rate 66.19 ± 1.67 70.94 ± 1.72 76.37 ± 2.45 .001 HS>NS
Heart rate variability 21.61 ± 3.75 27.06 ± 3.90 8.20 ± 2.25 .003 CH>HS
BCO=breath carbon monoxide (ppm); BMI=body mass index; Cig/day=average number of cigarettes smoked in a day; FTND=Fagerstrom Test for Nicotine
Dependence (score ranges between 0 for no dependence and 10 for high dependence); Heart rate (beats/min); HRV=heart rate variability (pNN50); Respiration
(breaths/min). Differences between groups are represented by P values (P) calculated using analysis of variance (ANOVA) and Kruskal-Wallis test for categorical
variables (race/ethnicity and education). P values < .05 are shown in bold. All measures represent mean ± standard error unless otherwise specied.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 00 5
Response toStress
On average participants responded that they felt moderately stressed
during the titrated Stroop task, with heavy smokers expressing the
most stress (Table3).
SmokingUrges
We limited the analysis of smoking urges to the smoking groups.
Craving was assessed before and after acute stress induction. Because
time since last cigarette may differentially impact heavy smokers and
chippers, we recorded if participants smoked or not during the visit.
We used this discrete variable as covariate in our analyses. Atwo-
factor repeated measures ANOVA with smoking urges as dependent
variable and time and group as independent variables indicated that
there was a signicant effect of time [F(1, 86)=9.81, P < .01] and
group [F(1, 86)=41.85, P < .0001; CH=25; HS=22]. There was no
signicant interaction, indicating that the effect of stress on smok-
ing urges was the same for heavy smokers as for chippers (Table3).
However, additional analyses showed a signicant increase in crav-
ing after stress only for heavy smokers [F(1, 42)=9.15, P < .01] but
not for chippers [F(1, 48)=3.43, P > .05].
Affect
Positive and negative affect were evaluated before and after stress. In
this case analysis includes all three study groups (NS=25; CH=25;
HS=23). Using a two-factor repeated measures ANOVA an effect of
time [F(1, 140)=8.88, P < .01] was identied on positive affect. There
was no signicant effect of group [F(2, 140)=3.03, P > .05] and no
interaction. Post hoc analyses using ANOVA with positive affect as
the dependent variable and time as the independent factor showed
that only heavy smokers signicantly decreased positive affect after
experimental stress [F(1, 44)= 7.21, P < .05]. An effect of group
[F(2, 140)=4.99, P < .01] and time [F(1, 140)=4.91, P < .05] were
identied for negative affect. As before, post hoc analysis showed
that heavy smokers were the only group in which stress signicantly
Figure 1. Fitted hyperbolic functions and median indifference points for
each study group as a result of performance of the delay discounting task
(k, discounting rate). One-way analysis of variance detected significant
differences in average rate of discounting (lnk, natural logarithm of k) between
groups (NS, −5.887 ± 0.32; CH, −4.076 ± 0.39; HS, −4.036 ± 0.35; F(2,69)=9.11,
P < .001). NS=nonsmokers; CH=tobacco chippers; HS=heavy smokers.
Table3. Effects of Acute Stress on Craving, Affect, and Stress-Associated Physiological Measures in Nonsmokers (NS), Chippers (CH),
and Heavy Smokers (HS)
Baseline
(mean ± SE)
Acute stress
(mean ± SE)P, group P, stress P, group × stress
Smoking urges NS 44.00 ± 2.12 41.40 ± 2.52 <.001a.002a.693a
CH 84.08 ± 5.88 102.92 ± 8.29
HS 137.91 ± 6.05 162.13 ± 5.55
Positive affect NS 32.48 ± 1.57 29.88 ± 1.55 .051 .003 .784
CH 33 ± 1.31 29.56 ± 1.74
HS 30.39 ± 1.06 25.74 ± 1.37
Negative affect NS 12.56 ± 0.56 13.2 ± 0.57 .008 .028 .612
CH 14.68 ± 1.29 16.92 ± 1.36
HS 13.69 ± 0.64 16.00 ± 0.90
Self-rated acute stress NS n/a 2.72 ± 0.17 <.001 n/a n/a
CH n/a 3.28 ± 0.17
HS n/a 3.74 ± 0.15
Respiration (breaths/
min)
NS 14.36 ± 0.83 20.53 ± 1.11 .146 <.001 .519
CH 14.97 ± 0.78 19.27 ± 0.57
HS 15.91 ± 0.63 21.50 ± 0.99
Heart rate (beats/
min)
NS 66.19 ± 1.67 70.13 ± 1.64 <.001 .009 .889
CH 70.94 ± 1.72 74.89 ± 1.70
HS 76.37 ± 2.45 82.08 ± 2.97
Heart rate variability
(pNN50)
NS 21.61 ± 3.75 15.43 ± 3.39 <.001 .013 .521
CH 27.06 ± 3.90 17.03 ± 3.02
HS 8.20 ± 2.25 5.25 ± 1.87
Salivary cortisol
(µg/dl)
NS 0.30 ± 0.03 0.27 ± 0.03 .020 .594 .239
CH 0.29 ± 0.03 0.36 ± 0.04
HS 0.24 ± 0.02 0.25 ± 0.03
SE=standard error. P values < .05 are shown in bold.
aOnly smoking groups comparison.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 006
increased negative affect [F(1, 44)= 4.37, P < .05]. No signicant
interaction between group and stress effect was found (Table3).
RespirationRate
A repeated measures ANOVA identied an effect of stress on respi-
ration rate [F(1, 129)=60.59, P < .0001] but no group differences
[F(2, 129)=1.95, P > .05; NS=24; CH= 22; HS= 23]. Post hoc
analyses showed a signicant increase in respiration rate for all three
groups [CH, F(1, 42)=19.77, P < .001; HS, F(1,42)=23.60, P <
.0001; NS, F(1, 45)=19.88, P < .001; Table3].
HeartRate
An effect of group [F(2, 126)= 13.96, P < .0001] and stress [F(1,
126)=7.04, P < .01] was observed on heart rate (NS=22; CH=23;
HS=22; Table3). However, there was no interaction between group
and stress. The effect of stress was not signicant when analyzing
groups separately (all Ps > .05). However, one-way ANOVA using
group as independent factor indicated that heavy smokers had sig-
nicant higher heart rate than nonsmokers at baseline and this dif-
ference remained constant throughout stress induction (P < .01).
Heart Rate Variability
A repeated measures ANOVA showed a signicant effect of group
and stress on heart rate variability measured using pNN50 ([F(2,
126)=13.37, P < .0001] and [F(1, 126)=6.32, P < .05], respectively;
NS=22; CH = 23; HS = 22). No interaction between group and
stress was observed. At baseline and during stress, heavy smokers
showed signicantly lower heart rate variability than chippers and
nonsmokers (P < .05). Post hoc analysis of the effect of stress by
study group showed a statistically signicant effect on chippers (P <
.05) but not on heavy smokers or nonsmokers (Table3).
Salivary Cortisol
We applied a repeated measures ANOVA using salivary cortisol as
the dependent variable (NS=25; CH=25; HS=23). Although the
model was not signicant (F(5, 140)=2.24, P=.053), there was an
effect of group [F(2, 140)= 4.02, P < .05]. There was no effect of
stress or any interaction. Post hoc analyses using a one-way ANOVA
conrmed the group effect with a signicant difference in post
stress salivary cortisol between chippers and heavy smokers [F(2,
70)=3.41, P < .05].
Variables Associated With Stress and Smoking
We performed pairwise correlation analyses using baseline one-time
measures. As expected, there was a signicant correlation between
perceived stress and neuroticism in the whole sample, r(69)=0.5885,
P < .0001. This correlation was signicant for heavy smokers
[r(19)=0.634, P < .05] and chippers [r(23)= 0.6247, P < .01] but
not for nonsmokers. In the heavy smoker group, perceived stress was
positively correlated with nicotine dependence [r(20)=0.6469, P <
.05] and negatively correlated with mindfulness trait (nonjudgment
facet) [r(20)=−0.6344, P < .05]. None of these correlations were
signicant for chippers or nonsmokers.
We explored if perceived stress would predict performance on
the delay discounting task. Linear regression analysis identied the
score on the perceived stress scale as a signicant predictor of rate
of discounting in the heavy smoker group [b=0.15, t(19)=3.30, P
< .01], suggesting that chronically stressed heavy smokers tend to
discountmore.
Baseline variables were also used in a regression model to iden-
tify predictors of stress effects on affect, smoking urges, heart rate
and respiration. In our sample, neuroticism was positively associ-
ated with increase in smoking urges after stress in heavy smokers
[b=2.75, t(15)=2.18, P < .05] and the number of cigarettes smoked
each day was a signicant predictor of increase in urges in chippers
[b= 7.52, t(19) = 2.28, P < .05]. Pairwise correlation analysis was
conducted among outcome variables (change after stress). In chip-
pers, change in positive affect was inversely correlated to change in
smoking urges [r(23)=−0.57, P < .05], and change in negative affect
positively correlated to change in urges [r(23)=0.63, P < .05]. No
signicant association was found for heavy smokers.
Discussion
To examine further the differences between low-level smoking and
heavy smoking, our study characterized and compared nicotine
dependent smokers (heavy smokers), nondependent smokers (chip-
pers), and nonsmokers in terms of impulsivity, stress perception, and
stress response. There is extensive literature about the relationship
between impulsivity and nicotine addiction, and stress and smoking.
However, the majority refers to dependent smokers as dened by the
number of cigarettes smoked per day and high dependence scores.31
Less is known about nondependent smokers. Our aim was to con-
tribute to the understanding of this group of smokers hypothesizing
that differences in impulsivity, personality traits, stress perception,
and stress reactivity might be associated to nicotine dependence
resistance.
Impulsivity and PersonalityTraits
Similar to previous studies,9,41,52,53 heavy smokers in our sample
showed greater discounting of delayed money than nonsmokers.
Literature on delay discounting in nondependent smokers is scarce.
Previous studies have described a signicant difference in rate of dis-
counting between dependent smokers and nondependent ones and a
relationship between degree of nicotine dependence and discounting
of delayed rewards.15,17 Our study found no signicant difference
in rate of discounting between chippers and heavy smokers, as well
as no signicant correlation with nicotine dependence or cigarettes
smoked daily, suggesting that nondependent smokers are as impul-
sive as dependent smokers. Several studies have documented the rela-
tionship between drinking alcohol and smoking in light smokers.54–57
In our sample alcohol consumption was signicantly higher in chip-
pers and could account for higher discounting (Table2). However,
after controlling for amount of alcohol, there still was no difference
in rate of discounting between chippers and heavy smokers. No dif-
ferences were found in response inhibition with performance on the
anker task. Delay discounting and response inhibition load onto
different factors to account for variance in smoking behavior.58,59
Although some studies nd response inhibition differences between
smokers and nonsmokers,60,61 studies comparing different impulsiv-
ity measures report that delay discounting discriminates controls
from addicts better than response inhibition.58,62,63 Our results might
reect that there are truly no differences in this facet of impulsiv-
ity between chippers and heavy smokers. However, alternatively,
response inhibition tasks such as the anker task might not be
sensitive enough to detect differences in impulsivity in our popula-
tion. If this is the case, response inhibition might still be associated
with chippers’ ability to maintain a pattern of long-term low level
smoking.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 00 7
We did not nd signicant differences in self-reported personal-
ity traits. Previously, smokers have been characterized as high on
facets related to impulsivity and neuroticism, low on agreeableness
and conscientiousness,64–66 and in some older studies smokers scored
high on extraversion.64,67,68 Sensation seeking has also been reported
as higher in nicotine dependent smokers than in nonsmokers.9,69–71
In our sample dependent smokers were not signicantly different
from chippers or nonsmokers in any of those traits. This discrep-
ancy might be explained by: (1) Differences in the average age of
the sample, since our population averaged 33years old while recent
studies have assessed personality traits and smoking in college and
adolescence.69,71 (2) Changes in the prole of heavy smokers asso-
ciated with cultural and environmental differences across geogra-
phy and/or time. For example, research in Europe and Japan found
extraversion associated with cigarette smoking.67,72 Additionally,
studies using a similar age sample to ours tend to be older studies
that precede the impact of smoking restrictions on the prole of cur-
rent smokers.9,70
Consistent with what has been published, we conrmed the rela-
tionship between smoking and chronic stress in nicotine dependent
smokers.23,24 Heavy smokers scored high in perceived stress, while
chippers were undistinguishable from nonsmokers. Mindfulness
was negatively correlated with stress only in dependent smokers.
This association, in addition to the association between nicotine
dependence and stress, suggests that nicotine dependence treatments
could be improved by addressing stress, and that mindfulness based
approaches might provide smokers with the useful skills to quit
successfully.73,74
Neuroticism has been associated to smoking and stress.75–77 In
our study, neuroticism was associated with higher perceived stress
in both smoking groups but not in nonsmokers. This observation is
consistent with the hypothesis that increased neuroticism is associ-
ated with self-medication of negative affect with nicotine and that
decreased serotonergic activity, the neurobiological substrate of neu-
roticism, is associated with increased likelihood of smoking.76
The stress vulnerability model suggests that stress inuences sub-
stance abuse through maladaptive response to the environment.78–80
Perceived stress was signicantly higher in our sample of heavy
smokers compared to nonsmokers. Furthermore, perceived stress
was a signicant predictor of performance in the delay discounting
task, suggesting that higher levels of stress result in a shift to a more
immediate-oriented mindset and, subsequently, an increased proba-
bility of relapse. Accordingly, a recent meta-analysis of the literature
on impulsivity and stress found a moderate to large effect of stress
on impulsive decision making.81
Acute Stress Effects
Our results indicate that nicotine-dependent and nondependent
smokers respond to acute stress with a similar increase in smok-
ing urges. Analyses of associated variables differed between smok-
ing groups. Only in chippers were increases in craving associated
with decreases in positive affect and increases in negative affect sug-
gesting that smoking behavior is more linked to emotional state in
nondependent smokers than in heavy regular smokers. Only heavy
smokers showed a signicant change in affect after stress. This, how-
ever, wasn’t associated to increases in craving, indicating that heavy
smokers might be more prone to smoke regardless of context, as
reported previously in nicotine deprived dependent smokers.82
Acute stress in all three groups increased breathing rate equiva-
lently. Thus, breathing rate might be a good physiological marker of
acute stress. However, breathing rate does not seem to be a marker
for chronic stress based on our sample or the literature.83 Similarly,
stress increased heart rate in the sample as a whole. As expected,84
heavy smokers showed elevated resting heart rate at baseline com-
pared to nonsmokers, and chippers were in between. Heart rate
variability was also signicantly lower in heavy smokers. Our obser-
vations agree with the well-established relationship between nicotine
consumption and cardiovascular symptoms, even in occasional or
light smokers.85–87
Limitations
While heavy smoking is relatively easy to dene (usually >15
cigarettes/d),30 there is little consensus when dening low-levels of
cigarette smoking.88 Anumber of operational denitions of low-level
smoking can be found in the literature.89–92 We based our distinction
between tobacco chippers and heavy smokers on the Fagerstrom Test
for Nicotine Dependence score. This score relies heavily on amount
of cigarettes smoked, which, as smoking restrictions increase, might
not be an accurate measure of dependence anymore.93 Future
research might examine alternative methods of classifying smokers
such as the measure of autonomy over smoking,94,95 the Diagnostic
and Statistical Manual-IV (DSM-IV) nicotine dependence criteria,96
or the Nicotine Dependence Syndrome Scale (NDSS).97
Regarding our salivary cortisol results, we cannot exclude the
possibility of Type II error. Cortisol’s circadian rhythm and rapid
morning decline might have masked some of the acute stress
effects.73,74 In addition, our sample size, which was sufcient to
detect signicant effects of stress on respiration, heart rate and heart
rate variability, might have been too small to detect changes in sali-
vary cortisol concentration. Finally, it might be worth enhancing
some aspects of the titrated Stroop (ie, performance feedback) to
maximize the physiological response.
Conclusions
Tobacco chippers are as impulsive as heavy smokers. However,
chippers report less stress than heavy smokers. Smoking urges were
associated to emotional state more in chippers than heavy smok-
ers. Autonomic activity differed between heavy smokers and con-
trols, but chippers trended between nonsmokers and heavy smokers.
Nicotine dependence treatments could benet from an emphasis on
stress reduction stress coping strategies.
Funding
This work was supported by the National Institutes of Health (grants
R21DA035877 to LC-T, T32AT002688, and K24AT005121 to BSO, and
UL1TR000128). NIH had no further role in study design, collection, analysis
and interpretation of data, manuscript writing, or in the decision to submit
for publication.
Declaration of Interests
None declared.
Acknowledgments
We are grateful to Roger Ellingson for adapting the titrated Stroop task and
to Vanessa Wilson for valuable help with recruitment and support throughout
the study. We thank all study participants for their participation.
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Nicotine & Tobacco Research, 2015, Vol. 00, No. 008
References
1. Shiffman S, Ferguson SG, Dunbar MS, Scholl SM. Tobacco dependence
among intermittent smokers. Nicotine Tob Res. 2012;14(11):1372–1381.
doi:10.1093/ntr/nts097.
2. Shiffman S, Zettler-Segal M, Kassel J, Paty J, Benowitz NL, O’Brien G.
Nicotine elimination and tolerance in non-dependent cigarette smok-
ers. Psychopharmacology (Berl). 1992;109(4):449–456. doi:10.1007/
BF02247722.
3. Gilbert DG, Gilbert BO. Personality, psychopathology, and nico-
tine response as mediators of the genetics of smoking. Behav Genet.
1995;25(2):133–147. doi:10.1007/BF02196923.
4. Kassel JD, Stroud LR, Paronis CA. Smoking, stress, and negative affect:
correlation, causation, and context across stages of smoking. Psychol Bull.
2003;129(2):270–304. doi:10.1037/0033-2909.129.2.270.
5. Nichter M, Vuckovic N, Quintero G, Ritenbaugh C. Smoking experimen-
tation and initiation among adolescent girls: qualitative and quantitative
ndings. Tob Control. 1997;6(4):285–295. doi:10.1136/tc.6.4.285.
6. Sinha R. Chronic stress, drug use, and vulnerability to addiction. Ann NY
Acad Sci. 2008;1141(1):105–130. doi:10.1196/annals.1441.030.
7. Ainslie G. Specious reward: a behavioral theory of impulsiveness and
impulse control. Psychol Bull. 1975;82(4):463–496. www.ncbi.nlm.nih.
gov/pubmed/1099599. Accessed May 20, 2015.
8. Reynolds B, Ortengren A, Richards JB, de Wit H. Dimensions of impul-
sive behavior: personality and behavioral measures. Pers Individ Dif.
2006;40(2):305–315. doi:10.1016/j.paid.2005.03.024.
9. Mitchell SH. Measures of impulsivity in cigarette smokers and non-smok-
ers. Psychopharmacology (Berl). 1999;146(4):455–464. doi:10.1007/
PL00005491.
10. Bari A, Robbins TW. Inhibition and impulsivity: behavioral and neural
basis of response control. Prog Neurobiol. 2013;108:44–79. doi:10.1016/j.
pneurobio.2013.06.005.
11. Zuckerman M, Kuhlman DM. Personality and risk-taking: common bioso-
cial factors. J Pers. 2000;68(6):999–1029. doi:10.1111/1467-6494.00124.
12. Ersche KD, Turton AJ, Pradhan S, Bullmore ET, Robbins TW. Drug
addiction endophenotypes: impulsive versus sensation-seeking per-
sonality traits. Biol Psychiatry. 2010;68(8):770–773. doi:10.1016/j.
biopsych.2010.06.015.
13. Enticott PG, Ogloff JRP, Bradshaw JL. Associations between laboratory
measures of executive inhibitory control and self-reported impulsivity.
Pers Individ Dif. 2006;41(2):285–294.
14. Luijten M, Littel M, Franken IH. Decits in inhibitory control in smokers
during a Go/NoGo task: an investigation using event-related brain poten-
tials. PLoS One. 2011;6(4):e18898. doi:10.1371/journal.pone.0018898.
15. Heyman GM, Gibb SP. Delay discounting in college cigarette chip-
pers. Behav Pharmacol. 2006;17(8):669–679. doi:10.1097/
FBP.0b013e3280116cfe.
16. Johnson MW, Bickel WK, Baker F. Moderate drug use and
delay discounting: a comparison of heavy, light, and never
smokers. Exp Clin Psychopharmacol. 2007;15(2):187–194.
doi:10.1037/1064-1297.15.2.187.
17. Sweitzer MM, Donny EC, Dierker LC, Flory JD, Manuck SB. Delay dis-
counting and smoking: association with the Fagerstrom Test for Nicotine
Dependence but not cigarettes smoked per day. Nicotine Tob Res.
2008;10(10):1571–1575. doi:10.1080/14622200802323274.
18. McFarlane A, Clark CR, Bryant RA, etal. The impact of early life stress
on psychophysiological, personality and behavioral measures in 740
non-clinical subjects. J Integr Neurosci. 2005;4(1):27–40. doi:10.1142/
S0219635205000689.
19. Norton R, Brown K, Howard R. Smoking, nicotine dose and the lat-
eralisation of electrocortical activity. Psychopharmacology (Berl).
1992;108(4):473–479. doi:10.1007/BF02247424.
20. Seeman TE, McEwen BS, Rowe JW, Singer BH. Allostatic load as a
marker of cumulative biological risk: MacArthur studies of successful
aging. Proc Natl Acad Sci USA. 2001;98(8):4770–4775. doi:10.1073/
pnas.081072698.
21. Oken BS, Chamine I, Wakeland W. A systems approach to stress, stress-
ors and resilience in humans. Behav Brain Res. 2015;282:144–154.
doi:10.1016/j.bbr.2014.12.047.
22. Siqueira L, Diab M, Bodian C, Rolnitzky L. Adolescents becom-
ing smokers: the roles of stress and coping methods. J Adolesc Health.
2000;27(6):399–408. doi:10.1016/S1054-139X(00)00167-1.
23. Parrott AC. Stress modulation over the day in cigarette smokers. Addiction.
1995;90(2):233–244. doi:10.1111/j.1360-0443.1995.tb01041.x.
24. Pomerleau OF, Pomerleau CS. Cortisol response to a psychological
stressor and/or nicotine. Pharmacol Biochem Behav. 1990;36(1):211–213.
doi:10.1016/0091-3057(90)90153-9.
25. Fleming SE, Lombardo TW. Effects of cigarette smoking on phobic anxiety.
Addict Behav. 1987;12(2):195–198. doi:10.1016/0306-4603(87)90027-x.
26. Perkins KA, Grobe JE. Increased desire to smoke during acute stress.
Br J Addict. 1992;87(7):1037–1040. doi:10.1111/j.1360-0443.1992.
tb03121.x.
27. Oken BS, Fonareva I, Wahbeh H. Stress-related cognitive dysfunction in
dementia caregivers. J Geriatr Psychiatry Neurol. 2011;24(4):191–198.
doi:10.1177/0891988711422524.
28. Carton S, Jouvent R, Widlocher D. Sensation seeking, nicotine depend-
ence, and smoking motivation in female and male smokers. Addict Behav.
1994;19(3):219–227. doi:10.1016/0306-4603(94)90026-4.
29. Wahbeh H, Lu M, Oken B. Mindful awareness and non-judging in rela-
tion to posttraumatic stress disorder symptoms. Mindfulness (NY).
2011;2(4):219–227. doi:10.1007/s12671-011-0064-3.
30. Shiffman S, Kassel JD, Paty J, Gnys M, Zettler-Segal M. Smoking typology
proles of chippers and regular smokers. J Subst Abuse. 1994;6(1):21–35.
www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&d
opt=Citation&list_uids=8081107. Accessed June 29, 2015.
31. Heatherton TF, Kozlowski LT, Frecker RC, Fagerstrom KO. The
Fagerstrom Test for Nicotine Dependence: a revision of the Fagerstrom
Tolerance Questionnaire. Br J Addict. 1991;86(9):1119–1127.
doi:10.1111/j.1360-0443.1991.tb01879.x.
32. Gianaros PJ, Derbyshire SW, May JC, Siegle GJ, Gamalo MA,
Jennings JR. Anterior cingulate activity correlates with blood pres-
sure during stress. Psychophysiology. 2005;42(6):627–635.
doi:10.1111/j.1469-8986.2005.00366.x.
33. Fan J, McCandliss BD, Sommer T, Raz A, Posner MI. Testing the ef-
ciency and independence of attentional networks. J Cogn Neurosci.
2002;14(3):340–347. doi:10.1162/089892902317361886.
34. Edwards S, Clow A, Evans P, Hucklebridge F. Exploration of the awaken-
ing cortisol response in relation to diurnal cortisol secretory activity. Life
Sci. 2001;68(18):2093–2103. doi:10.1016/S0024-3205(01)00996-1.
35. Dickerson SS, Kemeny ME. Acute stressors and cortisol responses: a
theoretical integration and synthesis of laboratory research. Psychol Bull.
2004;130(3):355–391. doi:10.1037/0033-2909.130.3.355.
36. Kirschbaum C, Pirke KM, Hellhammer DH. The ‘Trier Social Stress
Test’--a tool for investigating psychobiological stress responses in a labo-
ratory setting. Neuropsychobiology. 1993;28(1–2):76–81. doi:119004.
37. Dedovic K, Renwick R, Mahani NK, Engert V, Lupien SJ, Pruessner JC.
The Montreal Imaging Stress Task: using functional imaging to investigate
the effects of perceiving and processing psychosocial stress in the human
brain. J Psychiatry Neurosci. 2005;30(5):319–325. www.ncbi.nlm.nih.
gov/pubmed/16151536. Accessed May 15, 2015.
38. Chida Y, Hamer M. Chronic psychosocial factors and acute physiological
responses to laboratory-induced stress in healthy populations: a quantita-
tive review of 30years of investigations. Psychol Bull. 2008;134(6):829–
885. doi:10.1037/a0016852.
39. Bellingrath S, Weigl T, Kudielka BM. Chronic work stress and exhaustion
is associated with higher allostastic load in female school teachers. Stress.
2009;12(1):37–48. doi:10.1080/10253890802042041.
40. Lupien S. Well Stressed : How You Can Manage Stress Before It Turns
Toxic. Mississauga, ON: John Wiley & Sons Canada, Ltd; 2012.
41. Imhoff S, Harris M, Weiser J, Reynolds B. Delay discounting by depressed
and non-depressed adolescent smokers and non-smokers. Drug Alcohol
Depend. 2014;135:152–155. doi:10.1016/j.drugalcdep.2013.11.014.
at OHSU Main Library on February 17, 2016http://ntr.oxfordjournals.org/Downloaded from

Nicotine & Tobacco Research, 2015, Vol. 00, No. 00 9
42. Cohen S, Kamarck T, Mermelstein R. A global measure of perceived stress.
J Health Soc Behav. 1983;24(4):385–396. doi:10.2307/2136404.
43. Costa PT Jr, McCrae RR. Domains and facets: hierarchical personality
assessment using the revised NEO personality inventory. J Pers Assess.
1995;64(1):21–50. doi:10.1207/s15327752jpa6401_2.
44. Zuckerman M, Link K. Construct validity for the sensation-seeking scale.
J Consult Clin Psychol. 1968;32(4):420–426. doi:10.1037/h0026047.
45. Baer RA, Smith GT, Lykins E, et al. Construct validity of the ve facet
mindfulness questionnaire in meditating and nonmeditating samples.
Assessment. 2008;15(3):329–342. doi:10.1177/1073191107313003.
46. Watson D, Clark LA, Tellegen A. Development and validation of brief
measures of positive and negative affect: the PANAS scales. J Pers Soc
Psychol. 1988;54(6):1063–1070. doi:10.1037/0022-3514.54.6.1063.
47. Hughes JR, Hatsukami D. Signs and symptoms of tobacco with-
drawal. Arch Gen Psychiatry. 1986;43(3):289–294. doi:10.1001/archp
syc.1986.01800030107013.
48. Tiffany ST, Drobes DJ. The development and initial validation of a
questionnaire on smoking urges. Br J Addict. 1991;86(11):1467–1476.
doi:10.1111/j.1360-0443.1991.tb01732.x.
49. Wostmann NM, Aichert DS, Costa A, Rubia K, Moller HJ, Ettinger U.
Reliability and plasticity of response inhibition and interference control.
Brain Cogn. 2013;81(1):82–94. doi:10.1016/j.bandc.2012.09.010.
50. Casaletto KB, Umlauf A, Beaumont J, et al. Demographically Corrected
Normative Standards for the English Version of the NIH Toolbox
Cognition Battery. J Int Neuropsychol Soc. 2015;21(5):378–391.
doi:10.1017/S1355617715000351.
51. Mukherjee S, Yadav R, Yung I, Zajdel DP, Oken BS. Sensitivity to mental
effort and test-retest reliability of heart rate variability measures in healthy
seniors. Clin Neurophysiol. 2011;122(10):2059–2066. doi:10.1016/j.
clinph.2011.02.032.
52. Reynolds B, Fields S. Delay discounting by adolescents experi-
menting with cigarette smoking. Addiction. 2012;107(2):417–424.
doi:10.1111/j.1360-0443.2011.03644.x.
53. Friedel JE, DeHart WB, Madden GJ, Odum AL. Impulsivity and cigarette
smoking: discounting of monetary and consumable outcomes in current
and non-smokers. Psychopharmacology (Berl). 2014;231(23):4517–4526.
doi:10.1007/s00213-014-3597-z.
54. King AC, Epstein AM. Alcohol dose-dependent increases in smok-
ing urge in light smokers. Alcohol Clin Exp Res. 2005;29(4):547–552.
doi:10.1097/01.ALC.0000158839.65251.FE.
55. Harrison EL, McKee SA. Non-daily smoking predicts hazardous
drinking and alcohol use disorders in young adults in a longitudinal
U.S. sample. Drug Alcohol Depend. 2011;118(1):78–82. doi:10.1016/j.
drugalcdep.2011.02.022.
56. Ray LA, Miranda R Jr, Kahler CW, etal. Pharmacological effects of nal-
trexone and intravenous alcohol on craving for cigarettes among light
smokers: a pilot study. Psychopharmacology (Berl). 2007;193(4):449–
456. doi:10.1007/s00213-007-0794-z.
57. Shiffman S, Dunbar MS, Li X, etal. Smoking patterns and stimulus con-
trol in intermittent and daily smokers. PLoS One. 2014;9(3):e89911.
doi:10.1371/journal.pone.0089911.
58. Courtney KE, Arellano R, Barkley-Levenson E, et al. The relation-
ship between measures of impulsivity and alcohol misuse: an integra-
tive structural equation modeling approach. Alcohol Clin Exp Res.
2012;36(6):923–931. doi:10.1111/j.1530-0277.2011.01635.x.
59. Christiansen P, Cole JC, Goudie AJ, Field M. Components of behav-
ioural impulsivity and automatic cue approach predict unique variance
in hazardous drinking. Psychopharmacology. 2012;219(2):501–510.
doi:10.1007/s00213-011-2396-z.
60. Yakir A, Rigbi A, Kanyas K, etal. Why do young women smoke? III.
Attention and impulsivity as neurocognitive predisposing factors.
Eur Neuropsychopharmacol. 2007;17(5):339–351. doi:10.1016/j.
euroneuro.2006.09.004.
61. Spinella M. Correlations between orbitofrontal dysfunction and tobacco
smoking. Addict Biol. 2002;7(4):381–384. doi:10.1080/1355621021000
005964.
62. Torres A, Catena A, Megias A, et al. Emotional and non-emotional
pathways to impulsive behavior and addiction. Front Hum Neurosci.
2013;7:43. doi:10.3389/fnhum.2013.00043.
63. Ledgerwood DM, Alessi SM, Phoenix N, Petry NM. Behavioral assess-
ment of impulsivity in pathological gamblers with and without substance
use disorder histories versus healthy controls. Drug Alcohol Depend.
2009;105(1–2):89–96. doi:10.1016/j.drugalcdep.2009.06.011.
64. Malouff JM, Thorsteinsson EB, Schutte NS. The ve-factor model of per-
sonality and smoking: a meta-analysis. J Drug Educ. 2006;36(1):47–58.
doi:10.2190/9EP8-17P8-EKG7-66AD.
65. Paunonen SV, Ashton MC. Big ve factors and facets and the pre-
diction of behavior. J Pers Soc Psychol. 2001;81(3):524–539.
doi:10.1037/0022-3514.81.3.524.
66. Terracciano A, Costa PT. Smoking and the Five-Factor Model of personality.
Addiction. 2004;99(4):472–481. doi:10.1111/j.1360-0443.2004.00687.x.
67. Arai Y, Hosokawa T, Fukao A, Izumi Y, Hisamichi S. Smoking behav-
iour and personality: a population-based study in Japan. Addiction.
1997;92(8):1023–1033. doi:10.1111/j.1360-0443.1997.tb02982.x.
68. Munafò MR, Black S. Personality and smoking status: a lon-
gitudinal analysis. Nicotine Tob Res. 2007;9(3):397–404.
doi:10.1080/14622200701188869.
69. Balevich EC, Wein ND, Flory JD. Cigarette smoking and measures of
impulsivity in a college sample. Subst Abus. 2013;34(3):256–262. doi:10.
1080/08897077.2012.763082.
70. Harmsen H, Bischof G, Brooks A, Hohagen F, Rumpf HJ. The relation-
ship between impaired decision-making, sensation seeking and readi-
ness to change in cigarette smokers. Addict Behav. 2006;31(4):581–592.
doi:10.1016/j.addbeh.2005.05.038.
71. Rezvanfard M, Ekhtiari H, Mokri A, Djavid GE, Kaviani H. Psychological
and behavioral traits in smokers and their relationship with nicotine
dependence level. Arch Iran Med. 2010;13(5):395–405. doi:010135/
AIM.006.
72. Harakeh Z, Scholte RHJ, de Vries H, Engels RCME. Association between
personality and adolescent smoking. Addict Behav. 2006;31(2):232–245.
doi:10.1016/j.addbeh.2005.05.003.
73. Debono M, Ghobadi C, Rostami-Hodjegan A, et al. Modied-release
hydrocortisone to provide circadian cortisol proles. J Clin Endocrinol
Metab. 2009;94(5):1548–1554. doi:10.1210/jc.2008-2380.
74. Krieger DT, Allen W, Rizzo F, Krieger HP. Characterization of the normal
temporal pattern of plasma corticosteroid levels. J Clin Endocrinol Metab.
1971;32(2):266–284. doi:10.1210/jcem-32-2-266.
75. Oken BS, Fonareva I, Wahbeh H. Stress-related cognitive dysfunction in
dementia caregivers. J Geriatr Psychiatry Neurol. 2011;24(4):191–198.
doi:10.1177/0891988711422524.
76. Munafo MR, Zetteler JI, Clark TG. Personality and smok-
ing status: a meta-analysis. Nicotine Tob Res. 2007;9(3):405–413.
doi:10.1080/14622200701188851.
77. Lahey BB. Public health signicance of neuroticism. Am Psychol.
2009;64(4):241–256. doi:10.1037/a0015309.
78. Sinha R. Modeling stress and drug craving in the laboratory: implications
for addiction treatment development. Addict Biol. 2009;14(1):84–98.
doi:10.1111/j.1369-1600.2008.00134.x.
79. McKee SA, Sinha R, Weinberger AH, etal. Stress decreases the ability to resist
smoking and potentiates smoking intensity and reward. J Psychopharmacol.
2011;25(4):490–502. doi:10.1177/0269881110376694.
80. Ansell EB, Gu P, Tuit K, Sinha R. Effects of cumulative stress and impul-
sivity on smoking status. Hum Psychopharmacol. 2012;27(2):200–208.
doi:10.1002/hup.1269.
81. Fields SA, Lange K, Ramos A, Thamotharan S, Rassu F. The rela-
tionship between stress and delay discounting: a meta-analytic
review. Behav Pharmacol. 2014;25(5–6):434–444. doi:10.1097/
FBP.0000000000000044.
82. Sayette MA, Martin CS, Wertz JM, Shiffman S, Perrott MA. A
multi-dimensional analysis of cue-elicited craving in heavy smok-
ers and tobacco chippers. Addiction. 2001;96(10):1419–1432.
doi:10.1080/09652140120075152.
at OHSU Main Library on February 17, 2016http://ntr.oxfordjournals.org/Downloaded from

Nicotine & Tobacco Research, 2015, Vol. 00, No. 0010
83. Wahbeh H, Oken BS. Peak high-frequency HRV and peak alpha frequency
higher in PTSD. Appl Psychophysiol Biofeedback. 2013;38(1):57–69.
doi:10.1007/s10484-012-9208-z.
84. Winniford MD. Smoking and cardiovascular function. J Hypertens Suppl.
1990;8(5):S17–23. www.ncbi.nlm.nih.gov/pubmed/2286853. Accessed
May 20, 2015.
85. Thun MJ, Carter BD, Feskanich D, etal. 50-year trends in smoking-related
mortality in the United States. N Engl J Med. 2013;368(4):351–364.
doi:10.1056/NEJMsa1211127.
86. Jha P, Ramasundarahettige C, Landsman V, et al. 21st-century hazards
of smoking and benets of cessation in the United States. N Engl J Med.
2013;368(4):341–350. doi:10.1056/NEJMsa1211128.
87. Luoto R, Uutela A, Puska P. Occasional smoking increases total and car-
diovascular mortality among men. Nicotine Tob Res. 2000;2(2):133–139.
doi:10.1080/713688127.
88. WHO. WHO Report on the Global Tobacco Epidemic, 2008: The
MPOWER package. 2008. www.who.int/tobacco/mpower/2008/en/.
Accessed May 20, 2015.
89. Wortley PM, Husten CG, Trosclair A, Chrismon J, Pederson LL. Nondaily
smokers: a descriptive analysis. Nicotine Tob Res. 2003;5(5):755–759. doi
:10.1080/1462220031000158753.
90. The 2008 PHS Guideline Update Panel, Liaisons, and Staff. Treating tobacco
use and dependence: 2008 update U.S. Public Health Service Clinical Practice
Guideline executive summary. Respir Care. 2008;53(9):1217–1222. www.
ncbi.nlm.nih.gov/pubmed/18807274. Accessed June 29, 2015.
91. Biener L, Albers AB. Young adults: vulnerable new targets of tobacco mar-
keting. Am J Public Health. 2004;94(2):326–330. www.pubmedcentral.
nih.gov/articlerender.fcgi?artid=1448251&tool=pmcentrez&rendertype=
abstract. Accessed June 29, 2015.
92. Zvolensky MJ, Bernstein A, Cardenas SJ, Colotla VA, Marshall EC,
Feldner MT. Anxiety sensitivity and early relapse to smoking: a test among
Mexican daily, low-level smokers. Nicotine Tob Res. 2007;9(4):483–491.
doi:10.1080/14622200701239621.
93. Donny EC, Grifn KM, Shiffman S, Sayette MA. The relation-
ship between cigarette use, nicotine dependence, and craving in
laboratory volunteers. Nicotine Tob Res. 2008;10(5):934–942.
doi:10.1080/14622200802133681.
94. Wellman RJ, DiFranza JR, Wood C. Tobacco chippers report dimin-
ished autonomy over smoking. Addict Behav. 2006;31(4):717–721.
doi:10.1016/j.addbeh.2005.05.043.
95. Difranza JR, Savageau JA, Wellman RJ. A comparison of the autonomy
over tobacco scale and the Fagerstrom test for nicotine dependence.
Addict Behav. 2012;37(7):856–861. doi:10.1016/j.addbeh.2012.03.013.
96. Sledjeski EM, Dierker LC, Costello D, etal. Predictive validity of four
nicotine dependence measures in a college sample. Drug Alcohol Depend.
2007;87(1):10–19. doi:10.1016/j.drugalcdep.2006.07.005.
97. Shiffman S, Sayette MA. Validation of the nicotine dependence syn-
drome scale (NDSS): a criterion-group design contrasting chippers and
regular smokers. Drug Alcohol Depend. 2005;79(1):45–52. doi:10.1016/j.
drugalcdep.2004.12.009.
at OHSU Main Library on February 17, 2016http://ntr.oxfordjournals.org/Downloaded from