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Anxiety, Depression, and Cigarette Smoking: A TransdiagnosticVulnerability Framework to Understanding Emotion–Smoking Comorbidity
Adam M. LeventhalUniversity of Southern California
Michael J. ZvolenskyUniversity of Houston and University of Texas
MD Anderson Cancer Center
Research into the comorbidity between emotional psychopathology and cigarette smoking has oftenfocused upon anxiety and depression’s manifest symptoms and syndromes, with limited theoretical andclinical advancement. This article presents a novel framework to understanding emotion–smokingcomorbidity. We propose that transdiagnostic emotional vulnerabilities—core biobehavioral traits re-flecting maladaptive responses to emotional states that underpin multiple types of emotional psychopa-thology—link various anxiety and depressive psychopathologies to smoking. This framework is appliedin a review and synthesis of the empirical literature on 3 transdiagnostic emotional vulnerabilitiesimplicated in smoking: (a) anhedonia (Anh; diminished pleasure/interest in response to rewards), (b)anxiety sensitivity (AS; fear of anxiety-related sensations), and (c) distress tolerance (DT; ability towithstand distressing states). We conclude that Anh, AS, and DT collectively (a) underpin multipleemotional psychopathologies, (b) amplify smoking’s anticipated and actual affect-enhancing propertiesand other mechanisms underlying smoking, (c) promote progression across the smoking trajectory (i.e.,initiation, escalation/progression, maintenance, cessation/relapse), and (d) are promising targets forsmoking intervention. After existing gaps are identified, an integrative model of transdiagnostic pro-cesses linking emotional psychopathology to smoking is proposed. The model’s key premise is that Anhamplifies smoking’s anticipated and actual pleasure-enhancing effects, AS amplifies smoking’s anxio-lytic effects, and poor DT amplifies smoking’s distress terminating effects. Collectively, these processesaugment the reinforcing properties of smoking for individuals with emotional psychopathology toheighten risk of smoking initiation, progression, maintenance, cessation avoidance, and relapse. Weconclude by drawing clinical and scientific implications from this framework that may generalize to othercomorbidities.
Keywords: anxiety, depression, smoking, comorbidity, nicotine dependence
Despite large-scale public health campaigns to warn against thedangers of smoking and encourage cigarette smokers to quit, asignificant portion of the population initiate smoking each year andexisting smokers struggle to quit (Centers for Disease Control andPrevention [CDC], 2010). Therefore, a major public health prob-lem is to limit the incidence of new smokers, encourage currentsmokers to make a cessation attempt, and enhance quit success inthe population of recalcitrant smokers who are interested in quit-ting but are unable to successfully maintain abstinence.
The field of psychology is in a unique position to address thepublic health burden of smoking, given that depressive and anxiety
symptoms and syndromes (i.e., emotional disorders) are highlyprevalent in the general population and remarkably comorbid withsmoking (Grant, Hasin, Chou, Stinson, & Dawson, 2004; Hughes,1999, 2011; Japuntich et al., 2007; Leventhal, Japuntich, et al.,2012; Leventhal, Ramsey, Brown, LaChance, & Kahler, 2008;Piper, Cook, Schlam, Jorenby, & Baker, 2011; Piper et al., 2010;Zvolensky, Gibson, et al., 2008; Zvolensky, Stewart, Vujanovic,Gavric, & Steeves, 2009). The link between smoking and emo-tional psychopathology (a) generalizes across several emotionalconditions, including major depression (Leventhal, Japuntich, etal., 2012), dysthymic disorder (Weinberger, Pilver, Desai, Mazure,& McKee, 2013), minor depression (Weinberger, Pilver, et al.,2013), panic disorder (Piper et al., 2011), social anxiety disorder(Piper et al., 2011), posttraumatic stress disorder (PTSD; Zvolen-sky, Gibson, et al., 2008), and generalized anxiety disorder (GAD;Piper et al., 2011); and (b) extends to multiple stages of thesmoking trajectory, including initiation (Leventhal, Ray, Rhee, &Unger, 2012; Patton et al., 1998), progression to regular smoking(Audrain-McGovern, Rodriguez, Rodgers, & Cuevas, 2011), de-velopment and maintenance of nicotine dependence (McKenzie,Olsson, Jorm, Romaniuk, & Patton, 2010), and risk of smokingcessation failure (Hall, Muñoz, & Reus, 1994; Hitsman et al.,2013). The smoking–emotion relation is bidirectional, as increasesin tobacco use heightens risk of emotional disorder symptoms
Adam M. Leventhal, Department of Psychology and Department ofPreventive Medicine, Keck School of Medicine, University of SouthernCalifornia; Michael J. Zvolensky, Department of Psychology, University ofHouston, and Department of Behavioral Sciences, University of Texas MDAnderson Cancer Center.
Adam M. Leventhal was supported by National Institute on Drug AbuseGrant DA025041.
Correspondence concerning this article should be addressed to Adam M.Leventhal, Department of Preventive Medicine, Keck School of Medicine,University of Southern California, Los Angeles, CA 90033. E-mail:[email protected]
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Psychological Bulletin © 2014 American Psychological Association2014, Vol. 141, No. 1, 000 0033-2909/14/$12.00 http://dx.doi.org/10.1037/bul0000003
1
(Breslau & Klein, 1999; Breslau, Novak, & Kessler, 2004; J. G.Johnson et al., 2000; Khaled et al., 2012; Wu & Anthony, 1999)and sustained abstinence decreases emotional symptoms (Kahler,Spillane, Busch, & Leventhal, 2011).
Yet, strikingly little is known about the mechanisms underlyingthe relation between emotional disorders and smoking relative tothe volume of work published on this topic. Furthermore, behav-ioral, pharmacologic, or combination cessation programs designedto address emotional symptoms to facilitate quitting have generallyyielded modest (e.g., Cinciripini et al., 1995; McFall et al., 2005,2010; Piper et al., 2008) or mixed (e.g., R. A. Brown et al., 2007;Hitsman, Borrelli, McChargue, Spring, & Niaura, 2003; Hitsmanet al., 2013) results on cessation outcomes and, in some cases, pooreffects on emotional outcomes (Kahler et al., 2002). Hence, thecurrent research paradigm to studying emotion–smoking comor-bidity may need to be revised to propel further progress in under-standing etiologic mechanisms and advancing clinical services forthis population.
The traditional paradigm in the emotion–smoking literaturemainly focuses on individual psychiatric syndromes and the man-ifest symptoms of these disorders, which poses several scientificand clinical challenges. First, a syndrome-based approach does notadequately address the substantive heterogeneity within individualdepressive and anxiety disorders. For instance, major depressionmay have from two to four symptom factors that are empirically,conceptually, and phenomenologically distinct (Shafer, 2006).Such heterogeneity suggests that there are multiple, distinct etio-logic influences that underlie a single emotional syndrome (Hasler,Drevets, Manji, & Charney, 2004). Hence, individuals who sharethe same emotional disorder diagnosis may have different emo-tional influences on their smoking and, therefore, benefit fromdifferent smoking intervention approaches. Second, thissyndrome-based approach, which often focuses on each disorder inisolation from one another, does not sufficiently address the con-siderable co- and multimorbidity across multiple depressive andanxiety disorders (Gorman, 1996–1997). Certain disorders (e.g.,major depression and GAD) have exceedingly high rates of co-occurrence (Kessler, Chiu, Demler, & Walters, 2005), which hasprompted some to suggest that some emotional disorders may be“alternate manifestations” of a common underlying etiology (T. A.Brown, Chorpita, & Barlow, 1998). Thus, individuals with differ-ent emotional disorder syndromes may actually have shared emo-tional influences on their smoking and potentially benefit from acommon clinical strategy. Finally, focusing on syndromes assumesthat the manifest symptoms are important in explaining emotion–smoking comorbidity. However, certain manifest symptoms havelimited direct relations to smoking (e.g., increased appetite inmajor depression, intrusive nightmares in PTSD, and worry inGAD; Greenberg et al., 2012; Leventhal, Kahler, Ray, & Zimmer-man, 2009; Peasley-Miklus, McLeish, Schmidt, & Zvolensky,2012), and for some of the pathognomonic emotional symptoms(e.g., dysphoric affect), many individuals can effectively cope withsymptoms without smoking (Skrove, Romundstad, & Indredavik,2013; Tsourtos et al., 2011). Thus, underlying processes thatdirectly reflect the propensity to act on emotional disturbance withsmoking behavior, rather than the emotional symptomatology perse, may be particularly salient to smoking. Accordingly, an ap-proach focused on underlying vulnerability processes that govern
one’s reaction to emotion states and cut across multiple forms ofemotional disorder is warranted to advance research and practice.
The Current Article
Extant review, synthesis, or theory articles on emotion–smokingcomorbidity have limited their focus on manifest symptoms orsyndromes, factors germane to either depression or anxiety but notboth, or a particular stage of the smoking trajectory (e.g., R. A.Brown, Lejuez, Kahler, Strong, & Zvolensky, 2005; Covey, Glass-man, & Stetner, 1998; Hall, Muñoz, Reus, & Sees, 1993; Hitsmanet al., 2003; Morissette, Tull, Gulliver, Kamholz, & Zimering,2007; Weinberger, Mazure, Morlett, & McKee, 2013; Wilhelm,Wedgwood, Niven, & Kay-Lambkin, 2006). We are not aware ofany article that introduces an integrative theoretical framework forparsimoniously identifying key psychological mechanisms thatunderpin the relation of multiple manifestations of anxiety anddepression to progression across the smoking trajectory. To ad-dress this major gap in the literature, the present article puts fortha novel framework to synthesize recently emerging lines of em-pirical evidence on the role of transdiagnostic emotional vulnera-bility factors in emotion–smoking comorbidity. Here we focus onthree key transdiagnostic emotional vulnerabilities implicated inthe etiology of smoking: (a) anhedonia (Anh; defined as thetendency to experience reduced happiness, pleasure, and interest inresponse to rewards; Leventhal, Chasson, Tapia, Miller, & Pettit,2006), (b) anxiety sensitivity (AS; fear that anxiety symptoms areharmful; Reiss, Peterson, Gursky, & McNally, 1986), and (c)distress tolerance (DT; perceived or actual ability to tolerate emo-tional and physical distress; Leyro, Zvolensky, & Bernstein, 2010).
We first define terminology, discuss key conceptual tenets ofthe proposed transdiagnostic framework, explain why we extrap-olate the framework to Anh, AS, and DT specifically, and describethe review methodology. In the main body of the article, we defineAnh, AS, and DT and critically review the empirical literature onthe role of these three vulnerability factors in smoking, withseparate subsections devoted to each vulnerability factor. Thestructure of these subsections is organized similarly, covering thefollowing content areas: the vulnerability factor’s definition, mea-surement, and theoretical applicability to smoking; empirical rela-tions of the vulnerability factor to stages along the smoking tra-jectory; and implications for smoking interventions that target thevulnerability factor. We then point out key gaps in the literatureand synthesize the review results by proposing an integrativemodel for understanding the etiologic role of transdiagnostic vul-nerabilities in emotional disorder–smoking comorbidity. We con-clude with clinical and scientific implications drawn from thisapproach.
Transdiagnostic Emotion Vulnerability Framework:Defining Key Variables, Conceptual Tenets, and
Review Methodology
Key Variable Definitions
Stages in the trajectory of cigarette smoking. Smokers oftenfollow a generally well-specified sequence that includes the initi-ation, progression, maintenance, cessation, and relapse. Initiationreflects the initial cigarette smoked and further experimentation
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2 LEVENTHAL AND ZVOLENSKY
(irregular smoking). A sizable portion of initiators continue andescalate their smoking behavior, ultimately progressing to regularsmoking, ranging from weekly to daily use. The period in whichsmokers continue systematic regular smoking patterns is termedmaintenance; it is in this stage that smoking behavior is likely tobecome habitualized. For some individuals certain mechanismsthat maintain smoking may be more powerful and promote morechronic, compulsive, and severe smoking patterns, indicative oftobacco dependence (Japuntich, Piper, Schlam, Bolt, & Baker,2009). Typically, the longer that smoking is maintained, the moreentrenched and severe smoking behavior becomes. Although somesmokers avoid making a cessation attempt as a result of poormotivation to quit or severe tobacco dependence that overrides anyquit motivation, almost all who make a quit attempt relapse backto smoking after their first attempt (CDC, 2010). Following arelapse, many individuals return to their typical prequit-levelsmoking behavior or even exceed prequit levels (CDC, 2010),which recapitulates and extends the maintenance of smoking.From this point forward, many smoking trajectories enter into apersistent cyclic pattern of maintenance, cessation, and relapse.
Emotional symptoms and disorders. This article focuses ondiagnostic status and dimensional variation in symptom severitywithin emotional syndromes within the unipolar mood and anxietydisorders. We focus on major depression, dysthymic disorder,panic disorder, social anxiety disorder, specific phobia, GAD, andPTSD and other trauma-related disorders given their (a) common-alities with one another; (b) high prevalence rate; and (c) strongrelation with smoking initiation, maintenance, and relapse (Lev-enthal, Japuntich, et al., 2012; Piper et al., 2011; Weinberger,Pilver, et al., 2013; Zvolensky, Gibson, et al., 2008).
Transdiagnostic (“reactive”) emotional vulnerabilities.Recent work in psychopathological science proposes that the un-derlying cause of many forms of emotional symptoms and disor-ders as well as their comorbidity may be underpinned by a smallerset of transdiagnostic vulnerability processes (Dozois, Seeds, &Collins, 2009; Sauer-Zavala et al., 2012). This approach integrateswell with the National Institute of Mental Health’s ResearchDomain Criteria, which proposes that common cross-cutting di-mensions, traits, neural circuits, and biological pathways underpinand account for the presentation of various mental disorder diag-noses (Cuthbert & Insel, 2013). Our framework focuses on “reac-tive” transdiagnostic vulnerabilities, which denote characteristicmaladaptive responses to emotion stimuli and states. These typesof vulnerabilities play a key explanatory role in emotion experi-ence by (a) enhancing or diminishing the normative response toemotion stimuli and states, resulting in an excess or deficit, re-spectively, beyond typical emotional functioning; or (b) alteringthe type of response to emotion stimuli and states. In either case,these reactive processes may be maladaptive because they serve toreinforce the intensity and frequency of future manifest emotionalsymptoms. For example, when faced with negative emotion states,individuals with an emotional vulnerability factor that limits theircapacity to handle distress may be more apt to execute avoidancebehaviors that preclude habituation to negative emotion states,which could ultimately increase the intensity of future negativeaffect and solidify beliefs and learned responses that interfere withthe capacity to adaptively respond to distress (Leyro, Zvolensky, &Bernstein, 2010).
Transdiagnostic Emotional Vulnerabilities andSmoking: Core Conceptual Tenets of the Framework
Amplification of smoking’s anticipated and actual affect-modulatory effects. There is variability in smoking patternswithin the subpopulation of individuals with elevated emotionalpathology (e.g., Dierker & Donny, 2008), suggesting that many areable to cope with emotional disturbance without resorting to smok-ing, whereas others may have more difficulty. We propose thatunderlying vulnerabilities that directly amplify the propensity toact on emotion disturbance with smoking behavior, rather than thelevel or quality of emotional symptomatology per se, may parsi-moniously explain emotion–smoking comorbidity. The core tenetof the framework is that smoking reflects a critical manifestationof the maladaptive response to emotion states that characterizetransdiagnostic emotional vulnerabilities. Specifically, people withelevated vulnerabilities may be hypermotivated to respond toemotion states or stimuli with smoking behavior to achieve affectmodulation, which they might otherwise not be able to obtainthrough adaptive means. As a result, people with reactive vulner-abilities may be more sensitive to the effects of smoking onaffective states, place greater salience on the reinforcing value ofsmoking-induced affect modulation, and develop stronger expec-tancies for smoking-induced affect modulation, which collectivelymay transmit risk for movement along the smoking trajectory.
Conceptual rationale for focusing on Anh, AS, and DT. Wefocus on Anh, AS, and DT in this article because these threefactors are implicated in a wide variety of manifestations ofemotional disorder and have theoretical relevance to smoking.Smoking possesses three unique primary affect-modulatory prop-erties that make it a particularly potent reinforcer for individuals atrisk for emotional psychopathology: (a) pleasure/positive affectenhancement (Strong et al., 2011), (b) anxiety reduction (Kassel &Unrod, 2000), and (c) distress termination (Kassel, Stroud, &Paronis, 2003). As reviewed below, evidence indicates that Anhamplifies smoking’s anticipated and actual pleasure-enhancingproperties, AS amplifies smoking’s anticipated and actual anxio-lytic properties, and DT amplifies smoking’s anticipated and actualdistress-alleviating properties. Accordingly, Anh, AS, and DT maycollectively account for a wide range of emotional psychopathol-ogy as well as multiple affective mechanisms that transmit riskalong the smoking trajectory continuum. A heuristic for the trans-diagnostic framework to emotion–smoking comorbidity proposedhere is presented in Figure 1.
Scope and Methodology for Review ofEmpirical Literature on the Relation of Anh, AS, andDT to Smoking
Within a portion of each succeeding section focused on Anh,AS, and DT, we critically review and integrate the availableempirical literature examining the role of these three vulnerabilityfactors in smoking. We located citations via searches of Medline,PsycINFO, and Google Scholar as of May 1, 2014. Searches usedthe AND function that identified citations that crossed two typesof terms: a transdiagnostic vulnerability factor term and a smokingterm. For the vulnerability term, searches were repeated for each ofthe following: anhedonia, hedonia, hedonic, anhedonic, reduced/diminished pleasure, reduced/diminished interest, distress (in)tol-
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3EMOTIONAL VULNERABILITIES AND SMOKING
erance, persistence, frustration (in)tolerance, anxiety sensitivity,bodily vigilance, somatic threat, and interoception sensitivity. Forthe smoking term, searches were repeated for smoking, cigarette,nicotine, and tobacco. In addition, abstract catalogues for presen-tations for relevant professional meetings (e.g., Society for Re-search on Nicotine and Tobacco) were searched. Published arti-cles, conference abstracts, theses, and dissertations wereconsidered for inclusion (98% of final studies included werepublished articles). Study selection methods resulted in approxi-mately 500 citations. Studies that did not directly report data on theempirical relation of Anh, AS, or DT to a smoking variable orexamine Anh, AS, or DT in the context of a smoking-relatedmanipulation (e.g., tobacco deprivation, nicotine administration)were discarded. The remaining 79 studies were qualitatively re-viewed and synthesized. Table 1 describes final studies included inthe review.
We divided identified articles by relevance to one of the fol-lowing stages: (a) smoking initiation, (b) progression to regularsmoking, (c) maintenance, and (d) cessation and relapse processes.In the initiation and progression sections, we included both cross-sectional (e.g., relations of Anh, AS, and DT to lifetime smokingstatus) and prospective studies (e.g., predicting initiation or esca-lation). For the maintenance sections, we focused on studies ex-amining the relation of Anh, AS, and DT to mechanisms thatmaintain smoking (e.g., smoking expectancies, craving, with-drawal effects, smoking reinforcement) and indicators of smokingchronicity (e.g., years as a smoker), as well as the effects ofsmoking and nicotine manipulations on Anh, AS, and DT. Thecessation and relapse sections incorporated prospective and retro-spective studies of correlates of relapse and cessation-relevantconstructs (e.g., perceived barriers to quitting).
Transdiagnostic EmotionalVulnerabilities and Smoking
Anhedonia
Anhedonia: Construct and correlates.Definition. Anh reflects diminished appetitive functioning
and manifests as deficient happiness and enjoyment as well asdecreased pleasure from and interest in stimuli that are commonlyrewarding (Hatzigiakoumis, Martinotti, Giannantonio, & Janiri,2011). In some conceptualizations, Anh is considered a categoricalsymptom and acute state that onsets in conjunction with the onsetof a depressive episode and offsets during remission (AmericanPsychiatric Association, 2013). Though often present in majordepression, Anh symptom status is only modestly associated withother depressive symptoms (�s � .09–.58) and regularly occursoutside depression among psychiatric patients (Zimmerman,McGlinchey, Young, & Chelminski, 2006a, 2006b). The person-ality and psychopathology literature has conceptualized Anh as atrait-like continuous dimension normally distributed in the popu-lation (Fawcett, Clark, Scheftner, & Gibbons, 1983). Individuals atthe lower end of the Anh spectrum experience higher levels ofenjoyment and respond strongly to rewards, whereas those at theupper end of this spectrum exhibit prominent deficits in appetitiveexperience (Fawcett et al., 1983; Meehl, 1975). Anh is somewhatstable over time (Lyons et al., 1995; Meehl, 2001b) but canincrease following stress (Berenbaum & Connelly, 1993) and candecrease following clinical intervention (Stein, 2008). Thus, suchperspectives posit that Anh is a “trait-like” dimension that is stableyet malleable (Loas, 1996), which we apply in the current article.
Figure 1. General framework proposing that transdiagnostic emotional vulnerability factors explain therelation between various manifestations of emotional psychopathology and cigarette smoking.
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4 LEVENTHAL AND ZVOLENSKY
Tab
le1
Ove
rvie
wof
Art
icle
sIn
clud
edin
the
Rev
iew
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
Anh
edon
ia
Anh
-Alle
net
al.
(201
2)
N�
15sm
oker
sw
ithsc
hizo
phre
nia
(10�
cig/
day)
BD
I-A
nhC
ross
-sec
tiona
lco
rrel
atio
nal
MA
nhw
aspo
sitiv
ely
asso
ciat
edw
ithur
geto
smok
ein
smok
ers
with
schi
zoph
reni
a(r
�.6
0)bu
tno
tno
npsy
chia
tric
cont
rols
(ESU
).N
�16
nonp
sych
iatr
icco
ntro
lsm
oker
s(1
0�ci
g/da
y)A
udra
in-M
cGov
ern
etal
.(2
012)
N�
1,10
6ad
oles
cent
s(m
ean
age
�15
.5)
SHA
PSPr
ospe
ctiv
eco
rrel
atio
nal
I,P
Hig
her
base
line
Anh
was
asso
ciat
edw
ithgr
eate
rlik
elih
ood
ofpa
st30
-da
ysm
okin
gat
base
line
(OR
�2.
64)
and
incr
ease
inci
g/da
yov
erth
esu
bseq
uent
18m
onth
s(d
�0.
14).
Coo
ket
al.
(200
4)N
�35
adul
tno
ntre
atm
ent-
seek
ing
smok
ers
(10�
cig/
day)
FCPS
Lab
quas
i-ex
peri
men
tal
MH
ighe
rA
nhpr
edic
ted
grea
ter
incr
ease
sin
crav
ing
(r�
.47)
and
redu
ctio
nsin
acut
epo
sitiv
eaf
fect
(r�
�.4
0)bu
tno
tch
ange
sin
nega
tive
affe
ct(r
�.2
0)fo
llow
ing
24hr
ofto
bacc
ode
priv
atio
n.C
ook
etal
.(2
007)
N�
50ad
ult
nont
reat
men
t-se
ekin
gsm
oker
s(1
5�ci
g/da
y)FC
PSL
abqu
asi-
expe
rim
enta
lP,
MSm
oker
sw
ithhi
gh(v
s.lo
w)
Anh
did
not
diff
erin
nico
tine
depe
nden
cese
veri
ty(d
��
0.47
),ci
g/da
y(d
�0.
11),
orye
ars
smok
ing
(d�
0.07
).Sm
oker
sw
ithhi
gh(v
s.lo
w)
Anh
exhi
bite
dgr
eate
rin
crea
ses
inpo
sitiv
eaf
fect
duri
nga
posi
tive
moo
din
duct
ion
whe
nsm
okin
ga
ciga
rette
with
nico
tine
(d�
0.72
)ve
rsus
plac
ebo
ciga
rette
(d�
0.14
).C
ook
etal
.(2
010)
N�
45sm
oker
s(1
0�ci
g/da
y)m
akin
ga
quit
atte
mpt
FCPS
Pros
pect
ive
corr
elat
iona
lC
RB
asel
ine
Anh
pred
icte
dfa
ster
late
ncy
tore
laps
e(H
R�
1.55
).
Coo
ket
al.
(201
2)N
�1,
504
smok
ers
(10�
cig/
ay)
enro
lled
ina
cess
atio
ntr
ial
Thr
ee-i
tem
Anh
scal
eaPr
ospe
ctiv
eco
rrel
atio
nal
P,M
,CR
Anh
was
high
erpo
stqu
it(v
s.pr
equi
t)da
y(d
�0.
13).
Anh
was
asso
ciat
edw
ithhi
gher
cig/
day
(r�
.15)
and
nico
tine
depe
nden
cese
veri
ty(r
�.1
2)at
base
line.
Bas
elin
eA
nh(O
R�
0.93
),po
stqu
itA
nh(O
R�
0.91
),an
dpr
e-to
post
quit
chan
gein
Anh
(OR
�0.
88)
pred
icte
dlo
wer
8-w
eek
poin
tpr
eval
ence
abst
inen
ce.
Gre
gor
etal
.(2
007)
N�
276
youn
gad
ult
daily
smok
ers
MA
SQ-A
DC
ross
-sec
tiona
lco
rrel
atio
nal
P,M
Anh
was
posi
tivel
yas
soci
ated
with
cig/
day
(r�
.17)
and
year
sas
asm
oker
(r�
.15)
.K
.A
.Jo
hnso
net
al.
(200
9)N
�12
3ad
ult
daily
trea
tmen
t-se
ekin
gsm
oker
sM
ASQ
-AD
Cro
ss-s
ectio
nal
corr
elat
iona
lP
Anh
was
not
asso
ciat
edw
ithci
g/da
y(r
�.1
3).
Lev
enth
al,
Ram
sey,
etal
.(2
008)
N�
157
heav
yso
cial
drin
kers
(10�
cig/
day)
insm
okin
gce
ssat
ion
tria
l
CE
SD-A
nhPr
ospe
ctiv
eco
rrel
atio
nal
P,M
,CR
Anh
was
not
asso
ciat
edw
ithba
selin
eci
g/da
y(r
�.0
7)or
nico
tine
depe
nden
cese
veri
ty(r
�.0
7).
Anh
was
asso
ciat
edw
ithgr
eate
rw
ithdr
awal
sym
ptom
son
quit
day
(��
.25)
.A
nhw
aspo
sitiv
ely
asso
ciat
edw
ithre
laps
eat
8(d
�0.
44),
16(d
�0.
48),
and
24(d
�0.
47)
wee
ksaf
ter
quit
date
.L
even
thal
,A
mer
inge
r,et
al.
(201
3)
N�
187
nont
reat
men
t-se
ekin
gsm
oker
s(1
0�ci
g/da
y)M
ASQ
-AD
Lab
quas
i-ex
peri
men
tal
MA
nhpr
edic
ted
grea
ter
sens
itivi
tyto
the
dam
peni
ngef
fect
sof
16-h
rto
bacc
ode
priv
atio
non
emot
iona
lvi
gor
(��
�.1
7)an
del
atio
n(�
��
.20)
.L
even
thal
,K
ahle
r,et
al.
(200
9)N
�1,
568
psyc
hiat
ric
outp
atie
nts
SCID
-Anh
item
Cro
ss-s
ectio
nal
corr
elat
iona
lI,
CR
Patie
nts
with
curr
ent
DSM
–IV
nico
tine
depe
nden
ceha
dhi
gher
rate
sof
clin
ical
lysi
gnif
ican
tA
nh(S
CID
)an
dm
ore
seve
reA
nhra
tings
(SA
DS)
com
pare
dto
thos
ew
ithno
hist
ory
ofni
cotin
ede
pend
ence
(OR
�1.
83;
��
.33)
and
past
(OR
�1.
62;
��
.25)
nico
tine
depe
nden
ce.
SAD
S-A
nhite
mPa
tient
sw
ithpa
stve
rsus
nohi
stor
yof
nico
tine
depe
nden
cedi
dno
tsi
gnif
ican
tly(O
R�
1.13
;�
�.0
4).
Lev
enth
al,
Mun
afò,
etal
.(2
012)
N�
75no
ntre
atm
ent-
seek
ing
smok
ers
(10�
cig/
day)
SHA
PST
PI-R
Lab
quas
i-ex
peri
men
tal
MO
vern
ight
toba
cco
depr
ivat
ion
mod
erat
edth
ere
latio
nbe
twee
nba
selin
eA
nhan
dem
otio
nal
proc
essi
ngof
happ
yfa
ces
(SH
APS
:�
p2�
.06;
TPI
-R:
�p2
�.0
4),
such
that
Anh
pred
icte
ddi
min
ishe
dem
otio
nal
proc
essi
ngdu
ring
depr
ivat
ion
(SH
APS
:r
��
.28;
TPI
-R:
r�
.08)
,bu
tno
taf
ter
adlib
smok
ing
(SH
APS
:r
��
.33;
TPI
-R:
r�
�.1
0).
Lev
enth
al,
Pipe
r,et
al.
(201
4)N
�1,
469
smok
ers
(10�
cig/
day)
enro
lled
ina
cess
atio
ntr
ial
CID
Ian
ticip
ator
yA
nhite
mb
Pros
pect
ive
corr
elat
iona
lP,
CR
Lif
etim
ehi
stor
yof
Anh
was
asso
ciat
edw
ithm
ore
seve
reni
cotin
ede
pend
ence
atba
selin
e(r
�.0
6).
Anh
pred
icte
dgr
eate
rod
dsof
rela
pse
(OR
�1.
42).
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
5EMOTIONAL VULNERABILITIES AND SMOKING
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
Lev
enth
al,
Wat
ers,
etal
.(2
009)
N�
212
nont
reat
men
t-se
ekin
gsm
oker
s(5
�ci
g/da
y)SH
APS
Lab
quas
i-ex
peri
men
tal
P,M
Anh
was
not
asso
ciat
edw
ithba
selin
eci
g/da
y(r
�.0
4),
age
ofon
set
(r�
.02)
,ni
cotin
ede
pend
ence
seve
rity
(r�
.09)
,or
year
sas
asm
oker
(r�
.01)
.A
nhw
aspo
sitiv
ely
asso
ciat
edw
itha
num
ber
ofpa
stqu
itat
tem
pts
(r�
.23)
,hi
gher
prop
ortio
nof
past
quit
atte
mpt
sen
ding
inra
pid
rela
pse
(abs
tinen
ce�
24hr
;r
�.2
0),
and
grea
ter
beha
vior
alch
oice
mel
iora
tion
smok
ing
mot
ives
(e.g
.,“V
ery
few
thin
gsgi
vem
epl
easu
reea
chda
ylik
eci
gare
ttes”
;r
�.1
8).
Anh
was
posi
tivel
yas
soci
ated
with
grea
ter
sens
itivi
tyto
12-h
rto
bacc
ode
priv
atio
nef
fect
son
urge
tosm
oke
for
plea
sure
(��
.19)
but
not
urge
tosm
oke
for
nega
tive
affe
ctre
lief
(��
.13)
.L
even
thal
,T
rujil
lo,
etal
.(2
014)
N�
275
nont
reat
men
t-se
ekin
gsm
oker
s(1
0�ci
g/da
y)M
ultim
easu
reA
nhco
mpo
site
cL
abqu
asi-
expe
rim
enta
lP,
MA
nhw
asas
soci
ated
with
high
erci
g/da
y(r
�.1
4)bu
tno
tni
cotin
ede
pend
ence
seve
rity
(r�
�.0
2)at
base
line.
Anh
pred
icte
dsh
orte
rtim
eto
smok
ing
initi
atio
nw
hen
dela
ying
smok
ing
was
mon
etar
ilyre
war
ded
(��
�.1
0)an
dm
ore
ciga
rette
spu
rcha
sed
(��
.13)
.L
even
thal
(201
0)N
�21
2no
ntre
atm
ent-
seek
ing
smok
ers
(5�
cig/
day)
CE
SD-A
nhC
ross
-sec
tiona
lco
rrel
atio
nal
MA
nhw
asas
soci
ated
with
high
ersm
okin
gur
gele
vel
(r�
.27)
mea
sure
daf
ter
adlib
smok
ing.
Lev
enth
al,
Ray
,et
al.
(201
2)N
�1,
204
Chi
nese
adol
esce
nts
(mea
nag
e�
12.2
)C
ESD
-Anh
Cro
ss-s
ectio
nal
corr
elat
iona
lI
Anh
was
high
erin
adol
esce
nts
with
ahi
stor
yof
smok
ing
expe
rim
enta
tion
com
pare
dto
thos
ew
ithou
t(r
�.2
9).
Mic
kens
etal
.(2
011)
N�
212
nont
reat
men
t-se
ekin
gsm
oker
s(5
�ci
g/da
y)C
ESD
-Anh
Cro
ss-s
ectio
nal
corr
elat
iona
lP,
MA
nhw
asas
soci
ated
with
mor
ese
vere
nico
tine
depe
nden
cese
veri
ty(�
�.1
9)an
dbe
havi
oral
choi
ceam
elio
ratio
nm
otiv
es(�
�.2
6)bu
tno
tci
g/da
yor
othe
rsm
okin
gm
otiv
es.
McC
harg
ue&
Coo
k(2
007)
N�
77ad
ult
smok
ers
FCPS
and
Anh
scre
ener
dC
ross
-sec
tiona
lco
rrel
atio
nal
PA
nhle
vel
onth
eFC
PS(r
�.2
7)w
asas
soci
ated
with
high
erni
cotin
ede
pend
ence
seve
rity
.A
nhst
atus
onth
eD
SM-b
ased
scre
ener
item
was
not
sign
ific
antly
asso
ciat
edw
ithni
cotin
ede
pend
ence
(r�
.13)
.M
cLei
shet
al.
(200
6)N
�22
0no
ntre
atm
ent-
seek
ing
daily
smok
ers
MA
SQ-A
DC
ross
-sec
tiona
lco
rrel
atio
nal
PA
nhw
aspo
sitiv
ely
asso
ciat
edci
g/da
y(r
�.1
8).
McL
eish
etal
.(2
008)
N�
222
youn
gad
ults
MA
SQ-A
DC
ross
-sec
tiona
lco
rrel
atio
nal
IA
nhw
ashi
gher
inda
ily(v
s.ne
ver)
smok
ers
(r�
.27)
.N
iaur
aet
al.
(200
1)N
�72
smok
ers
enro
lled
insm
okin
gce
ssat
ion
prog
ram
sA
ntic
ipat
ory
Anh
item
eC
ross
-sec
tiona
lco
rrel
atio
nal
CR
Anh
was
posi
tivel
yre
late
dto
mor
era
pid
rela
pse
over
ase
lf-g
uide
dqu
itat
tem
ptov
er30
days
(ESU
).Po
mer
leau
etal
.(2
003)
N�
931
adul
tw
omen
CE
SD-A
nhC
ross
-sec
tiona
lco
rrel
atio
nal
I,C
RR
elat
ive
tone
ver
smok
ers,
Anh
was
sign
ific
antly
high
erin
curr
ent
smok
ers
(d�
0.21
)an
dm
argi
nally
high
erin
ex-s
mok
ers
(d�
0.18
).C
urre
ntan
dex
-sm
oker
sdi
dno
tsi
gnif
ican
tlydi
ffer
inA
nh(d
�0.
03).
Pow
ell
etal
.(2
004)
N�
78da
ilysm
oker
sSH
APS
Lab
expe
rim
enta
lM
Ove
rnig
htde
priv
edsm
oker
sre
ceiv
ing
plac
ebo
(vs.
nico
tine)
loze
nge
repo
rted
grea
ter
Anh
(d�
0.39
).St
one
&L
even
thal
(201
4)N
�50
4ad
oles
cent
neve
rsm
oker
s(m
ean
age
�14
.5)
SHA
PSC
ross
-sec
tiona
lco
rrel
atio
nal
IA
nhw
asas
soci
ated
with
grea
ter
expe
ctan
cies
that
smok
ing
wou
ldpr
oduc
epl
easu
re(�
�.1
4),
grea
ter
curi
osity
abou
ttr
ying
smok
ing
(��
.12)
,an
dlo
wer
nega
tive
smok
ing
expe
ctan
cies
(��
�.1
6).
Anh
was
not
rela
ted
tow
illin
gnes
s(�
�.0
7)or
inte
ntio
n(�
�.0
4)to
smok
e.Z
vole
nsky
,K
otov
,et
al.
(200
8)N
�39
0R
ussi
anad
ults
MA
SQ-A
DC
ross
-sec
tiona
lco
rrel
atio
nal
IA
nhdi
dno
tdi
ffer
betw
een
smok
ers
and
nons
mok
ers
(r�
.03)
.Z
vole
nsky
,Jo
hnso
n,et
al.
(200
9)
N�
144
daily
nont
reat
men
t-se
ekin
gad
ult
smok
ers
MA
SQ-A
DC
ross
-sec
tiona
lco
rrel
atio
nal
P,M
Anh
was
not
asso
ciat
edw
ithci
g/da
y(r
�.0
1),
year
sas
asm
oker
(r�
.13)
,or
num
ber
ofpa
stqu
itat
tem
pts
(r�
.01)
.
Anx
iety
sens
itivi
ty
Abr
ams,
Schl
osse
r,et
al.
(201
1)
N�
58he
avy
smok
ers
(20�
cig/
day)
and
27no
nsm
oker
sA
SIL
abqu
asi-
expe
rim
enta
lI,
MA
Sw
asno
tsi
gnif
ican
tlyhi
gher
insm
oker
sco
mpa
red
tono
nsm
oker
s(d
s�
0.38
to0.
53).
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
6 LEVENTHAL AND ZVOLENSKY
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
At
base
line,
AS
was
posi
tivel
yco
rrel
ated
with
reas
ons
for
smok
ing
for
tens
ion
redu
ctio
n(r
�.3
0)bu
tno
tsi
gnif
ican
tlyco
rrel
ated
with
reas
ons
for
smok
ing
due
tosu
bjec
tive
addi
ctio
nto
smok
ing
(r�
.18)
amon
gsm
oker
s.T
heex
tent
tow
hich
depr
ivat
ion
heig
hten
edpa
nic
resp
onse
toa
rebr
eath
ing
chal
leng
ew
asdi
min
ishe
dam
ong
smok
ers
with
high
AS
men
tal
conc
erns
(i.e
.,fe
arof
the
nega
tive
cons
eque
nces
ofco
gniti
vean
xiet
ysy
mpt
oms;
“It
scar
esm
ew
hen
Iam
unab
leto
keep
my
min
don
ata
sk”;
ESU
).A
Sso
cial
conc
erns
(e.g
.,“O
ther
peop
leno
tice
whe
nI
feel
shak
y”)
and
phys
ical
conc
erns
(e.g
.,“I
tsc
ares
me
whe
nm
yhe
art
beat
sra
pidl
y”)
did
not
mod
erat
eef
fect
sof
depr
ivat
ion
onre
spon
seto
the
brea
thin
gch
alle
nge
(ESU
).A
bram
s,Z
vole
nsky
,et
al.
(201
1)
N�
326
adul
tda
ilysm
oker
s(a
tle
ast
5ci
g/da
yfo
rat
leas
t1
year
)
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lM
AS
was
corr
elat
edw
ithth
eSA
EQ
full
scal
e(r
�.5
0)an
dsu
bsca
les
tapp
ing
expe
ctin
gne
gativ
em
ood,
som
atic
sym
ptom
s,an
dha
rmfu
lco
nseq
uenc
esin
resp
onse
toab
stin
ence
(rs
�.3
7to
.52)
.A
ssay
aget
al.
(201
2)N
�67
adul
tda
ilysm
oker
sin
smok
ing
cess
atio
ntr
eatm
ent
ASI
Pros
pect
ive
corr
elat
iona
lC
RT
hose
with
mai
ntai
ned
high
AS
from
pret
reat
men
tto
1m
onth
post
trea
tmen
t,co
mpa
red
toth
ose
who
expe
rien
ced
asi
gnif
ican
tre
duct
ion
inA
Sle
vels
duri
ngth
ispe
riod
,w
ere
atin
crea
sed
risk
for
laps
ean
dre
laps
e(d
�0.
55).
R.
A.
Bro
wn
etal
.(2
001)
N�
60sm
oker
sw
ithpa
stm
ajor
depr
esse
den
rolle
din
asm
okin
gce
ssat
ion
tria
l
ASI
Pros
pect
ive
corr
elat
iona
lM
,CR
AS
was
asso
ciat
edw
ithin
crea
sed
odds
ofla
psin
gdu
ring
the
firs
tw
eek
afte
rqu
itda
y(R
R�
2.0)
.A
Sw
asco
rrel
ated
with
the
incr
ease
dex
pect
atio
nsfo
rne
gativ
eaf
fect
redu
ctio
nfr
omsm
okin
gat
base
line
(��
.39)
.E
vatt
&K
asse
l(2
010)
N�
32ad
ult
smok
ers
(ave
rage
of10
cig/
day)
ASI
Lab
quas
i-ex
peri
men
tal
MH
igh
(vs.
low
)A
Ssm
oker
sdi
ffer
edin
the
exte
ntto
whi
chsm
okin
gre
duce
dac
ute
anxi
ety
afte
ra
stre
ssfu
lsp
eech
(vs.
cont
rol)
cond
ition
(�p2
�.1
1),
such
that
smok
ing
redu
ced
acut
ean
xiet
yin
resp
onse
toth
esp
eech
(vs.
cont
rol)
cond
ition
inhi
gh-A
Ssm
oker
s(�
p2�
.36)
but
not
low
-AS
smok
ers
(ESU
).H
igh
(vs.
low
)A
Ssm
oker
sm
argi
nally
diff
ered
inth
eex
tent
tow
hich
smok
ing
redu
ced
perc
eive
dar
ousa
laf
ter
ast
ress
ful
spee
ch(v
s.co
ntro
l)co
nditi
on(�
p2�
.07)
,su
chth
atsm
okin
gre
duce
dac
ute
anxi
ety
inre
spon
seto
the
spee
ch(v
s.co
ntro
l)co
nditi
onin
high
-AS
smok
ers
(�p2
�.2
2)bu
tno
tlo
w-A
Ssm
oker
s(E
SU).
Hig
h(v
s.lo
w)
AS
smok
ers
did
not
diff
erin
the
exte
ntto
whi
chsm
okin
gim
pact
edsu
bjec
tive
stre
ss,
hear
tra
te,
orsk
inco
nduc
tanc
eaf
ter
ast
ress
ful
spee
ch(v
s.co
ntro
l)co
nditi
on(E
SU).
Feld
ner
etal
.(2
008)
N�
96hi
gh-A
Sda
ilysm
oker
sin
aps
ycho
soci
alin
terv
entio
nta
rget
ing
AS
and
smok
ing
orhe
alth
info
rmat
ion
cont
rol
grou
p
ASI
Pros
pect
ive
expe
rim
enta
lC
RA
Sre
duct
ion
inte
rven
tion
(com
pare
dto
cont
rol)
sign
ific
antly
redu
ced
AS
(�2
�.0
8)an
dm
argi
nally
redu
ced
cig/
day
(p�
.06;
�2
�.0
3).
Gre
gor
etal
.(2
008)
N�
125
daily
smok
ers
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lM
AS
was
corr
elat
edw
ithgr
eate
rsm
okin
gex
pect
anci
esfo
rne
gativ
ere
info
rcem
ent,
nega
tive
cons
eque
nce,
posi
tive
rein
forc
emen
t,an
dap
petit
eco
ntro
las
wel
las
with
grea
ter
perc
eive
dba
rrie
rsto
cess
atio
n(r
s�
.33
to.5
5).
Gon
zale
zet
al.
(200
8)N
�18
9da
ilysm
oker
s(a
vera
geof
15�
cig/
day)
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lM
,CR
AS
was
sign
ific
antly
corr
elat
edw
ithst
imul
atio
n,ha
bitu
al,
addi
ctiv
e,an
dco
ping
reas
ons
for
smok
ing
asw
ell
aspe
rcei
ved
barr
iers
toqu
ittin
g(�
s�
.22
to.2
3).
Gui
llot
etal
.(2
014)
N�
205
nont
reat
men
t-se
ekin
gad
ult
smok
ers
(10
cig/
day)
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lM
AS
was
asso
ciat
edw
ithst
rong
erex
pect
anci
esth
atsm
okin
gal
levi
ates
nega
tive
affe
ct(�
�.3
0)an
dsm
okin
gab
stin
ence
exac
erba
tes
aver
sive
with
draw
alsy
mpt
oms
(��
.24)
.K
.A
.Jo
hnso
net
al.
(201
2)N
�12
3ad
ult
daily
smok
ers
enro
lled
ina
cess
atio
nst
udy
ASI
Pros
pect
ive
corr
elat
iona
lP,
MA
Sw
aspo
sitiv
ely
asso
ciat
edw
ithgr
eate
rba
selin
eni
cotin
ew
ithdr
awal
sym
ptom
s(r
�.5
5)bu
tno
tni
cotin
ede
pend
ence
seve
rity
(r�
.04)
.
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
7EMOTIONAL VULNERABILITIES AND SMOKING
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
Gre
ater
leve
lsof
base
line
AS
wer
eas
soci
ated
with
ast
rong
erre
latio
nbe
twee
nav
erag
ele
vels
ofst
ate
anxi
ety
and
aver
age
leve
lsof
nico
tine
with
draw
alsy
mpt
oms
expe
rien
ced
duri
ngth
eco
urse
offi
rst
two
wee
ksof
the
quit
atte
mpt
(ESU
).A
Sw
asas
soci
ated
with
slow
erde
crea
sein
with
draw
alsy
mpt
oms
duri
ngth
esa
me
time
peri
od(E
SU).
Mar
shal
let
al.
(200
9)N
�99
daily
smok
ers
ASI
Lab
quas
i-ex
peri
men
tal
M,C
RA
Sw
aspo
sitiv
ely
corr
elat
edw
ithqu
it-da
yni
cotin
ew
ithdr
awal
(r�
.53)
.In
tera
ctio
nbe
twee
nA
San
dpa
nic
resp
onsi
vity
toa
volu
ntar
yhy
perv
entil
atio
nch
alle
nge
pred
icte
dqu
it-da
yni
cotin
ew
ithdr
awal
sym
ptom
seve
rity
abov
ean
dbe
yond
the
mai
nef
fect
s(�
p2�
.046
,�
��
.29)
.M
cLei
shet
al.
(200
8)N
�22
2yo
ung
adul
tsA
SIC
ross
-sec
tiona
lco
rrel
atio
nal
IA
Sph
ysic
alco
ncer
nssu
bsca
le(e
.g.,
“It
scar
esm
ew
hen
my
hear
tbe
ats
rapi
dly”
)w
ashi
gher
insm
oker
sve
rsus
nons
mok
ers
(r�
.24)
.A
Sph
ysic
alco
ncer
nsm
oder
ated
the
asso
ciat
ion
ofsm
okin
gst
atus
with
body
vigi
lanc
ean
dan
xiet
ysy
mpt
oms
(�s
�.2
3an
d.2
7),
such
that
the
posi
tive
rela
tion
ofth
ese
two
aspe
cts
ofan
xiet
yto
smok
ing
was
high
eram
ong
thos
ew
ithhi
gher
AS.
Mor
isse
tteet
al.
(200
6)N
�52
7in
divi
dual
sw
ithan
xiet
ydi
sord
ers
seek
ing
anxi
ety
trea
tmen
t
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lI
AS
was
sign
ific
antly
high
eram
ong
smok
ers
com
pare
dto
nons
mok
ers
(d�
0.54
).
Perk
ins
etal
.(2
010)
N�
71no
ntre
atm
ent-
seek
ing
adul
tsm
oker
s(�
10ci
g/da
y)A
SIL
abqu
asi-
expe
rim
enta
lM
Hig
her
vers
uslo
wer
AS
was
asso
ciat
edw
ithgr
eate
rci
gare
ttelik
ing
(rew
ard)
duri
nga
stre
ssfu
lsp
eech
prep
arat
ion
proc
edur
eve
rsus
othe
rco
nditi
ons
(�p2
�.0
46).
Neg
ativ
eaf
fect
decr
ease
dm
ore
afte
rsm
okin
gin
thos
ew
ithhi
ghve
rsus
low
AS,
but
only
duri
ngst
ress
ful
spee
chpr
epar
atio
nve
rsus
othe
rco
nditi
ons
(�p2
�.0
31,
�p2
�.0
44).
AS
did
not
sign
ific
antly
infl
uenc
eor
inte
ract
with
nega
tive-
affe
ct-
rela
ted
expe
rim
enta
lco
nditi
ons
onsm
okin
gre
info
rcem
ent
(i.e
.,ad
libsm
okin
g).
Vuj
anov
ic&
Zvo
lens
ky(2
009)
N�
90no
ntre
atm
ent-
seek
ing
daily
smok
ers
(15�
cig/
day)
ASI
Lab
quas
i-ex
peri
men
tal
MA
Sby
toba
cco
depr
ivat
ion
inte
ract
ion
was
sign
ific
antly
pred
ictiv
eof
acut
ean
xiet
ydu
ring
aC
O2
chal
leng
e(a
nxie
tydu
ring
the
chal
leng
e;�
2�
.05)
,su
chth
atlo
w-A
Ssm
oker
sex
peri
ence
dle
ssan
xiet
yw
hen
depr
ived
(vs.
nond
epri
ved)
and
high
-AS
smok
ers
expe
rien
ced
sim
ilar
anxi
ety
asa
func
tion
ofde
priv
atio
nst
atus
.W
ong
etal
.(2
013)
N�
87ad
ult
smok
ers
(10�
cig/
day)
ASI
Lab
quas
i-ex
peri
men
tal
MA
Spr
edic
ted
grea
ter
incr
ease
sin
posi
tive
affe
ctfr
ompr
e-to
post
ciga
rette
(��
.30)
asw
ell
asgr
eate
rsm
okin
gsa
tisfa
ctio
nan
dps
ycho
logi
cal
rew
ard
(��
.23
to.4
8).
AS
was
not
sign
ific
antly
rela
ted
tosm
okin
g-in
duce
dch
ange
sin
nega
tive
affe
ct,
urge
,or
aver
sive
effe
cts
ofsm
okin
g(|�
|s�
.16)
.Z
vole
nsky
,B
erns
tein
,et
al.
(200
7)
N�
130
“low
-lev
elsm
oker
s”(�
10ci
g/da
y)fr
omM
exic
oA
SIC
ross
-sec
tiona
lco
rrel
atio
nal
P,C
RA
Sph
ysic
al-c
once
rns
low
eror
der
fact
orw
asre
late
dto
retr
ospe
ctiv
ere
port
sof
earl
ysm
okin
gre
laps
e(O
R�
1.19
).A
Sw
asco
rrel
ated
with
high
erci
g/da
y(r
�.4
3).
Zvo
lens
kyet
al.
(200
6)N
�75
daily
smok
ers
(20�
cig/
day)
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lC
RA
Sw
assi
gnif
ican
tlyas
soci
ated
with
retr
ospe
ctiv
ere
port
sof
earl
ysm
okin
gre
laps
e(O
R�
1.06
)ab
ove
and
beyo
ndth
eef
fect
sof
nega
tive
affe
ctiv
ity.
Zvo
lens
ky,
Farr
is,
Schm
idt,
&Sm
its(2
014)
N�
466
adul
ttr
eatm
ent-
seek
ing
daily
smok
ers
ASI
-3C
ross
-sec
tiona
lco
rrel
atio
nal
P,M
,CR
AS
was
posi
tivel
yre
late
dto
high
erni
cotin
ede
pend
ence
leve
l(r
�.1
4),
perc
eive
dba
rrie
rsto
smok
ing
cess
atio
n(r
�.3
2),
prob
lem
atic
sym
ptom
sdu
ring
prev
ious
quit
atte
mpt
s(r
�.3
8),
and
expe
ctan
cies
for
smok
ing-
indu
ced
nega
tive
rein
forc
emen
t(r
�.2
9).
AS
was
not
sign
ific
antly
asso
ciat
edw
ithlif
etim
enu
mbe
rof
quit
atte
mpt
s(r
�.0
3).
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
8 LEVENTHAL AND ZVOLENSKY
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
AS
sign
ific
antly
indi
rect
lyre
late
dto
barr
iers
toce
ssat
ion,
grea
ter
num
ber
ofqu
itat
tem
pts,
and
grea
ter
nega
tive
rein
forc
emen
tsm
okin
gex
pect
anci
esth
roug
hth
ete
nden
cyto
avoi
ddi
stre
ssin
gth
ough
ts,
feel
ings
,an
din
tern
alse
nsat
ions
(ESU
;st
atis
tical
med
iatio
nof
rela
tion
ofA
Sto
smok
ing
via
avoi
danc
e).
Zvo
lens
ky,
Feld
ner,
etal
.(2
004)
N�
90yo
ung
adul
tre
gula
rsm
oker
sA
SIC
ross
-sec
tiona
lco
rrel
atio
nal
MA
Sph
ysic
alco
ncer
nsan
dm
enta
lin
capa
cita
tion
conc
erns
wer
esi
gnif
ican
tlyre
late
dto
smok
ing
expe
ctan
cies
for
nega
tive
rein
forc
emen
tan
dne
gativ
ehe
alth
cons
eque
nces
(rs
�.3
0to
.32)
.Z
vole
nsky
,Jo
hnso
n,et
al.
(200
9)
N�
144
adul
tsm
oker
s(1
5�ci
g/da
y)A
SIC
ross
-sec
tiona
lco
rrel
atio
nal
CR
AS
was
corr
elat
edw
ithgr
eate
rnu
mbe
rof
past
quit
atte
mpt
s(r
�.2
8).
Zvo
lens
ky,
Kot
ov,
etal
.(2
003)
N�
95ad
ult
smok
ers
from
Mos
cow
ASI
Cro
ss-s
ectio
nal
corr
elat
iona
lP,
MA
Sw
asno
tsi
gnif
ican
tlyas
soci
ated
with
cig/
day
(r�
.04)
.A
Sam
plif
ied
the
exte
ntto
whi
chhi
gher
cig/
day
pred
icte
dag
orap
hobi
cav
oida
nce
(sr2
�.1
0;A
S
Smok
ing
Stat
usin
tera
ctio
n).
AS
did
not
sign
ific
antly
mod
erat
eth
ere
latio
nof
cig/
day
tonu
mbe
rof
pani
cat
tack
s(s
r2�
.02)
oran
xiet
ysy
mpt
omse
veri
tyex
peri
ence
d(s
r2�
.02)
duri
ngth
epa
stw
eek.
Zvo
lens
ky,
Lej
uez,
etal
.(2
003)
A43
-yea
r-ol
dC
auca
sian
mal
ere
ceiv
ing
inte
roce
ptiv
eex
posu
re-
base
dpr
ogra
mof
smok
ing
cess
atio
nan
dco
gniti
vebe
havi
oral
ther
apy
for
pani
cdi
sord
er
ASI
Pros
pect
ive
case
repo
rtC
RPa
rtic
ipan
tre
port
edre
duct
ion
inA
Ssc
ore
(fro
m35
pret
reat
men
tto
25po
sttr
eatm
ent)
and
mai
ntai
ned
abst
inen
cefo
r12
mon
ths
follo
win
gqu
itat
tem
pt(i
psat
ive
z-sc
ore
diff
eren
ce�
0.92
).
Zvo
lens
ky,
Yar
tz,
etal
.(2
008)
N�
3fe
mal
eda
ilysm
oker
sw
ithhi
ghA
San
dni
cotin
ede
pend
ence
rece
ivin
gin
tero
cept
ive
expo
sure
-ba
sed
smok
ing
cess
atio
ntr
eatm
ent
ASI
Pros
pect
ive
case
seri
esC
RR
esul
tsin
dica
ted
sign
ific
ant
redu
ctio
nin
AS
com
pare
dto
base
line
(ips
ativ
ez-
scor
edi
ffer
ence
�0.
86to
1.53
).A
llpa
rtic
ipan
tsre
mai
ned
abst
inen
tat
4-m
onth
follo
w-u
p.
Dis
tres
sto
lera
nce
Abr
ante
set
al.
(200
8)
N�
81ad
ult
smok
ers
com
plet
ing
beha
vior
alD
Tta
sks
prio
rto
thei
rsm
okin
gce
ssat
ion
inte
rven
tion
Bre
ath
hold
ing,
CO
2,
inha
latio
npe
rsis
tenc
e,PA
SAT
Pros
pect
ive
corr
elat
iona
lC
RC
ompa
red
toth
ose
high
inD
Ton
aco
mpo
site
inde
x,sm
oker
slo
win
DT
atba
selin
ew
ere
atgr
eate
rri
skof
laps
ing
onqu
itda
y(O
R�
9.22
).N
egat
ive-
affe
ct-r
elat
edri
skfo
rea
rly
laps
ew
asst
rong
est
amon
gth
ose
with
low
DT
vers
ushi
ghD
T(E
SU).
Ber
nste
inet
al.
(200
8)N
�43
mod
erat
esm
oker
s(1
1–20
cig/
day)
Bre
ath-
hold
ing
dura
tion
Lab
quas
i-ex
peri
men
tal
MD
Tw
aslo
wer
follo
win
g12
-hr
smok
ing
depr
ivat
ion
than
duri
ngsm
okin
g-as
-usu
al(d
�0.
76).
The
leve
lof
psyc
hiat
ric
sym
ptom
sw
assi
gnif
ican
tlyne
gativ
ely
corr
elat
edw
ithD
Tdu
ring
the
smok
ing
depr
ivat
ion
sess
ion
(r�
�.3
5)bu
tno
tth
esm
okin
g-as
-usu
alse
ssio
n(r
��
.18)
.B
rand
onet
al.
(200
3)N
�14
4tr
eatm
ent-
seek
ing
smok
ers
APT
,M
TPT
Pros
pect
ive
corr
elat
iona
lC
RD
Tw
asne
gativ
ely
rela
ted
toni
cotin
ede
pend
ence
atba
selin
e(r
��
.21
for
APT
and
r�
�.1
8fo
rM
TPT
).M
TPT
was
asi
gnif
ican
tpr
edic
tor
ofsu
stai
ned
abst
inen
ce(H
R�
0.99
8).
APT
was
not
rela
ted
tola
pse
(ESU
).R
.A
.B
row
net
al.
(200
2)N
�32
smok
ers
(10
cig/
day)
with
hist
ory
ofqu
itat
tem
pts
Bre
ath
hold
ing,
CO
2,
inha
latio
npe
rsis
tenc
e,PA
SAT
Cro
ss-s
ectio
nal
corr
elat
iona
lC
RR
elat
ive
tosm
oker
sw
ithat
leas
ton
esu
stai
ned
quit
atte
mpt
of3
mon
ths
orlo
nger
,sm
oker
sw
hoha
dfa
iled
tosu
stai
nan
ypr
evio
usqu
itat
tem
ptfo
rm
ore
than
24hr
exhi
bite
dlo
wer
DT
onth
ePA
SAT
(AO
R�
4.6)
,C
O2
pers
iste
nce
(AO
R�
12.2
),an
dbr
eath
-hol
ding
dura
tion
(d�
0.93
).R
.A
.B
row
net
al.
(200
9)N
�81
smok
ers,
mot
ivat
edfo
rce
ssat
ion,
prio
rto
unai
ded
quit
atte
mpt
s
PASA
T,
CO
2in
hala
tion
pers
iste
nce,
brea
th-
hold
ing
pers
iste
nce
Pros
pect
ive
corr
elat
iona
lC
RSm
oker
sw
ithhi
gh(v
s.lo
w)
DT
onC
O2
pers
iste
nce
and
brea
thho
ldin
gat
base
line
wer
eat
redu
ced
risk
ofla
psin
g(R
Rs
�.5
5an
d.9
8,re
spec
tivel
y).
DT
onth
ePA
SAT
did
not
pred
ict
laps
eri
sk(R
R�
1.0)
.
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
9EMOTIONAL VULNERABILITIES AND SMOKING
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
Bol
det
al.
(201
3)N
�35
DT
S,br
eath
-hol
ding
dura
tion
Lab
quas
i-ex
peri
men
tal
MO
na
smok
ing
choi
ceta
sk,
smok
ers
with
low
erD
Ton
the
DT
Sw
ere
mar
gina
llym
ore
likel
yto
smok
esm
okin
gup
totw
oci
gare
ttes
ina
15-m
inw
indo
wve
rsus
wai
ting
and
rece
ivin
gfo
urci
gare
ttes
afte
ra
dela
yof
45m
in(d
�0.
43,
p�
.08)
and
took
mor
epu
ffs
(R2
�.2
01).
DT
onth
eD
TS
was
not
asso
ciat
edw
ithot
her
outc
omes
(ESU
).D
Ton
brea
thho
ldin
gw
asno
tas
soci
ated
with
smok
ing
task
outc
omes
(ESU
).C
amer
onet
al.
(201
3)N
�40
smok
ers
part
icip
atin
gin
ace
ssat
ion
stud
yPA
SAT
,M
TPT
Pros
pect
ive
corr
elat
iona
lC
RSm
oker
sw
ithlo
wer
DT
onPA
SAT
rela
psed
mor
equ
ickl
ydu
ring
the
quit
atte
mpt
(r�
.43)
.D
Ton
the
MT
PTw
asno
tas
soci
ated
with
time
tore
laps
e(r
��
.05)
.D
ahne
etal
.(2
014)
N�
153
adul
tsPA
SAT
Cro
ss-s
ectio
nal
corr
elat
iona
lI
DT
mar
gina
llyin
tera
cted
with
race
topr
edic
tsm
okin
gst
atus
(p�
.052
),su
chth
atw
ithin
Afr
ican
Am
eric
ans
low
DT
was
sign
ific
antly
rela
ted
tosm
okin
gst
atus
(OR
�0.
23),
whe
reas
with
inW
hite
sth
ere
was
nore
latio
nbe
twee
nD
Tan
dsm
okin
gst
atus
(OR
�1.
07).
Haj
eket
al.
(198
7)N
�56
trea
tmen
t-se
ekin
gsm
oker
sB
reat
h-ho
ldin
gpe
rsis
tenc
ePr
ospe
ctiv
eco
rrel
atio
nal
CR
Low
erD
Tm
easu
red
befo
retr
eatm
ent
was
asso
ciat
edw
ithpo
orer
smok
ing
cess
atio
nou
tcom
e(r
�.4
4).
Ley
roet
al.
(201
1)N
�17
4no
ntre
atm
ent-
seek
ing
daily
smok
ers
DT
SC
ross
-sec
tiona
lco
rrel
atio
nal
P,M
Low
erD
Tw
asas
soci
ated
with
grea
ter
num
ber
ofye
ars
smok
ing
(r�
�.1
6),
mor
ese
vere
nico
tine
depe
nden
ce(r
��
.22)
,an
dgr
eate
rex
pect
anci
esof
smok
ing-
indu
ced
nega
tive
cons
eque
nces
(r�
�.2
3),
nega
tive
rein
forc
emen
t(r
��
.27)
,an
dap
petit
ere
duct
ion
(r�
�.3
0).
DT
was
not
sign
ific
antly
asso
ciat
edw
ithci
g/da
y(r
��
.13)
orex
pect
anci
esof
smok
ing-
indu
ced
posi
tive
rein
forc
emen
t(r
��
.13)
.M
acPh
erso
n,R
eyno
lds,
etal
.(2
010)
N�
230
earl
yad
oles
cent
s(a
ged
9–13
)B
IRD
Pros
pect
ive
corr
elat
iona
lI
Low
erD
Tw
asno
tas
soci
ated
with
aco
mpo
site
risk
beha
vior
inde
xin
clud
ing
smok
ing
atba
selin
eor
1-ye
arfo
llow
-up.
DT
inte
ract
edw
ithri
sk-t
akin
gpr
open
sity
topr
edic
thi
gh-r
isk
beha
vior
at1-
year
follo
w-u
p.Pe
rkin
set
al.
(201
0)N
�71
heal
thy
adul
tD
TS
Lab
quas
i-ex
peri
men
tal
MA
dlib
smok
ing
beha
vior
inth
ela
bw
asgr
eate
rin
thos
ew
ithlo
w(v
s.hi
gh)
DT
follo
win
gac
ute
abst
inen
cere
lativ
eto
othe
rco
nditi
ons
(�p2
�.0
52).
DT
did
not
dire
ctly
pred
ict
orm
oder
ate
the
effe
cts
ofne
gativ
eaf
fect
man
ipul
atio
nson
smok
ing
rew
ard
and
affe
ct(E
SU).
Qui
nnet
al.
(199
6)N
�52
heav
ysm
oker
s(
10ci
g/da
y)an
dN
�57
nons
mok
ers
MT
PT,
APT
Lab
quas
i-ex
peri
men
tal
ISm
oker
sco
mpa
red
tono
nsm
oker
sde
mon
stra
ted
low
erD
Ton
the
APT
(d�
0.68
)an
dM
TPT
(d�
0.67
).R
agla
n(2
013)
38cu
rren
tsm
oker
s(
10ci
g/da
y),
21fo
rmer
smok
ers
(10
cig/
day,
quit
for
1
year
),an
d27
neve
rsm
oker
s
MT
PT,
FDS
Cro
ss-s
ectio
nal
corr
elat
iona
lI,
P,M
,CR
Cur
rent
and
form
ersm
oker
sex
hibi
ted
low
erD
Ton
the
MT
PTth
anne
ver
smok
ers
(ds
�0.
76an
d0.
71,
resp
ectiv
ely)
but
did
not
diff
erfr
omea
chot
her
(d�
�0.
08).
Gro
ups
did
not
sign
ific
antly
diff
erin
DT
onth
eFD
S(d
s�
0.27
).A
mon
gcu
rren
tsm
oker
slo
wer
DT
onFD
Sw
assi
gnif
ican
tlyco
rrel
ated
with
urge
tosm
oke
(r�
.37)
and
mar
gina
llyco
rrel
ated
with
seve
rity
ofni
cotin
ede
pend
ence
(r�
.30)
.D
Ton
the
MT
PTw
asno
tas
soci
ated
with
urge
orni
cotin
ede
pend
ence
(rs
��
.25)
.St
einb
erg
etal
.(2
012)
Smok
ers
with
psyc
hotic
diso
rder
(N�
71)
and
nonp
sych
iatr
icsm
oker
s(N
�78
)in
smok
ing
cess
atio
ntr
eatm
ent
MT
PT,
brea
th-h
oldi
ngpe
rsis
tenc
ePr
ospe
ctiv
eco
rrel
atio
nal
CR
Low
erD
Ton
the
MT
PTpr
edic
ted
grea
tri
skof
rela
pse
(ESU
).D
Ton
the
brea
th-h
oldi
ngpe
rsis
tenc
ete
stw
asno
tas
soci
ated
with
rela
pse
likel
ihoo
d(E
SU).
Tru
jillo
etal
.(2
012)
N�
212
nont
reat
men
t-se
ekin
gsm
oker
s(5
�ci
g/da
y)D
TS
Cro
ss-s
ectio
nal
corr
elat
iona
lP,
MD
Tw
asno
tsi
gnif
ican
tlyas
soci
ated
with
seve
rity
ofni
cotin
ede
pend
ence
onth
eFa
gers
tröm
Tes
tof
Nic
otin
eD
epen
denc
e(E
SU).
Low
erD
Tw
assi
gnif
ican
tlyas
soci
ated
with
high
erse
veri
tyof
depe
nden
ceon
the
Nic
otin
eD
epen
denc
eSy
ndro
me
Scal
e(�
�.1
9)an
dW
isco
nsin
Inve
ntor
yof
Smok
ing
Dep
ende
nce
Mot
ives
tota
lsc
ale
(��
.32)
.
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
10 LEVENTHAL AND ZVOLENSKY
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
Low
erD
Tw
asas
soci
ated
with
high
ersm
okin
gfo
rne
gativ
ere
info
rcem
ent
purp
oses
(��
.33)
and
urge
tosm
oke
toal
levi
ate
nega
tive
affe
ct(�
�.3
4).
Vol
zet
al.
(201
4)56
vete
rans
and
com
mun
itym
embe
rspa
rtic
ipat
ing
ina
MT
PTPr
ospe
ctiv
eco
rrel
atio
nal
M,C
RB
asel
ine
DT
did
not
have
am
ain
effe
cton
pred
ictin
gcr
avin
gfo
llow
ing
the
quit
atte
mpt
(ESU
).sm
okin
gce
ssat
ion
tria
lB
asel
ine
DT
mod
erat
edth
ere
latio
nbe
twee
nda
ilyha
ssle
san
dcr
avin
gdu
ring
the
quit
atte
mpt
(exp
lain
ed4%
and
2%of
betw
een-
pers
onan
dw
ithin
-per
son
vari
ance
,re
spec
tivel
y),
such
that
low
erD
Tw
asas
soci
ated
with
stro
nger
rela
tions
betw
een
hass
les
and
crav
ing.
Con
com
itant
rela
tion
ofm
ultip
leem
otio
nal
vuln
erab
ilitie
sto
smok
ing
Kra
emer
etal
.(2
013)
N�
126
daily
nont
reat
men
t-se
ekin
gsm
oker
sA
SI-3
DT
SC
ross
-sec
tiona
lco
rrel
atio
nal
P,C
RA
Sw
asno
tsi
gnif
ican
tlyas
soci
ated
with
cig/
day
(r�
.04)
ornu
mbe
rof
prio
rqu
itat
tem
pts
(r�
.13)
.
AS
was
sign
ific
antly
asso
ciat
edw
ithgr
eate
rpe
rcei
ved
barr
iers
for
cess
atio
nre
late
dto
addi
ctio
n(e
.g.,
“Qui
tting
will
mak
em
eth
ink
ofci
gare
ttes
all
the
time”
;r
�.2
0),
exte
rnal
(e.g
.,“N
oen
cour
agem
ent
from
wor
kfo
rno
tsm
okin
g”;
r�
.25)
,an
din
tern
al(e
.g.,
“Qui
tting
will
mak
em
efe
elle
ssin
cont
rol
ofm
ym
oods
”;r
�.2
5)so
urce
s.D
Tw
asno
tsi
gnif
ican
tlyas
soci
ated
with
cig/
day
(r�
.12)
,nu
mbe
rof
prio
rqu
itat
tem
pts
(r�
�.0
8),
orad
dict
ion-
rela
ted
perc
eive
dba
rrie
rsto
cess
atio
n(r
��
.12)
.L
ower
DT
was
sign
ific
antly
asso
ciat
edw
ithgr
eate
rpe
rcei
ved
barr
iers
for
cess
atio
nre
late
dto
exte
rnal
(r�
�.3
0)an
din
tern
al(r
��
.42)
sour
ces.
Aft
erco
ntro
lling
for
AS,
low
erD
Tw
assi
gnif
ican
tlyas
soci
ated
with
grea
ter
perc
eive
din
tern
alba
rrie
rsto
cess
atio
n(�
��
.31)
but
not
sign
ific
antly
with
addi
ctio
n-re
late
d(�
��
.05)
orex
tern
alba
rrie
rsto
cess
atio
n(�
��
.19)
orpr
ior
faile
dqu
itat
tem
pts
(��
.06)
.L
angd
onet
al.
(201
3)N
�65
smok
ers
enro
lled
ina
cess
atio
nst
udy
ASI
Pros
pect
ive
corr
elat
iona
lC
RA
Sw
assi
gnif
ican
tly(p
ositi
vely
)re
late
dto
all
ofth
ety
pes
ofin
divi
dual
with
draw
alsy
mpt
oms
onqu
itda
yex
cept
crav
ing
and
appe
tite
inun
ivar
iate
anal
yses
(rs
�.0
8to
28).
MA
SQ-A
nhA
nhw
assi
gnif
ican
tly(p
ositi
vely
)re
late
dto
all
ofth
ein
divi
dual
with
draw
alsy
mpt
oms
exce
ptcr
avin
gin
univ
aria
tean
alys
es(r
s�
.17
to30
).A
fter
cont
rolli
ngfo
rA
San
dot
her
cofa
ctor
s,A
nhpr
edic
ted
quit
day
depr
essi
on,
anxi
ety,
and
inso
mni
abu
tno
tot
her
with
draw
alsy
mpt
oms
(ESU
).A
fter
cont
rolli
ngfo
rA
nhan
dot
her
cofa
ctor
s,A
Sw
asno
tsi
gnif
ican
tlyas
soci
ated
with
quit
day
with
draw
alsy
mpt
oms
(ESU
).A
fter
cont
rolli
ngfo
rA
San
dot
her
cofa
ctor
s,A
nhsi
gnif
ican
tlypr
edic
ted
fast
erde
clin
esin
inso
mni
aov
ertim
edu
ring
the
firs
t2
wee
ksof
quit
atte
mpt
but
was
not
rela
ted
toch
ange
sin
othe
rw
ithdr
awal
sym
ptom
s(E
SU).
Aft
erco
ntro
lling
for
Anh
and
othe
rco
fact
ors,
AS
sign
ific
antly
pred
icte
dsl
ower
decl
ines
inal
lw
ithdr
awal
sym
ptom
sex
cept
conc
entr
atio
npr
oble
ms
and
crav
ing
(ESU
).A
fter
cont
rolli
ngfo
rco
fact
ors,
the
inte
ract
ion
ofA
San
dA
nhpr
edic
ted
chan
ges
infr
ustr
atio
nan
dre
stle
ssne
ssov
ertim
ebu
tno
tot
her
with
draw
alsy
mpt
oms
(ESU
),su
chth
atin
divi
dual
sw
ithel
evat
edA
San
dA
nhha
ddi
spro
port
iona
tely
high
erra
tes
ofes
cala
tion
offr
ustr
atio
n/re
stle
ssne
ssdu
ring
cess
atio
n.Z
vole
nsky
,St
ewar
t,et
al.
(200
9)N
�12
3da
ilyC
anad
ian
smok
ers
enro
lled
ina
cess
atio
ntr
eatm
ent
stud
y
MA
SQ-A
DPr
ospe
ctiv
eco
rrel
atio
nal
P,M
,CR
Anh
was
asso
ciat
edw
ithhi
gher
preq
uit
nico
tine
depe
nden
cese
veri
ty(r
�.2
1)an
dpr
equi
tni
cotin
ew
ithdr
awal
sym
ptom
seve
rity
(r�
.28)
.
(tab
leco
ntin
ues)
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
11EMOTIONAL VULNERABILITIES AND SMOKING
Tab
le1
(con
tinu
ed)
Stud
ySa
mpl
eE
mot
iona
lvu
lner
abili
tym
easu
reD
esig
nSm
okin
gtr
ajec
tory
rele
vanc
eM
ain
find
ing
ASI
Aft
erco
ntro
lling
for
AS,
base
line
Anh
was
asso
ciat
edw
ithod
dsof
laps
ing
onD
ay1
(OR
�1.
04)
but
not
Day
7(H
R�
1.02
)or
14(H
R�
1.02
)of
the
quit
atte
mpt
.A
fter
cont
rolli
ngfo
rA
S,A
nhw
asas
soci
ated
with
odds
ofre
laps
ing
onD
ays
1(O
R�
1.04
),7
(HR
�1.
02),
and
14(H
R�
1.02
)of
the
quit
atte
mpt
.A
Sw
asno
tsi
gnif
ican
tlyas
soci
ated
with
preq
uit
nico
tine
depe
nden
cese
veri
ty(r
�.0
4).
AS
was
sign
ific
antly
asso
ciat
edpr
equi
tni
cotin
ew
ithdr
awal
sym
ptom
seve
rity
(r�
.25)
.A
fter
cont
rolli
ngfo
rA
nh,
AS
was
asso
ciat
edw
ithod
dsof
laps
ing
onD
ays
1(O
R�
1.04
),7
(HR
�1.
02),
and
14(H
R�
1.02
)of
the
quit
atte
mpt
.A
fter
cont
rolli
ngfo
rA
nh,
AS
was
not
sign
ific
antly
asso
ciat
edod
dsof
rela
psin
gon
Day
1(O
R�
1.04
),7
(HR
�1.
01),
or14
(HR
�1.
00)
ofth
equ
itat
tem
pt.
Not
e.C
ig/d
ay�
ciga
rette
ssm
oked
per
day;
Anh
�an
hedo
nia;
AS
�an
xiet
yse
nsiti
vity
;D
T�
dist
ress
tole
ranc
e;C
O2
�ca
rbon
diox
ide.
Em
otio
nal
vuln
erab
ility
mea
sure
s:A
PT�
Ana
gram
Pers
iste
nce
Tas
k(E
isen
berg
er&
Leo
nard
,19
80);
ASI
�A
nxie
tySe
nsiti
vity
Inde
x(R
eiss
etal
.,19
86);
ASI
-3�
Anx
iety
Sens
itivi
tyIn
dex–
III
(Tay
lor
etal
.,20
07);
BD
I-A
nh�
Bec
kD
epre
ssio
nIn
vent
ory–
II–A
nhed
onia
subs
cale
(Bec
k,19
96);
BIR
D�
Beh
avio
ral
Indi
cato
rof
Res
ilien
cyto
Dis
tres
s(L
ejue
zet
al.,
2006
);C
ESD
-Anh
�C
ente
rfo
rE
pide
mio
logi
cSt
udie
sD
epre
ssio
nSc
ale–
Anh
edon
iaSc
ale
(Rad
loff
,197
7);C
IDI
�W
orld
Men
talH
ealth
Surv
eyIn
itiat
ive
vers
ion
ofth
eC
ompo
site
Inte
rnat
iona
lDia
gnos
ticIn
terv
iew
(Kes
sler
&U
stun
,200
4);D
TS
�D
istr
ess
Tol
eran
ceSc
ale
(Sim
ons
&G
aher
,20
05);
FCPS
�Fa
wce
tt–C
lark
Plea
sure
Scal
e(F
awce
ttet
al.,
1983
);FD
S�
Frus
trat
ion
Dis
com
fort
Scal
e(H
arri
ngto
n,20
05);
MA
SQ-A
D�
Moo
dan
dA
nxie
tySy
mpt
omQ
uest
ionn
aire
–Anh
edon
icD
epre
ssio
nSc
ale
(Wat
son
etal
.,19
95);
MT
PT�
Mir
ror
Tra
cing
Pers
iste
nce
Tas
k(B
rand
onet
al.,
2003
);PA
SAT
�Pa
ced
Aud
itory
Seri
alA
dditi
onT
ask
(Lej
uez
etal
.,20
03);
SAD
S�
Sche
dule
for
Aff
ectiv
eD
isor
ders
and
Schi
zoph
reni
a(E
ndic
ott&
Spitz
er,1
978)
;SA
EQ
�Sm
okin
gA
bstin
ence
Exp
ecta
ncie
sQ
uest
ionn
aire
(Abr
ams,
Zvo
lens
ky,e
tal.,
2011
);SC
ID�
Stru
ctur
edC
linic
alIn
terv
iew
for
DSM
–IV
(Fir
stet
al.,
1997
);SH
APS
�Sn
aith
–Ham
ilton
Plea
sure
Scal
e(S
naith
etal
.,19
95);
TPI
-R�
Tri
part
itePl
easu
reIn
vent
ory–
Res
pons
iven
ess
subs
cale
(Lev
enth
al,M
unaf
ò,et
al.,
2012
).R
elev
ance
tost
age
insm
okin
gtr
ajec
tory
:I�
initi
atio
n;P
�pr
ogre
ssio
n;M
�m
aint
enan
ce;C
R�
cess
atio
nan
dre
laps
e.E
ffec
tsiz
em
etri
cs:d
�C
ohen
’sd;
OR
�od
dsra
tio;
AO
R�
adju
sted
odds
ratio
;H
R�
haza
rds
ratio
;R
R�
rela
tive
risk
;r
�Pe
arso
n’s
corr
elat
ion
coef
fici
ent;
��
stan
dard
ized
regr
essi
onw
eigh
t;E
SU�
effe
ctsi
zeun
avai
labl
e;D
SM–I
V�
Dia
gnos
tic
and
Stat
isti
cal
Man
ual
ofM
enta
lD
isor
ders
(4th
ed.)
.a
Plea
sure
rece
ived
from
(a)
cont
act
with
othe
rs,
(b)
perf
orm
ance
(wor
k,sc
hool
,or
chor
es),
and
(c)
recr
eatio
n.b
Res
pons
eto
“Hav
eyo
uev
erha
da
peri
odla
stin
gse
vera
lda
ysor
long
erw
hen
you
lost
inte
rest
inm
ostt
hing
syo
uus
ually
enjo
ylik
ew
ork,
hobb
ies,
and
pers
onal
rela
tions
hips
?”(y
es/n
o).
cM
ean
ofT
empo
ralE
xper
ienc
eof
Plea
sure
Scal
e(a
ntic
ipat
ory
and
cons
umm
ator
yA
nh;G
ard
etal
.,20
06)
and
the
Subj
ectiv
eH
appi
ness
Scal
e(L
yubo
mir
sky
&L
eppe
r,19
99).
dR
espo
nse
to“H
ave
you
ever
lost
inte
rest
orpl
easu
rein
thin
gsyo
uty
pica
llyen
joy
mos
tof
the
day
near
lyev
eryd
ayfo
r2
wee
ksor
mor
e?”
eR
espo
nse
to“D
urin
gth
epa
stw
eek,
Iw
asa
lot
less
inte
rest
edin
thin
gs.”
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
12 LEVENTHAL AND ZVOLENSKY
We conceptualize Anh as a multilevel construct—a sharedhigher order dimension indicative of diminished appetitive func-tioning that is composed of related but distinct lower order dimen-sions of (a) global Anh (reduced happiness and enjoyment derivedin one’s life; Carleton et al., 2013), (b) consummatory Anh (inca-pacity to experience pleasure in response to rewarding stimuli;Gard, Gard, Kring, & John, 2006), and (c) anticipatory Anh(diminished subjective desire and anticipation of pleasant events;Gard et al., 2006). Anh is conceptually and empirically distinctfrom other emotional constructs, such as extraversion, positiveemotionality, alexithymia, affective flattening (i.e., dampened ex-perience of both positive and negative emotions), overall level ofdepressive symptoms, and negative affect (Fiorito & Simons,1994; Franken & Muris, 2006; Leventhal et al., 2006).
Although those with higher levels of Anh may respond lessstrongly to typical rewards, they are not entirely incapable offeeling pleasure and do not necessarily lack a desire to experiencepleasure (Gard et al., 2006). Rather, anhedonic individuals requirea higher threshold of reward stimulation and more potent reinforc-ers to experience pleasure (Schlaepfer et al., 2008; Wise, 2008).Low to moderate potency-rewarding stimuli that may be pleasantor interesting to most individuals (e.g., viewing a picturesquescene from a high vantage point) may have limited emotional andmotivational effects in anhedonic individuals, whereas high po-tency rewards may still elicit emotional effects (Franken, Zijlstra,& Muris, 2006).
Anh is considered to be a key risk factor for depression onsetand chronicity by causing a cyclic cascade of diminished levels ofpositive reinforcement from and engagement in rewarding antide-pressant behaviors (Lewinsohn, 1974; Loas, 1996). Specifically,repeated experience of diminished pleasure in response to activi-ties that are enjoyable for most other individuals is likely topromote cognitive expectations that many activities are unenjoy-able, which in turn can contribute to anticipatory Anh (i.e., lack ofinterest or desire in pleasurable activities). Resulting elevations ofanticipatory Anh may diminish reward-seeking behavior and sub-sequent exposure to pleasure-eliciting stimuli. Reduced exposureto and pleasure from reward may promote broad deficits in hap-piness (i.e., global Anh) and potentially feed back into furtheranhedonic cognitions and experiences. These processes, eitheralone or in conjunction with other vulnerability factors, may es-calate into a pattern of behavioral withdrawal, diminished motiva-tion, fatigue, and other depression features (Loas, 1996), whichtend to present in melancholic subtypes of depression (Leventhal& Rehm, 2005). Although it is most frequently linked to depres-sion, Anh is elevated in many psychopathologies involving dys-regulated appetitive functioning, including psychosis (Cohen, Na-jolia, Brown, & Minor, 2011), borderline personality disorder(Bandelow, Schmahl, Falkai, & Wedekind, 2010; Marissen, Ar-nold, & Franken, 2012), social anxiety disorder (Watson &Naragon-Gainey, 2010), attention-deficit/hyperactivity disorder(Meinzer, Pettit, Leventhal, & Hill, 2012), PTSD (Kashdan, Elhai,& Frueh, 2006), and obsessive-compulsive disorder (Abramovitch,Pizzagalli, Reuman, & Wilhelm, 2014). Hence, Anh reflects atransdiagnostic process.
Measurement. Distinct facets of the Anh construct have beenmeasured with different methodologies. Global Anh has ben mea-sured with questionnaires assessing reduced happiness and lifeenjoyment (e.g., “I enjoyed life”; Center for Epidemiologic Studies
Depression Scale–Anh subscale; Radloff, 1991; Shafer, 2006). Theconsummatory Anh construct is often assessed in questionnaireswhereby individuals rate imagined hedonic responses to variousexperiences that are commonly pleasurable that span hobbies,interests, food, sensory, and social activities (e.g., “Would you findpleasure in a bright sunny day?” Snaith–Hamilton Pleasure Scale;Snaith, Hamilton, Morley, & Humayan, 1995). Similarly, theanticipatory Anh construct has been measured by questionnairesasking participants to rate interest, desire, and anticipation of suchactivities (e.g., “When I hear about a new movie starring myfavorite actor, I can’t wait to see it”; Temporal Experience ofPleasure Scale; Gard et al. 2006). Measures of these distinct facetsof Anh evidence moderate correlations with one another, suggest-ing that they are nonredundant but related constructs; yet, thesemeasures also load onto a common higher order latent dimension(Leventhal, Trujillo, et al., 2014). Each of these types of measuresexhibits strong internal consistency, convergent validity, and dis-criminant validity from measure of global depression constructs(Franken, Rassin, & Muris, 2007; Gard et al., 2006; Leventhal etal., 2006, 2008).
Anh and smoking.Theoretical applicability of Anh to smoking. Because anhe-
donic individuals may recognize that they experience significantpleasure only in response to high-potency rewards (Franken et al.,2006), they may expect particularly strong positive effects frompharmacological rewards like smoking (Stone & Leventhal, 2014).Indeed, data suggest a correlation between Anh and sensationseeking (i.e., trait indicative of needing novel situations or stimu-lation; Carton, Houezec, Lagrue, & Jouvent, 2000) and the ten-dency to seek out high-intensity reinforcers (e.g., skydiving; Fran-ken et al., 2006). Hence, anhedonic individuals may be more proneto seek out pharmacological and other high-potency reinforcers inorder to experience a pleasure response that may otherwise bedeficient. Anhedonic individuals may be more likely to progressfrom experimentation to regular smoking because of potentialpsychopharmacological diatheses between Anh and nicotine (Lev-enthal, Munafò, et al., 2012). Nicotine stimulates mesolimbicdopaminergic release, which amplifies the reinforcing andpleasure-inducing properties of other rewards (Dawkins, Acaster,& Powell, 2007; Paterson, 2009). At the same time, researchimplicates deficient activity within the brain’s mesocorticolimbicdopamine system as potential underpinning of Anh (Tremblay,Naranjo, Cardenas, Herrmann, & Busto, 2002; Tremblay et al.,2005; Wise, 1982). We suspect that nicotine may temporarilycounteract deficient mesolimbic activity and hedonic response torewards in anhedonic individuals, which could sensitize anhedonicexperimenters to the reward-enhancing effects of smoking (Cook,Spring, & McChargue, 2007), enhance the reinforcing propertiesof smoking, and accelerate smoking progression.
Chronic nicotine exposure produces neuroadaptations to themesolimbic dopamine system, such that nicotine needs to bemaintained in order to preserve a homeostatic level of mesolimbic(and hedonic) tone (Watkins, Koob, & Markou, 2000). Whenchronic nicotine use is discontinued, neuroadaptations to the me-solimbic dopamine system are expressed and the system is in ahypoactive state (Watkins et al., 2000), which may underlieabstinence-induced manifestations of deficient acute positive af-fect (Leventhal, Waters, Moolchan, Heishman, & Pickworth,2010), diminished incentive salience of reward-associated stimuli
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
lied
publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
13EMOTIONAL VULNERABILITIES AND SMOKING
(Powell, Pickering, Dawkins, West, & Powell, 2004), and acuteelevations of state Anh (Dawkins et al., 2007) that have beenillustrated in general samples of smokers. Anh may amplify thepsychobiological effects of smoking abstinence via promoting theexpression and exacerbation of preexisting appetitive deficits dueto interactions between Anh-related neuropathology and the neu-robiological sequelae of nicotine withdrawal (Watkins et al.,2000). The expression of such deficits could theoretically producea strong motivation to return to smoking in order to counteractthese deficits. Overall, these processes could underlie heightenedpropensity to resume smoking either following brief periods ofabstinence (e.g., overnight) or during an intentional cessationattempt in anhedonic individuals, which could ultimately explainAnh’s relation with maintenance of regular smoking.
Empirical data on the relation of Anh to smoking initiation.Several cross-sectional studies have examined the association be-tween Anh and smoking status (i.e., smoker vs. nonsmoker) inadults. Pomerleau, Zucker, and Stewart (2003) showed that globalAnh was higher in current versus never smokers in a sample ofwomen. Similarly, global Anh was higher among daily smokersthan never smokers in a sample of U.S. young adults (McLeish,Zvolensky, Yartz, & Leyro, 2008). By contrast, Zvolensky, Kotov,Bonn-Miller, Schmidt, and Antipova (2008) did not find a relationbetween global Anh and smoking status in a representativepopulation-based sample of Moscow, Russia, residents, whichcould suggest that country of origin or age may alter the strengthof the Anh-smoking status relation.
Anh has also been studied as a correlate of early smokingexperimentation in adolescents. In a cross-sectional study of 14-year-olds who had never had a single puff of a cigarette, those withhigher Anh reported greater curiosity about trying smoking but didnot differ in willingness or intention to smoke after controlling foroverall depression symptoms and demographics (Stone & Lev-enthal, 2014). The disparate findings across susceptibility indicescould reflect differential sensitivity of measures of curiosity(Pierce, Distefan, Kaplan, & Gilpin, 2005). This study also foundthat teens with higher Anh reported greater expectancies thatsmoking caused pleasure, despite never smoking a cigarette, sug-gesting that anticipated effects of smoking in smoking-naive an-hedonic youths may confer initiation risk. It is possible that ob-servation of others or extrapolation from direct experience of otherhigh-potency reinforcers (e.g., drugs of abuse, high sugar foods,extreme sports) may cause anhedonic teens to develop expectan-cies for smoking-induced pleasure, even prior to their first smok-ing experience.
Research on teen initiation has found that Anh was higheramong Chinese adolescents who reported ever “trying a cigarette,even a few puffs” (Leventhal, Ray, et al., 2012). A separate studyof U.S. adolescents found that consummatory Anh was cross-sectionally associated with smoking status and frequency at age 15after controlling for depressive symptoms and other cofactors(Audrain-McGovern et al., 2012). However, Anh did not predictlikelihood of initiating smoking over the 1.5-year follow-up periodin that study, indicating that Anh’s relation with smoking experi-mentation may have occurred prior to age 15.
Empirical data on the relation of Anh to smoking progressionand regular smoking. In the only prospective study of smokingprogression, Audrain-McGovern et al. (2012) examined escalationpatterns and found that age-15 Anh prospectively predicted esca-
lation of smoking frequency over the subsequent 1.5 years. Thisstudy controlled for depressive symptoms and other cofactors,suggesting that Anh is unlikely to be an epiphenomenon ofdepression-related processes that confer smoking progression.Rather these findings suggest a unique source of affective risk thatperhaps may emanate from Anh.
Smoking severity level within the population of individuals whohave already established a pattern of regular smoking, which maybe an indirect indicator of progression, has also been studied as across-sectional correlate of Anh. Several studies have shown thatAnh is associated with greater number of cigarettes smoked perday (cig/day) among daily smokers across a range of populations(e.g., treatment seekers, smokers not interested in quitting, youngadults), suggesting that Anh may confer risk for more severepatterns of smoking (Cook, Spring, McChargue, & Doran, 2010;Gregor, Zvolensky, Bernstein, Marshall, & Yartz, 2007; Lev-enthal, Trujillo, et al., 2014; Leventhal, Waters, Kahler, Ray, &Sussman, 2009; McLeish, Zvolensky, Bonn-Miller, & Bernstein,2006). Furthermore, Anh is associated with measures of nicotinedependence in some investigations (Leventhal, Kahler, et al.,2009; Leventhal, Piper, Japuntich, Baker, & Cook, 2014; McCha-rgue & Cook, 2007; Mickens et al., 2011; Zvolensky, Stewart, etal., 2009). Other studies have not found evidence that Anh isrelated to cig/day (Cook et al., 2007; K. A. Johnson, Stewart,Zvolensky, & Steeves, 2009; Leventhal et al., 2008; Leventhal,Waters, et al., 2009; Mickens et al., 2011; Zvolensky, Johnson,Leyro, Hogan, & Tursi, 2009) and nicotine dependence (Cook,Piper, Kim, Schlam, & Baker, 2012; Cook et al., 2007; Leventhalet al., 2008; Leventhal, Trujillo, et al., 2014; Leventhal, Waters, etal., 2009) in daily smokers. Hence, evidence is mixed on this topic.
Results in studies of daily smokers are apt to be at least partiallyconditional on study entry criteria (e.g., some studies have 10�cig/day or regular smoking for at least 2 years as inclusion criteria,which could restrict the range at the lower end of the severityspectrum). Further, while cross-sectional analyses in samples ofdaily smokers are relevant to understanding progression fromregular daily smoking to heavier patterns of daily smoking, they donot shed light on progression earlier in the smoking trajectory, norcan they rule out alternative causal relations (e.g., smoking influ-ences Anh). Other methodological factors (e.g., variation in sam-ple size and statistical power across studies) may also influence thepattern of results, given data suggesting small relations betweenAnh and smoking severity that are statistically significant in largersamples (e.g., r � .06 for nicotine dependence; N � 1,469;Leventhal, Piper, et al., 2014) but not smaller samples (e.g., r �.09; N � 212; Leventhal, Waters, et al., 2009). Given such meth-odological considerations, the overall pattern of data, and theprospective evidence illustrating Anh as a risk factor for smokingescalation in youths (Audrain-McGovern et al., 2012), it is likelythat Anh plays some role in smoking progression.
Empirical data on the relation of and mechanisms linking Anhto the maintenance of smoking. Literature on whether Anh iscross-sectionally associated with a longer history of smoking ismixed (Cook et al., 2007; Gregor et al., 2007; Leventhal, Waters,et al., 2009; Zvolensky, Johnson, et al., 2009), although suchstudies are difficult to interpret because of potential confoundingbetween age of participant and years smoking. Regarding themechanisms maintaining smoking in anhedonic individuals, themotivation to smoke for positive affect and reward enhancement
Thi
sdo
cum
ent
isco
pyri
ghte
dby
the
Am
eric
anPs
ycho
logi
cal
Ass
ocia
tion
oron
eof
itsal
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publ
ishe
rs.
Thi
sar
ticle
isin
tend
edso
lely
for
the
pers
onal
use
ofth
ein
divi
dual
user
and
isno
tto
bedi
ssem
inat
edbr
oadl
y.
14 LEVENTHAL AND ZVOLENSKY
appears to be an important factor for anhedonic individuals, whomay otherwise derive little pleasure or reinforcement from re-wards. Cook et al. (2007) found that smokers who scored high ona measure of consummatory Anh (i.e., anhedonic smokers) showeda positive affect boost during a positive mood induction when theyconcurrently smoked a cigarette that contained nicotine. However,when anhedonic smokers smoked a placebo cigarette during themood induction, their affect did not increase. By contrast, low-Anhsmokers showed similar positive affect boosts regardless of thenicotine content of the cigarette smoked during the mood induc-tion. Hence, nicotine may help anhedonic smokers affectivelyrespond to rewards, which otherwise may have little affectiveimpact.
On the other hand, acute smoking abstinence may induce theexpression of deficits in reward and positive affect among indi-viduals with high Anh, which may, in turn, motivate the resump-tion of smoking to offset such deficits. Smokers with higherconsummatory and global Anh are more sensitive to the effects ofovernight tobacco abstinence (vs. sated states) on declines in statepositive affect and reductions in automatic cognitive processing ofreward-related stimuli (Cook, Spring, McChargue, & Hedeker,2004; Leventhal, Ameringer, Osborn, Zvolensky, & Langdon,2013; Leventhal, Munafò, et al., 2012), even after controlling fordepression, negative affect, and/or nicotine dependence. Addi-tional results indicate that measures of consummatory Anh predictgreater urge to smoke, in some cases over and above negativeaffect and nicotine dependence (Cook et al., 2004; Leventhal,Waters, et al., 2009), although measures of global Anh appear tobe less robustly related to urge (AhnAllen et al., 2012; Leventhal,Ameringer, et al., 2013). Importantly, evidence suggests that theseresults may be specific to an appetitive (but not an aversive) driveto smoke. Cook et al. (2004) showed that the relation between Anhand abstinence-induced increases in smoking urge was mediatedby greater abstinence-induced reductions in state positive affect.The same mediational pathway was not found for acute negativeaffect. Similarly, Leventhal, Waters, et al. (2009) found that Anhpredicted greater sensitivity to the amplifying effect of abstinenceon the appetitive aspect of smoking urge (e.g., “A cigarette wouldtaste good”), but did not moderate abstinence effects on aversiveurge (e.g., “A cigarette would make me less depressed”).
Additional lines of evidence implicate the importance of adisparity between the lack of positive reinforcement from non-smoking rewards and the reinforcement derived from smoking asa maintaining mechanism in anhedonic smokers. Two cross-sectional studies of daily smokers have explored relations betweenAnh and 13 qualitatively unique types of self-reported smokingdependence motives (Leventhal, Waters, et al., 2009; Mickens etal., 2011). These studies found that global and consummatoryforms of Anh were positively associated with the behavioralchoice melioration subscale of the Wisconsin Inventory of Smok-ing Dependence Motives (Piper et al., 2004). This scale taps thetendency to place higher priority on smoking as a reinforcer incomparison to other reinforcers (e.g., “Very few things give mepleasure each day like cigarettes,” “Smoking is the fastest way toreward myself”). Leventhal, Trujillo, et al. (2014) explored thisnotion further in a laboratory study of daily smokers who com-pleted an objective behavioral economics choice procedure. Theyshowed that Anh predicted choices indicative of a biased relativereward value of smoking versus an alternative reinforcer (i.e.,
money), such that anhedonic participants were less willing to delaysmoking for money and were more likely to pay for cigaretteswhen given the opportunity to smoke. These relations were medi-ated by high negative affect and low positive affect prior tocompleting the task and persisted after controlling for depressivesymptoms, nicotine dependence, and gender.
In addition to studies examining Anh as a trait-like construct,changes in acute Anh as a result of nicotine exposure have beenreported. Laboratory studies of regular smokers show that exper-imentally manipulated acute tobacco abstinence increases states ofconsummatory Anh, diminishes ability to modulate behavior as afunction of reward (i.e., reward learning), and attenuates the at-tentional salience of reward-associated stimuli (Dawkins et al.,2007; Powell, Dawkins, & Davis, 2002; Powell et al., 2004;Powell, Tait, & Lessiter, 2002). Additional data indicate that acutenicotine administration alleviates Anh on some of these outcomes(Barr, Pizzagalli, Culhane, Goff, & Evins, 2008; Dawkins, Powell,West, Powell, & Pickering, 2006). Effects of nicotine administra-tion and deprivation on state Anh are thought to be mediated byenhancement of and neuroadaptations to mesolimbic pathway,respectively (Caggiula et al., 2009; D’Souza & Markou, 2010).Thus, Anh appears to be a consequence of regular smoking.
It is plausible that there may be a bidirectional etiologicalpositive feedback loop whereby Anh increases vulnerability toregular smoking and chronic smoking increases Anh, which, inturn, increases smoking and so on. A clinical study showed thatconsummatory Anh increased from pre- to postquit and the degreeof increase predicted relapse following cessation treatment (Cooket al., 2012). Hence, those with higher trait Anh prior to smokingmay be at risk for smoking initiation and maintenance, as well asthe exacerbation of their Anh as a result of nicotine-inducedneuroadaptations, which may further motivate smoking.
Empirical data on the relation of Anh to smoking cessationand relapse. Studies have found that Anh increases risk of smok-ing cessation failure. Leventhal, Ramsey, et al. (2008) assessed thepredictive influence of depression symptom constructs on cessa-tion outcomes in smokers enrolled in a clinical trial involvingsmoking cessation counseling and nicotine replacement therapy(NRT). Four dimensions were measured prior to quit date: globalAnh, negative affect (i.e., sadness, crying), somatic features (i.e.,sleep, appetite, psychomotor, and concentration problems), andinterpersonal problems (i.e., social difficulties). When each dimen-sion was examined in isolation, Anh, negative affect, and somaticfeatures all predicted lower cessation success, with Anh having thestrongest effect. When the dimensions were considered concomi-tantly, only Anh significantly predicted poorer outcomes incre-mentally to the other dimensions. Both negative affect and somaticfeatures no longer significantly predicted outcomes when control-ling for the influence of Anh. These relations remained aftercontrolling for gender, nicotine dependence, cig/day, and historyof major depression.
Evidence that Anh incrementally increases risk of cessationfailure over and above other factors has been replicated in threestudies. Among smokers receiving NRT and counseling, Zvolen-sky, Stewart, et al. (2009) showed that prequit levels of global Anhsignificantly predicted increased risk of lapse (i.e., any smoking)within 24 hr of quitting and increased likelihood of relapse at threesuccessive postquit assessments over and above nicotine depen-dence and anxiety symptoms. Among smokers with a history of
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15EMOTIONAL VULNERABILITIES AND SMOKING
major depression who attended a 1-day smoking cessation coun-seling workshop, Cook et al. (2010) found that greater precessationconsummatory Anh was associated with shorter time to relapseafter covarying for depressive symptom level and cig/day across a25-day follow-up. More recently, Leventhal, Piper, et al. (2014)examined smokers taking part in a clinical trial involving multis-ession cessation counseling and randomization to one of severalmedication or placebo treatment conditions. They found that par-ticipants with a lifetime history of anticipatory Anh were morelikely to relapse at 8 weeks’ and 6 months’ postquit over and abovegender, depressed mood, depressive disorder, anxiety or substanceuse disorder, and nicotine dependence. History of major depres-sion or recurrent depression did not significantly predict cessationafter controlling for Anh.
Anh also appears to predict rapid relapses shortly after quitting.Global Anh predicted lapse within the 1st day following cessationin smokers receiving counseling and NRT (Zvolensky, Stewart, etal., 2009). In a study of smokers motivated to quit who obtainedminimal self-help cessation reading materials, Niaura et al. (2001)showed that smokers who endorsed anticipatory Anh lapsedquicker (median time to lapse � 0.9 days) than those with noanticipatory Anh (median time to lapse � 1.75 days). Similarly, across-sectional study of nontreatment-seeking smokers found thatconsummatory Anh was positively associated with a greater num-ber of prior failed quit attempts as well as a greater proportion ofquit attempts that ended in a lapse within the first 24 hr of theattempt (Leventhal, Waters, et al., 2009). These results were in-cremental to variance in negative affect and suggest that whileanhedonic smokers are indeed interested in quitting, their quitattempts tend to end in rapid failure.
Implications for targeting Anh in smoking prevention andcessation. Given evidence implicating Anh in smoking initiationand progression, smoking prevention that targets Anh may befruitful. Though a formal smoking prevention program that spe-cifically targets Anh has yet to be investigated, Sussman andLeventhal (2014) suggested that educational strategies to promotenormalization or acceptance of one’s anhedonic status and increaserecognition of subtle increases in pleasure in anhedonic youthsmight prevent them from experimenting with smoking to obtainpleasure. Methods to counteract Anh directly, such as facilitatingexposure to novel, high-threshold rewards that are healthy (e.g.,roller coasters, vigorous exercise), might naturally engender plea-sure and offset motivation to initiate smoking to obtain pharma-cological reward in Anh individuals. School-based activities couldbe developed that can be completed by individuals, small work-groups, or the whole classroom for universal prevention of smok-ing that targets Anh. For instance, in the self-esteem enhancementsession of the Towards No Drug Abuse prevention program uti-lized in high school settings (Sussman, Dent, & Stacy, 2002),students note their personal assets and pass compliment to otherstudents, which may perhaps be potent enough social rewards toenhance pleasure in anhedonic teens.
When considering the role of Anh in cessation treatment, it isimportant to note that Anh predicts poor quit outcomes across anumber of studies that apply different efficacious medications,including NRT and bupropion (Leventhal, Piper, et al., 2014;Leventhal et al., 2008; Zvolensky, Stewart, et al., 2009), as well asstudies that apply different behavioral intervention approaches,including self-help materials (Niaura et al., 2001), 1-day work-
shops (Cook et al., 2010), and standard multisession cessationcounseling (Leventhal, Piper, et al., 2014; Leventhal et al., 2008;Zvolensky, Stewart, et al., 2009). Furthermore, one of these studiesfound that medication condition (NRT/bupropion vs. placebo) didnot significantly moderate the relation of prequit lifetime Anh tosmoking cessation outcome (Leventhal, Piper, et al., 2014). Thus,existing standard interventions may do little to offset Anh-relatedrisk of cessation failure, and identifying tailored treatments thatmay offset the particular mechanisms underlying Anh’s effects onsmoking is warranted.
Diminished reward and positive affective response to nonsmok-ing alternative rewards as well as heightened reward and affectiveresponse to smoking may be important factors that maintain smok-ing in anhedonic individuals. Hence, candidate medications foroffsetting Anh’s effects might successfully mitigate nicotine’ssubjective effects without having detrimental effects on the hedo-nic properties of nonsmoking rewards. A recent laboratory studyshowed that in comparison to placebo, varenicline—a partial ag-onist of the �4�2 nicotinic acetylcholine receptor that has shownstrong efficacy for smoking cessation (Jorenby et al., 2006)—reduced the subjective rewarding effects of smoking followingabstinence and diminished the relative reward value of smokingversus an alternative reinforcer (i.e., money) on a behavioraleconomics measure (McClure, Vandrey, Johnson, & Stitzer,2013). Hence, future exploration of whether varenicline may beparticularly efficacious for anhedonic smokers may be fruitful.
Other pharmacotherapy targets for the nicotine receptor systemmay be warranted. Anh predicts poorer outcomes and higherpostquit withdrawal symptoms among studies involving standarddoses of NRT (Langdon et al., 2013; Leventhal, Piper, et al., 2014;Leventhal et al., 2008; Zvolensky, Stewart, et al., 2009). A stan-dard dose of NRT may not provide enough nicotine to entirelyoffset nicotine withdrawal in anhedonic smokers. Future researchis needed to determine whether a higher dose of NRT may berequired to more fully ameliorate reward and positive affect def-icits that are prominent when anhedonic individuals make a quitattempt.
Candidate behavioral interventions that may heighten the re-ward and hedonic effects of alternative nondrug reinforcers areworthy of consideration. Behavioral activation (BA), which isbased on behavioral approaches to addressing diminished appeti-tive functioning in depression, aims to enhance one’s ability toaccess healthy reinforcers and recognize mood-enhancing effects(Lejuez, Hopko, & Hopko, 2001). This treatment has recently beenadapted for smoking cessation (Behavioral Activation Treatmentfor Smoking [BATS]) by integrating BA-specific strategies (e.g.,activity monitoring, mood tracking, identifying and planning val-ued activities) to standard cessation counseling, with the overallaim of structuring reinforcing activities to promote a more reward-ing nonsmoking lifestyle (MacPherson, Tull, et al., 2010). In apilot trial of smokers with elevated depressive symptoms, aneight-session BATS (vs. standard cessation counseling alone) pro-duced significantly higher rates of smoking abstinence (MacPher-son, Tull, et al., 2010). Pending replication and extension, theseresults highlight the promise of BA as a strategy to prevent relapsein anhedonic smokers.
Positive psychotherapy (PPT; Seligman, Rashid, & Parks, 2006)is another candidate intervention for offsetting Anh’s impact onsmoking. PPT aims to cultivate positive emotions and traits and
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16 LEVENTHAL AND ZVOLENSKY
has recently been adapted into an integrated format for smokingcessation (i.e., Positive Psychotherapy for Smoking Cessation[PPT-S]; Kahler et al., 2014). PPT-S includes several PPT exer-cises that are designed to teach smokers means of obtainingpleasure, satisfaction, and meaning without relying on smoking.For instance, in the savoring exercise, individuals are asked tosavor at least two experiences (e.g., their morning coffee, the sunon their face) each day for 1 week, for at least 2–3 min perexperience. To effectively savor, participants were encouraged tobe mindful, “in the moment,” and “take in” all that a givenexperience had to offer. In a preliminary open-label trial for PPT-Sin high-Anh smokers, point prevalence abstinence rates were47.4% at 8 weeks, 36.9% at 16 weeks, and 31.6% at 26 weeks,which exceeds abstinence benchmarks reported in meta-analysesin U.S. Public Health Service clinical practice guidelines forsmoking cessation (U.S. Department of Health and Human Ser-vices, 2008). Hence, PPT may be a promising strategy for address-ing the role of Anh in smoking cessation.
Summary. Empirical data suggestively implicate Anh as a riskfactor for smoking initiation and progression across early stages ofthe smoking trajectory. There is consistent empirical evidence thatAnh increases risk of smoking cessation failure both early and latein quit attempts. Anticipated and actual amplification of smokingeffects on reward and positive affect appears to be a key mecha-nism that maintains smoking in anhedonic individuals and under-lies Anh’s possible effects on progression across several stages ofthe smoking trajectory. Efforts to cultivate pleasure and preventsmoking behavior as an unhealthy means of obtaining pleasure inanhedonic individuals are candidate smoking interventions thatrequire future evaluation. In many cases, the relation of Anh tosmoking processes is incremental to other factors, such as depres-sive, anxiety symptoms, and nicotine dependence. Thus, evidenceis broadly consistent with the transdiagnostic formulation pro-posed here that Anh may be one common pathway that channelsdistal risk of smoking carried by emotional disorders.
Anxiety Sensitivity
Anxiety sensitivity: Construct and correlates.Definition. The AS construct, defined as the extent to which
individuals believe anxiety and anxiety-related sensations haveharmful personal consequences (Reiss & McNally, 1985), is arelatively stable, but malleable, factor. The global AS constructencompasses lower order fears of physical, mental, and publiclyobservable experiences (Zinbarg, Barlow, & Brown, 1997).High-AS individuals are afraid to experience interoceptive sensa-tions indicative of arousal or other anxiety symptoms because theybelieve these experiences signal or will lead to cardiac arrest orother feared outcomes; low-AS individuals believe such sensationsto be benign. If a person perceives anxiety-related experiences area sign of imminent harm, they will likely experience anxiety andarousal in response to such cognitions, which could trigger phys-iological arousal reactions and more anxiety sensations, and in turnincrease risk for panic.
Empirically, AS is distinguishable from the tendency to expe-rience more frequent anxiety symptoms (trait anxiety) and othernegative affect propensity variables (e.g., neuroticism; Rapee &Medoro, 1994; Zvolensky, Kotov, Antipova, & Schmidt, 2003). Inaddition to a robust influence of AS on panic psychopathology
(McNally, 2002), research also documents AS’s role in the etiol-ogy of PTSD (Fedoroff, Taylor, Asmundson, & Koch, 2000),major depressive disorder (Taylor, Koch, Woody, & McLean,1996), social anxiety disorder (Scott, Heimberg, & Jack, 2000),hypochondrias (Eifert & Zvolensky, 2005), chronic pain (Asmund-son, Wright, & Hadjistavropoulos, 2000), obsessive-compulsivedisorder (Naragon-Gainey, 2010), and other clinical conditions(e.g., asthma; McLeish, Zvolensky, & Luberto, 2011). The dataimplicating AS in mood and anxiety pathology are strong, consis-tent across cultures and distinct national groups, and incremental toother risk factors (Hayward, Killen, Kraemer, & Taylor, 2000; Li& Zinbarg, 2007; Maller & Reiss, 1992; G. N. Marshall, Miles, &Stewart, 2010; Schmidt et al., 2010; Schmidt, Lerew, & Jackson,1997, 1999; Schmidt, Zvolensky, & Maner, 2006). AS may play arole in multiple disorders involving negative mood dysregulation,as AS-related tendencies may promote avoidance behavior andprevent the development of adaptive coping responses to a widevariety of emotionally aversive circumstances, and hence nega-tively reinforce more frequent negative emotional states. Further,AS reduction appears to be a chief explanatory element (mecha-nism) that promotes the reduction and remission in emotionalsymptomatology (Smits, Berry, Tart, & Powers, 2008).
Measurement. AS is most commonly assessed via self-reportmeans on the 16-item Anxiety Sensitivity Index (ASI; Reiss et al.,1986). Items are rated on a 5-point Likert scale and cover physical(e.g., “When I notice that my heart is beating rapidly, I worry thatI might have a heart attack”), mental (e.g., “When I cannot keepmy mind on a task, I worry that I might be going crazy”), andpublicly observable experiences (e.g., “It is important not to appearnervous”), which may reflect empirically distinct manifestations ofAS (Zinbarg et al., 1997). Efforts to improve the psychometricproperties of ASI have yielded additional variants of the measures,including the Anxiety Sensitivity Index–Revised (ASI-R; Taylor& Cox, 1998b), the Anxiety Sensitivity Profile (ASP; Taylor &Cox, 1998a), and the 18-item Anxiety Sensitivity Index–3 (ASI-3;Taylor et al., 2007). The ASI-R and ASP perform relatively poorlyin terms of replicability of factor structure and discriminant valid-ity (Armstrong, Khawaja, & Oei, 2006; Deacon, Abramowitz,Woods, & Tolin, 2003), whereas the ASI-3 has shown generallystrong psychometric properties (Taylor et al., 2007). Amongyouths, AS has been measured via the Childhood Anxiety Sensi-tivity Index (CASI), which has shown good psychometric proper-ties (Silverman, Fleisig, Rabian, & Peterson, 1991). The 18-itemCASI asks youths to rate their fear to similar experiences on theadult ASI, but its language is simplified and context is tailored(e.g., “When I cannot keep my mind on my schoolwork I worrythat I might be going crazy”).
Anxiety sensitivity and smoking.Theoretical applicability of AS to smoking. A major theoret-
ical premise of work linking AS and smoking is that smokingserves critically important and immediate acute affect regulatoryfunctions, which may override fears about the long-term healthconsequences of smoking. Perhaps for those high in AS, smokingmay be a potential means for offsetting anxiety symptoms orlimiting the negative consequences of anxiety in those yet toinitiate, which could in turn enhance motivation to experimentwith smoking. These expectations may be based in a pharmaco-logical reality, as the administration of tobacco and nicotineacutely diminishes anxiety symptoms and tobacco abstinence in-
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17EMOTIONAL VULNERABILITIES AND SMOKING
creases anxiety in regular smokers (Evans, Blank, Sams, Weaver,& Eissenberg, 2006; Evatt & Kassel, 2010; Leventhal, Waters, etal., 2010). As a result, high-AS individuals may find the anxiolyticeffects of smoking highly negatively reinforcing, which couldaccelerate the progression from experimentation to regular smok-ing. In the absence of other, more adaptive coping strategies,smokers high in AS may learn to rely on smoking to manageanxiety states and fears of bodily sensations in the relatively shortterm and overlook long-term health consequences of smoking(Zvolensky & Bernstein, 2005).
Over longer periods, smoking itself will lead to increasedanxiety-related sensations via a number of routes, includingnicotine-based withdrawal symptoms, perceived and objectivehealth impairment, and physical illness (CDC, 2010). For thosewith preexisting elevated AS, the development of smoking-induced aversive sensations may heighten one’s fear of suchsymptoms. Hence, smoking may increase AS. Furthermore, bidi-rectional learning mechanisms may serve to create a positivefeedback loop in which smoking and AS both increase one an-other. Indeed, because high-AS individuals may experience short-term anxiolysis from smoking, particularly in the presence ofanxiety-inducing situations (Evatt & Kassel, 2010), high-ASsmokers’ cognitions that internal cues can be personally harmful,dangerous, and anxiety evoking may be maintained because oflimited opportunity for exposure to anxiety symptoms and result-ing extinction and learning processes to ensue. Once regular smok-ing is established, high-AS smokers may be afraid to make quitattempts, because these persons are apt to be particularly fearful of,and emotionally reactive to, distressing nicotine-withdrawal-related sensations (e.g., anxiety, heart rate slowing, concentrationdifficulty) that occur during smoking abstinence. Thus, a forwardfeed cycle may develop, whereby smoking is used as a copingstrategy for managing aversive states in the short term yet para-doxically confers longer term risk for the maintenance of smokingin high-AS individuals (Zvolensky, Schmidt, & McCreary, 2003).
Empirical data on the relation of AS to smoking initiation.Some cross-sectional studies have found that smokers reporthigher levels of AS than nonsmokers (McLeish et al., 2008;Morissette, Brown, Kamholz, & Gulliver, 2006; cf. Abrams,Schlosser, et al., 2011), which provide indirect evidence that ASmay be related to smoking initiation. Given AS-smoking statusrelations extend to a sample of individuals with anxiety disorders(Morissette et al., 2006), it is possible that AS is not solely a proxyfor manifest anxiety psychopathology and rather a transdiagnosticfactor explains variance in smoking status among the population ofanxiety-disordered individuals. McLeish et al. (2008) found thatthe extent to which panic-relevant anxiety symptoms was cross-sectionally associated with greater likelihood of smoking wasamplified for individuals who scored high on the ASI–PhysicalConcerns subscale (e.g., “It scares me when my heart beats rap-idly”). These findings raise the possibility that high-AS individualsmay initiate smoking as a protective response to their own phys-iologic anxiety symptoms, as they may expect smoking to helpthem cope with anxiety and have a strong drive to limit anxiety dueto their fear of anxiety-related consequences. Perhaps high-ASindividuals might be prone to developing expectancies forsmoking-induced anxiety reduction even prior to initiation basedon observation of other smokers and extrapolation from other
behaviors that have acute anxiolytic properties (e.g., alcohol use;O’Connor, Farrow, & Colder, 2008).
Empirical data on the relation of AS to smoking progressionand regular smoking. Although no study has examined AS inthe progression from initiation to regular smoking, cross-sectionalstudies have examined whether AS is associated with more severesmoking profiles in those who have already established dailysmoking patterns. Results are mixed on this issue, with a widerange of effect sizes for relations of AS to cig/day and nicotinedependence severity in daily smokers (rs � .03–.44; K. A. John-son, Stewart, Rosenfield, Steeves, & Zvolensky, 2012; Zvolensky,Farris, Schmidt, & Smits, 2014; Zvolensky, Kotov, et al., 2003).Given the methodological caveats with these studies (e.g., cross-sectional, do not assess progression from nondaily to daily smok-ing), prospective work is warranted to clarify whether AS accel-erates progression from irregular to regular smoking.
Empirical data on the relation of and mechanisms linking ASto the maintenance of smoking. AS has frequently been linkedto stronger smoking outcome expectancies for negative reinforce-ment (e.g., beliefs smoking will reduce negative affect) acrossadult treatment-seeking heavy smokers (20 cig/day; R. A.Brown, Kahler, Zvolensky, Lejuez, & Ramsey, 2001), collegestudent daily smokers (Zvolensky, Feldner, et al., 2004), and adultdaily smokers from the community (Abrams, Schlosser, et al.,2011; Gonzalez, Zvolensky, Vujanovic, Leyro, & Marshall, 2008;Gregor, Zvolensky, McLeish, Bernstein, & Morissette, 2008; Guil-lot, Pang, & Leventhal, 2014). Similarly, AS is correlated withgreater expectations that abstinence will exacerbate negative affectand other undesired outcomes in regular smokers (Abrams, Zvo-lensky, Dorman, Gonzalez, & Mayer, 2011; Guillot et al., 2014).In many of these studies, relations involving AS were evidentabove and beyond the variance accounted for demographic, man-ifest psychopathology, and nicotine dependence level. AS alsorelates to stronger beliefs of smoking leading to health conse-quences (e.g., Zvolensky, Feldner, et al., 2004), which is in linewith theoretical models of AS (i.e., expectancy of negative con-sequences). The overall weight of scientific evidence is consistentwith the perspective that expectations of (and motivation to obtain)smoking’s acute affect-modulatory effects are paramount and out-weigh heightened perceptions of smoking’s potential negativeconsequences in high-AS individuals.
Consistent with evidence linking AS to expectancies that absti-nence provokes negative affect, AS also is related to the actualexperience of more severe nicotine withdrawal symptoms amongthose initiating an abstinence attempt in the early phases of absti-nence (i.e., 1 week postquit; K. A. Johnson et al., 2012; E. C.Marshall, Johnson, Bergman, Gibson, & Zvolensky, 2009), butless so in later phases of abstinence (Mullane et al., 2008). Impor-tantly, AS-related amplification of withdrawal during abstinence ismore robust for withdrawal symptoms that are affective andanxiety-related in nature (i.e., frustration, restlessness, depression,anxiety, irritability) than nonaffective withdrawal symptoms (i.e.,cigarette craving, concentration problems).
Experimental psychopathology paradigms to study AS, whichoften utilize some type of emotion elicitation paradigm and mon-itor real-time responsivity (Zvolensky & Forsyth, 2002), have beenleveraged to understand AS-smoking relations. For example, twostudies have examined the effect of 12-hr tobacco deprivation orad lib smoking on subjective anxiety during a carbon dioxide
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18 LEVENTHAL AND ZVOLENSKY
(CO2) procedure provocation challenge. Both studies showed thatalthough AS amplifies response to CO2 provocation, high-AS (vs.low-AS) smokers do not appear to show an enhanced sensitivity tothe subjective effects of CO2 provocation during abstinence(Abrams, Schlosser, et al., 2011; Vujanovic & Zvolensky, 2009).Taken together with results above, high (vs. low) AS smokers maybe more susceptible to the anticipated and actual effects of absti-nence on sustained (“tonic”) levels of subjective anxiety, yet maynot experience an amplification of subjective reaction to anx-iogenic stimuli (“phasic” anxiety responses) during abstinentstates.
In the tobacco administration literature, evidence suggests thatAS enhances sensitivity to the anxiolytic effects of acute smokingduring stressful anxiogenic conditions (i.e., smoking-induced pha-sic anxiety reductions). For example, using a stressful speechparadigm, Evatt and Kassel (2010) found that laboratory in vivosmoking reduced anxiety in high-AS smokers who smoked duringa stressful situation, but not a no-stress situation; low AS smokersendorsed anxiolysis in both conditions. These results are in linewith those of Perkins, Karelitz, Giedgowd, Concklin, and Sayette(2010), who reported that AS predicted greater smoking-inducedchanges in some measures of state positive and negative affectunder certain conditions of stress or smoking abstinence. Morerecently, Wong et al. (2013) indicated that AS predicted greaterincreases in positive affect pre- to postcigarette as well as greatersmoking satisfaction and psychological reward during a cigaretteadministration following ad lib smoking; effects remained signif-icant after adjusting for anxiety symptom severity. AS did notpredict degree of negative affect and craving suppression orpostcigarette aversive effects. Thus, positive reinforcement mech-anisms may be salient etiological processes that maintain smokingin high-AS individuals, at least when not acutely abstinent orstressed. Yet, negative reinforcement (including smoking-inducedanxiolysis) mechanisms may be enhanced in high-AS smokers ina stressed state.
Empirical data on the relation of AS to smoking cessation andrelapse. Studies of cessation outcomes have shown that AS isassociated with greater risk of lapse and relapse. One study foundthat AS was associated with an increased likelihood of smokinglapse (any smoking behavior) during the 1st week of a quit attemptamong depressed smokers receiving combination psychosocialtherapy and NRT (R. A. Brown, Kahler, et al., 2001). A separateprospective investigation found AS was related to increased re-lapse likelihood among adult daily smokers by 1 month followingcessation (Mullane et al., 2008). In a more recent study of smokersreceiving cessation counseling and NRT, Zvolensky, Stewart, et al.(2009) found that prequit AS was significantly associated with anincreased risk of early smoking lapse (i.e., any smoking behavior)at Days 1, 7, and 14 following the quit day, but not full relapse(i.e., 7 consecutive days of smoking). In separate work, adult dailysmokers with higher levels of AS reported their longest (lifetime)quit attempts as consisting of relapse within 1 week postcessationin smokers residing in Mexico (Zvolensky, Bernstein, et al., 2007)and the United States (Zvolensky, Bonn-Miller, Bernstein, & Mar-shall, 2006). Finally, a recent study examined lapse and relapseduring a 4-week group NRT-aided cognitive behavioral tobaccointervention program (Assayag, Bernstein, Zvolensky, Steeves, &Stewart, 2012). Results indicated that participants whom main-tained high levels of AS from pretreatment to 1-month posttreat-
ment, compared to those who demonstrated a significant reductionin AS levels during this period, showed a significantly increasedrisk for lapse and relapse. Importantly, the observed AS-smokingquit effects across the reviewed studies are not explained bysmoking rate, nicotine dependence, gender, other concurrent sub-stance use (e.g., alcohol, cannabis), manifest emotional symptom-atology, withdrawal symptoms, or trait-like negative mood pro-pensity. Hence, high-AS individuals who do not show a reductionin AS during cessation treatment may be at risk of cessationfailure, suggesting that treatments that attenuate AS during thesmoking cessation process may perhaps improve quit outcomes.
Evidence also highlights the importance of barriers and otherfactors that thwart quit attempts in high-AS smokers. AS is relatedto greater perceived barriers for quitting among daily adult smok-ers, and such an effect is not attributable to negative affectivity,Axis I psychopathology, history of nonclinical panic attacks,smoking rate, and alcohol consumption (Zvolensky, Johnson, etal., 2009). Thus, AS may prevent regular smokers from making acessation attempt. In line with this perspective, Zvolensky, Farris,Schmidt, and Smits (2014) recently found in treatment-seekingdaily smokers that AS was indirectly related (i.e., statistical me-diation) to greater perceived barriers to cessation, greater numberof prior quit attempts, and greater mood management smokingexpectancies through the tendency to escape and avoid aversivesmoking-related thoughts, feelings, and internal sensations. Be-cause high-AS individuals may be more apt to excessively worryabout the stress of quitting because they inflexibly rely on smokingto cope with anxiety, they may be at risk for treatment dropout.Indeed, in a study of smokers recruited to participate in a self-guided (unaided) quit attempt, Langdon et al. (2013) found thatthat after controlling for the effects of a number of cofactorsincluding prequit levels of motivation to quit, AS predicted in-creased odds of study dropout prior to scheduled quit day. Despitethese barriers, AS has been related to increased motivation to quit(Zvolensky, Feldner, et al., 2004), perhaps due to concerns aboutthe health effects of smoking (Zvolensky, Bernstein, et al., 2007).Thus, if practitioners could harness such motivation prior to andearly in cessation attempts, quit success might be enhanced forhigh-AS smokers.
Implications for targeting AS in smoking prevention andcessation. If AS in fact confers risk for smoking initiation andexpectancies that smoking offsets anxiety plays a role in smokingexperimentation, smoking prevention targeting AS-related beliefsmay be useful. For example, psychoeducation that acknowledgesthat although smoking may have some acute anxiolytic properties,the long-term harmful cardiovascular effects of nicotine smokingmay actually exacerbate anxiety symptoms and other negativehealth outcomes, may have preventive effects for high-AS indi-viduals through harnessing healthy fears of smoking-related neg-ative consequences. In addition, extensive mental illness preven-tion programs that challenge maladaptive fears of anxiety-relatedsensations and prevent avoidance behaviors might have usefulindirect effects on smoking prevention as speculated by someauthors (Dudas, Hans, & Barabas, 2005). Existing preventionprograms that aim to reduce AS by incorporating behavioral ex-posure exercises to anxiety-related sensations without executingescape behaviors in which individuals learn corrective informationthat such sensations are not harmful could be expanded (Schmidtet al., 2007). We speculate that encouraging youths to avoid
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19EMOTIONAL VULNERABILITIES AND SMOKING
smoking (and other substances) as escape behaviors in anxietyprevention programs may perhaps enhance any preventive effectthat AS reduction interventions have on smoking. Yet, prospectiveevidence linking AS to risk of smoking initiation and progressionamong youths will be needed prior to full-fledged application ofAS-based smoking prevention.
Based on the potential negative effects of AS on smokingcessation outcomes, efforts have been made to target reductions inAS to improve cessation success. Nontobacco-oriented interven-tion programs for anxiety-mood psychopathology, which target ASvia psychoeducation, cognitive restructuring, and interoceptiveexposure (Broman-Fulks & Storey, 2008; Gardenswartz & Craske,2001; Schmidt et al., 2007; Vujanovic, Bernstein, Berenz, &Zvolensky, 2012), have been integrated with smoking cessationprograms. In an initial case study, a 16-session integrated AS-smoking cessation treatment successfully reduced AS and im-proved quit success (Zvolensky, Lejuez, Kahler, & Brown, 2003).Subsequent controlled work has shown that a single-session pro-gram can reduce AS and facilitate reductions in smoking rate at1-month follow-up (Feldner, Zvolensky, Babson, Leen-Feldner, &Schmidt, 2008). Based upon such work, an eight-session programfor smokers high in AS entitled the Anxiety Sensitivity ReductionProgram for Smoking Cessation was developed (Zvolensky, Yartz,Gregor, Gonzalez, & Bernstein, 2008). The treatment appliedcognitive restructuring and acceptance-oriented behavioral strate-gies as well as interoceptive exposure to anxiety-related sensationswith a specific focus on reducing AS-related beliefs, combinedwith evidenced-based behavioral counseling for smoking cessation(for comprehensive session-by-session descriptions of the treat-ment, see Zvolensky & Farris, 2012; Zvolensky, Yartz, et al.,2008). In a case series evaluation (n � 3), this program reducedAS and facilitated smoking cessation success at 1-month follow-up(Zvolensky, Yartz, et al., 2008). These findings have now beenreplicated and extended to 3-month follow-up (Zvolensky, Bogi-aizian, Salazar, Farris, & Bakhshaie, 2014), yielding positive re-sults in terms of acceptability and adherence, positive smokingcessation outcome (five out of six participants were abstinent at12-week follow-up), and statistically significant reductions in AS.While additional work testing AS reduction strategies in largercontrolled trials is necessary, initial results suggest possible clin-ical value of such approaches.
Summary. While AS may theoretically play a role in smokinginitiation and potentially progression, the empirical evidence baseis too limited to draw firm conclusions regarding AS’s role earlyin the smoking trajectory. Yet, AS is consistently associated withfactors that likely drive smoking behavior across the later stages ofthe smoking trajectory, including impeding the initiation of cessa-tion attempts and derailing their success very early upon absti-nence. A key mechanism underlying and maintaining smoking inhigh-AS individuals involves amplification of anticipated and ac-tual anxiolytic and negative reinforcing effects of smoking. Ap-plying psychoeducation and exposure-based strategies to alleviateAS may perhaps be useful in smoking intervention and should befurther evaluated. In many studies, AS is associated with smoking-related processes over and above variance in emotional symptom-atology and other factors, which is consistent with the notion thatAS is a transdiagnostic processes that is a key underlying factorlinking anxiety and depressive pathology to smoking.
Distress Tolerance
Distress tolerance: Construct and correlates.Definition. The literature generally characterizes two broad,
conceptually distinct forms of DT (Leyro et al., 2010): (a) theperceived capacity to withstand negative emotional or other aver-sive states (e.g., physical discomfort) and (b) the objective behav-ioral act of withstanding distressing internal states elicited by sometype of stressor. We conceptualize DT as a higher order constructthat reflects one’s ability to tolerate and withstand any type ofexperience that is aversive in nature, which spans a variety ofnegative emotional states (e.g., stress, frustration, anxiety, nonspe-cific perceptions of feeling upset) or physical sensations that oftenprovoke negative affect, such as pain or other forms of physicaldiscomfort. DT is theorized to be related to, though conceptuallydistinct from, other variables (e.g., avoidant coping, emotion reg-ulation, experiential avoidance; Leyro et al., 2010). Individualswith lower DT are prone to maladaptively respond to distress, acommon manifestation of which involves avoidance and escape ofdistress-eliciting contexts. In contrast, high-DT individuals may bemore able to adaptively respond to distress or distress-elicitingcontexts. Theoretically, DT may affect, and be affected by, avariety of processes involved in self-regulation, including atten-tion, cognitive appraisals of distressing emotional and physicalstates, and emotional as well as behavioral responses to distress.Individuals with a more extensive or qualitatively unique historyof emotional experiences may have a greater opportunity to de-velop a more entrenched or qualitatively distinct type of perceivedor behavioral response to distress, which may manifest in low orhigh DT. The literature shows that DT can be context dependent(e.g., exacerbated by triggers such as stress, ameliorated by inter-vention), yet tends to be somewhat stable over time (Cummings etal., 2013; Leyro et al., 2010). Hence, it is plausible that, similar toAnh and AS, DT reflects a stable, yet malleable, construct that canbe targeted by intervention.
DT is believed to be an explanatory construct implicated in awide variety of psychopathological symptoms and disorders(Leyro et al., 2010). There is evidence of a consistent empiricalrelation of low DT to depressive symptoms in a variety of samples(Buckner, Keough, & Schmidt, 2007; Dennhardt & Murphy, 2011;Gorka, Ali, & Daughters, 2012) and poor depression treatmentoutcome (Williams, Thompson, & Andrews, 2013). There is alsoa consistent relation between poor DT and anxiety symptoms(Keough, Riccardi, Timpano, Mitchell, & Schmidt, 2010), includ-ing in samples of children (O’Neil Rodriguez & Kendall, 2014).DT’s relations extend across several manifestations of anxiety,including PTSD, panic, obsessive-compulsive, general worry, andsocial anxiety symptoms (Marshall-Berenz, Vujanovic, Bonn-Miller, Bernstein, & Zvolensky, 2010; Norr et al., 2013). Inaddition to its role in emotional pathology, DT is inversely asso-ciated with substance dependence status, substance abstinenceduration, and substance use treatment retention (Quinn, Brandon,& Copeland, 1996); antisocial (Daughters, Sargeant, Bornovalova,Gratz, & Lejuez, 2008), and borderline (Bornovalova et al., 2008)personality disorder; eating psychopathology (Anestis, Selby,Fink, & Joiner, 2007); and several other maladaptive processes(e.g., risk-taking propensity and risk-taking behavior; MacPher-son, Reynolds, et al., 2010). Hence, DT has transdiagnostic rele-
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20 LEVENTHAL AND ZVOLENSKY
vance to various emotional disorders and other psychopathologicalconditions involving emotional disturbance.
Poorer DT is likely to confer risk for emotional pathology via anumber of mechanisms. Individuals with low DT are likely toavoid and engage in escape behavior in response to stimuli andsituations that produce distress. As a result, negative affectivereactions to aversive stimuli are unlikely to habituate due tolimited extinction learning and a proneness toward avoidance,which may escalate emotional pathology in various contexts (e.g.,social events, physiological arousal). Furthermore, certain mani-festations of DT (e.g., tendency to become cognitively absorbedwhen experiencing distress, feeling ashamed in response to dis-tress; Simons & Gaher, 2005) may prolong negative affect, con-tribute to maladaptive depressogenic and anxiogenic cognitions,and interfere with one’s ability to effectively function. In addition,avoidance behavior associated with poor DT may prevent thedevelopment of positive coping skills, which may in turn worsenemotional psychopathology trajectories.
Measurement. The perceived capacity to tolerate distress hasbeen operationalized in several ways, with two conceptualizationsmost often applied in the smoking literature (Zvolensky, Vu-janovic, Bernstein, & Leyro, 2010). Tolerance of negative emo-tional states reflects individual differences in the perceived capac-ity to withstand negative emotional states (Simons & Gaher,2005). This construct can be measured via self-report indices, suchas the Distress Tolerance Scale (Simons & Gaher, 2005), whichinstruct participants to agree or disagree with self-statements re-garding responses to distressing states (e.g., “I’ll do anything toavoid feeling distressed or upset”). Tolerance of physical sensa-tions reflects perceived capacity to withstand uncomfortable phys-ical sensations (Schmidt, Richey, & Fitzpatrick, 2006). This con-struct has been assessed via self-report questionnaires, such as theDiscomfort Intolerance Scale (Schmidt et al., 2006), which instructrespondents to indicate the extent to which self-statements ofdiscomfort tolerance are characteristic of their typical behavior(e.g., “When I begin to feel physically uncomfortable, I quicklytake steps to relieve the discomfort”).
Behavioral indicators of DT typically measure the duration oftime that an individual can withstand exposure to a specific type ofexperimentally presented aversive task or stimulus. Tolerance tothe experiential distress elicited by such stimuli or tasks is inferredby longer persistence on such tasks. In one area of study, proce-dures that acutely change levels of oxygen and CO2 in order toinduce physiological sensations associated with anxious arousal(e.g., shortness of breath, dizziness) are applied (e.g., voluntaryhyperventilation or breath holding, carbon-dioxide-enriched airchallenge [CO2 challenge]). In another line of study, DT has beenevaluated by means of persistence in completing stressful or frus-trating cognitive tasks, such as the Paced Auditory Serial AdditionTest (PASAT), Mirror-Tracing Persistence Test (MTPT), andAnagram Persistence Task. DT is operationalized as how long onecan continue engagement in the distressing task prior to termina-tion.
DT and smoking.Theoretical applicability of DT to smoking. Application of
DT to smoking has grown, in part, out of Eisenberger’s (1992)learned industriousness theory, which proposed that receiving re-inforcement for high-effort behaviors would lead to an increasedlikelihood of a person putting forth greater effort in later endeav-
ors. As applied to smoking, low-DT individuals may be more aptto smoke because they have learned to utilize “low-effort copingskills” for distress throughout their lives (Quinn et al., 1996). Thus,low-DT individuals are likely to be attuned to identifying behav-iors that are low effort and maximizing efficacy for reducing oravoiding distress. Hence, low-DT individuals may be susceptibleto the development of affect modulation expectancies for suchbehaviors that circumvent distress and are likely to extrapolate thatsmoking is one such distress-terminating behavior via observationof other individuals who smoke or translation of expectancies fromother acute affect-modulatory behaviors (e.g., emotional eating).Hence, those with poor DT should presumably be more likely toinitiate smoking in order to manage experiential discomfort. Uponsmoking initiation, those with low DT may be more susceptible toany negative reinforcement from smoking because of the highpriority they place on distress escape, which ultimately may ac-celerate smoking progression for low-DT individuals. Continuednegative reinforcement via smoking-induced alleviation of a vari-ety of aversive states, including physical pain (e.g., Ditre, Bran-don, Zale, & Meagher, 2011), may be a salient factor maintainingsmoking for low-DT smokers.
DT theoretically impacts smoking cessation, as individuals whohave lower DT may be at the greatest risk of terminating theirlong-term goal (e.g., abstinence, reductions in use) when in dis-comfort in favor of the short-term goal of distress termination.During a quit attempt, low-DT smokers may have a low thresholdfor tolerating aversive states that routinely occur during cessation(e.g., withdrawal symptoms, bodily sensations associated withdeclining nicotine levels, coping with the stress and frustration ofnot being able to smoke). Thus, low-DT smokers are likely torespond to such states experienced during cessation with the re-sumption of smoking behavior aimed at temporarily amelioratingexperiential distress.
Empirical data on the relation of DT to smoking initiation.In an early study, Quinn et al. (1996) found that nonsmokerspersisted significantly longer than smokers on frustrating cognitivetasks. Later, MacPherson, Reynolds, et al. (2010) found that levelsof a self-reported risky behavior index that included cigarettesmoking were highest among adolescents with lower DT andhigher levels of impulsivity; this interactive effect was evidentabove and beyond the variance accounted for by a number ofsociodemographic factors. There was no main effect of DT onrisky behaviors in that study. In a more recent study, Raglan(2013) explored DT across current smokers, former smokers, andnever smokers. Participants completed the self-report tolerance-for-frustration scale (e.g., “I can’t stand doing tasks that seem toodifficult”) and a behaviorally based DT task that involved mirrortracing (i.e., MTPT). There were no significant differences betweengroups on perceived tolerance for frustration. Yet, never smokerspersisted longer on the MTPT than former or current smokers; therewas not a significant difference between current smokers and formersmokers. Although these results are notion that low DT may precedesmoking, the cross-sectional design precludes conclusions regardingtemporality.
Empirical data on the relation of DT to smoking progressionand regular smoking. We know of no study of DT in relation toprogression across the early end of the smoking trajectory (e.g.,initiation to irregular to regular smoking). Studies on the associa-tion of DT to nicotine dependence and smoking heaviness among
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21EMOTIONAL VULNERABILITIES AND SMOKING
daily smokers tend to show modest or nonsignificant associations.For example, across numerous behavioral tasks measuring DTamong daily smokers, no significant associations of DT to cig/dayor nicotine dependence were found (R. A. Brown et al., 2009).Similar findings have been reported in treatment-seeking smokingsamples (Brandt, Johnson, Schmidt, & Zvolensky, 2012). By con-trast, two studies reported modest significant associations of per-ceived DT to nicotine dependence severity among daily smokersnot seeking treatment (Leyro, Bernstein, Vujanovic, McLeish, &Zvolensky, 2011; Trujillo et al., 2012), but DT was not associatedwith cig/day. Hence, perceived incapacity to handle distress maybe more strongly linked with more severe dependence than actualbehavioral persistence in the face of distress.
Empirical data on the relation of and mechanisms linking DTto the maintenance of smoking. Cross-sectional evidence indi-cates that daily smokers with lower DT may have a longer historyof smoking (Leyro et al., 2011), suggesting that DT may be amaintaining factor that prolongs regular smoking. Work on themechanisms linking DT and smoking maintenance indicates thatDT may prolong smoking behavior by amplifying the reinforcingproperties of smoking. Perkins et al. (2010) found that lowerself-reported DT enhanced acute smoking reinforcement (definedas ad lib smoking) due to abstinence in a laboratory study; DT didnot moderate smoking’s effect on mood state. Similarly, in a smallexploratory study, Bold, Yoon, Chapman, and McCarthy (2013)found that while completing a smoking choice task, smokers withlower perceived DT (a) were marginally more likely to choose tosmoke now versus delay smoking for a greater reward and (b) tookmore puffs after smoking. Other work indicates that perceived DTis significantly and uniquely related to smoking motives aimed atnegative affect management and addiction as well as expectanciesfor smoking-induced negative affect reduction (Leyro, Zvolensky,Vujanovic, & Bernstein, 2008; Trujillo et al., 2012). Indeed, onestudy found that even after controlling for level of anxiety anddepressive symptoms, lower perceived DT was associated withgreater reported urge to smoke to alleviate negative affect andgreater motivation to smoke for negative reinforcement purposes,but not motives for smoking or desire to smoke for positive affectenhancement (Trujillo et al., 2012). Hence, DT may be a transdi-agnostic factor incremental to emotional disorder symptoms thatmaintains smoking via anticipation that smoking aids in negativeaffect reduction motivation.
Some work has explored the possible exacerbating influence ofsmoking on acute DT. In a laboratory tobacco deprivation study,Bernstein, Trafton, Ilgen, and Zvolensky (2008) found that smok-ers’ breath-holding duration was significantly shorter following a12-hr smoking deprivation period than during a smoking-as-usualsession. They also found that psychiatric symptoms were nega-tively correlated with breath-holding duration during smokingdeprivation, but not after smoking-as-usual. These findings sug-gest that (a) DT may be context sensitive and perhaps acutelydiminished by smoking abstinence, and (b) the expression of poorDT during abstinence may couple with the expression of psychi-atric symptoms.
Empirical data on the relation of DT to smoking cessation andrelapse. There are fairly consistent associations between poorDT and lower ability to sustain abstinence using retrospectivereports of quit history (R. A. Brown, Lejuez, Kahler, & Strong,2002), prospective analyses of prequit DT as a predictor of cessa-
tion outcomes (Brandon et al., 2003; R. A. Brown et al., 2009;Cameron, Reed, & Ninnemann, 2013; Hajek, 1991; Hajek,Belcher, & Stapleton, 1987; Steinberg et al., 2012), and laboratoryexperimental analogues of relapse behavior (Kahler, McHugh,Metrik, Spillane, & Rohsenow, 2013). Much of this work docu-ments that low DT increases risk of very early lapse behavior,including within the first several hours or days of abstinence (e.g.,Abrantes et al., 2008; R. A. Brown et al., 2002; Kahler et al.,2013). Associations of low DT to faster relapse latency generallyextend across various measures, including breath-holding duration(R. A. Brown et al., 2002, 2009; Hajek, 1991; Hajek et al., 1987;cf. Steinberg et al., 2012), persistence on a CO2 challenge (R. A.Brown et al., 2002, 2009), and persistence on psychologicallystressful and frustrating tasks (Brandon et al., 2003; R. A. Brownet al., 2009, 2002; Cameron et al., 2013). They have also beendocumented in several populations, including a mixed sample ofsmokers with and without schizophrenia who were provided ces-sation counseling and pharmacotherapy (Steinberg et al., 2012). Inone of these studies, precessation DT reflected as persistence on astressful cognitive task increased monotonically across (a) cessa-tion treatment dropouts, (b) lapsers, and (c) abstinence maintainers(Brandon et al., 2003). Hence, low DT is prognosticative of poorcessation outcome in several contexts.
In a mechanistic analysis of the role of DT in cessation outcome,Abrantes et al. (2008) divided smokers who completed laboratory-based, behavioral DT tasks (PASAT, breath-holding duration, andCO2 persistence) prior to an unaided quit attempt into low, aver-age, and high DT on the tasks. Low-DT smokers were significantlymore likely to lapse on the assigned quit day than high-DT smok-ers. Furthermore, the extent to which negative affect on quit daypredicted lapse was stronger in smokers with low versus high DT.These results were not explained by overall level of depressivesymptoms, which did not meaningfully predict cessation outcomein this study. Addressing a similar mechanism, Volz et al. (2014)showed that low baseline DT amplified the relation between dailyself-reported hassles and cigarette craving that took place during acessation attempt. Hence, low-DT smokers appear to be morelikely to respond to the distress occurring in abstinence with strongmotivations to resume smoking, perhaps to terminate such distress,and this risk pathway is potentially more proximal than any distalinfluence on relapse caused by depressive symptomatology.
Implications for targeting DT in smoking prevention andcessation. Although prospective studies examining relations ofDT with smoking initiation in youth samples is needed prior todeveloping smoking prevention interventions that specifically tar-get DT, a potential contextual role of DT in smoking preventionmight be considered. Many empirically supported smoking pre-vention programs teach youths refusal skills to promote assertiveresistance to social pressures by their peers to smoke (Botvin &Griffin, 2007). In theory, individuals with lower DT might find ita particularly difficult to tolerate stress associated with goingagainst social influences to smoke and ultimately give in andsmoke to terminate uncomfortable feelings that may accompanyresisting offers to smoke. While targeting DT per se in preventionmay not yet be indicated, based on the dearth of DT and initiationresearch, considering the contextual backdrop of DT in relation tothe psychosocial processes that confer smoking initiation risk maybe a worthwhile pursuit in smoking prevention efforts.
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22 LEVENTHAL AND ZVOLENSKY
To the extent low DT impairs sustained smoking abstinence,interventions that cultivate a greater willingness to tolerate oraccept experiential distress should promote greater success inquitting or maintaining abstinence (e.g., R. A. Brown et al., 2005).In fact, there have been efforts to apply acceptance-oriented treat-ment strategies to smokers more generally (Bricker, Mann, Marek,Liu, & Peterson, 2010; Gifford et al., 2004; Hernández-López,Luciano, Bricker, Roales-Nieto, & Montesinos, 2009), althoughthis work has not focused on DT per se. In the first smoking studythat specifically targeted DT, R. A. Brown et al. (2008) developedan intervention for smokers with a history of early lapses (i.e.,individuals with no quit attempts lasting longer than 72 hr in thelast 10 years). The treatment included six 50-min individual ses-sions, nine 2-hr group sessions, and 8 weeks of NRT over thecourse of 10 weeks. Specific treatment components included psy-choeducation about smoking triggers, self-management strategiesfor dealing with external triggers, withdrawal-based exposure ex-ercises aimed at enhancing tolerance of withdrawal-related statesand sensations via increasing exposure to tobacco abstinence,NRT, and a collection of acceptance strategies. In a small single-group pilot study, the end-of-treatment (4 weeks postquit) 7-daypoint prevalence of abstinence was 31%. By 8, 13, and 26 weekspostquit, abstinence rates were 25%, 18%, and 0%, respectively.Despite the low abstinence rates, these participants, who reporteda history of no quit attempts lasting longer than 3 days in the last10 years, achieved a median of 24 days of continuous abstinenceand 40.5 days of noncontinuous abstinence. Further, although mostparticipants lapsed quickly, they did not evidence full-blown re-lapse (7 consecutive days of smoking) until much later into theirattempt (Mdn � 45.5 days), and many continued to make quitattempts after lapsing (Mdn � 2.5 attempts).
In a follow-up preliminary randomized trial of smokers withearly lapse history, R. A. Brown et al. (2013) compared thisDT-based cessation treatment (n � 27) to standard smoking ces-sation counseling (n � 22), with all receiving transdermal NRT.Results indicated that DT treatment participants were more likelyto be abstinent at the end of behavioral treatment and were alsomore likely to recover from lapses that occurred during treatment.Relative to standard cessation treatment, DT treatment participantsalso reported a larger decrease in emotional avoidance, a hypoth-esized DT treatment mediator, prior to quit day. The trajectory ofnegative mood and withdrawal symptoms in DT treatment differedfrom standard treatment and was largely consistent with hypoth-eses. However, there were no group differences in abstinence ratesat long-term follow-ups (8, 13, and 26 weeks after quit day).
Summary. Although direct empirical evidence of the role ofDT in the early stages of the smoking trajectory is sparse, DT istheoretically relevant to smoking initiation and progression and isworthy of consideration at least as a contextual factor in smokingprevention. Evidence consistently implicates DT in the mainte-nance of regular smoking behavior over time and the precipitationof relapse early in a quit attempt. A key putative mechanism is thatindividuals with lower DT may be more likely to anticipate or acton sources of distress (elicited by a variety of mechanisms) withsmoking in order to terminate such distress. While efforts tocultivate DT may improve cessation outcomes, therapeutic tacticsto target DT applied up to this point show promise but requirefurther refinement to meaningfully enhance cessation outcomes.Some results suggest that DT independently relates to smoking
processes over and above depressive and anxiety symptoms, whichis consistent with a transdiagnostic formulation of DT as a linkingmechanism between emotional symptomatology and smoking.
Concomitant Relations of Multiple TransdiagnosticEmotional Vulnerabilities to Smoking
We have thus far focused on how each of the three transdiag-nostic emotional vulnerabilities operates independently withoutconsidering their collective relation to smoking. Understanding theextent to which Anh, AS, and DT have unique, overlapping, orinteractive relations to smoking would provide a comprehensive,yet nuanced, view of how transdiagnostic vulnerabilities mayunderlie the comorbidity between smoking and a variety manifes-tations of emotional disorders that may involve multiple emotionalinfluences on smoking. We are aware of only three studies of theseconcomitant relations below.
In a cross-sectional test, Kraemer, McLeish, Jeffries, Avallone,and Luberto (2013) showed that after controlling for the covari-ance between AS and DT as well as other factors, lower perceivedDT significantly predicted self-reported internal barriers to cessa-tion (e.g., “Quitting will make me feel less in control of mymoods”) but not external or addiction-related barriers to cessationor number of prior quit attempts. The effects of AS over and aboveDT were not reported. Univariate analyses illustrated that higherAS and lower DT were correlated with higher levels of perceivedcessation barriers across a number of domains in that study.
In a cessation study, Zvolensky, Stewart, et al. (2009) found thatafter controlling for the covariance between AS and Anh and otherfactors, prequit levels of AS incrementally predicted risk of earlysmoking lapse (i.e., any smoking behavior) at each assessmentpoint during the first 14 days postquit but did not predict relapse(i.e., 7 consecutive days of smoking). In addition, Anh incremen-tally predicted lapse only on quit day, but also predicted relapsethroughout the 14 days of follow-up. In a follow-up report, prequitlevels of Anh, but not AS, predicted quit day levels of mood-basednicotine withdrawal symptoms when the covariance of Anh andAS was adjusted for (Langdon et al., 2013). Alternatively, AS, butnot Anh, predicted change in most nicotine withdrawal symptomsacross the 14 days following cessation, with high-AS individualsshowing slower declines in withdrawal symptoms over time. Fur-thermore, there were interactive effects between the two vulnera-bility factors, such that individuals with elevated AS and Anhshowed continued escalation of frustration and restlessness duringthe first 2 weeks of cessation, whereas the majority of the sampleshowed a decline in these symptoms. Collectively, these findingssuggest that AS and Anh may be play unique roles in smokingcessation failure, with regard to both risk prediction and mecha-nisms of relapse and which stage of the cessation process theyexert their influence (e.g., lapse vs. relapse and quit day vs. later).
Remaining Gaps in the Literature
Little integrative work across emotional vulnerabilities andtheir role in diverse manifestations of emotional disorders.
Importance of Anh, AS, and DT relative to one another.There is very little study of possible unique, overlapping, andinteractive relations of Anh, AS, and DT to smoking. Hence, it isunclear the extent to which these vulnerabilities relate to smoking
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23EMOTIONAL VULNERABILITIES AND SMOKING
via unique etiological mechanisms. Although theory suggestssome unique mechanisms (e.g., anxiety-specific avoidance throughsmoking vs. general distress avoidance and termination throughsmoking), it is plausible that AS and DT may have some commonlinkages to smoking via shared negative reinforcement mecha-nisms whereby both vulnerability factors affect and result fromefforts to avoid or terminate any type of aversive state (e.g.,Kraemer et al., 2013). If relations of the vulnerability factors tosmoking are indeed nonoverlapping, as has been shown withregard to AS and Anh in the prediction of lapse and relapse riskand withdrawal (Langdon et al., 2013; Zvolensky, Stewart, et al.,2009), smoking interventions may benefit from targeting multipletransdiagnostic vulnerabilities. Further, if several factors have in-teractive effects that multiplicatively increase smoking processes(e.g., Langdon et al., 2013), individuals high on multiple transdi-agnostic vulnerability factors may require especially high-intensityand specialized smoking interventions.
Explanatory power of Anh, AS, and DT relative to multiplemanifestations of emotional disorder. The transdiagnostic for-mulation proposed here purports that Anh, AS, and DT reflectcommon pathways that explain risk marked by manifest symptomsof emotional disorders (see Figure 1). There is a significant bodyof work supporting this proposition, by illustrating that Anh, AS,and DT relate to smoking incrementally to emotional disorders andsymptoms (e.g., Audrain-McGovern et al., 2012; R. A. Brown etal., 2009; Leventhal, Piper, et al., 2014; Leventhal et al. 2008;Wong et al., 2013; Zvolensky, Stewart, et al., 2009). However,much of this work has studied such effects relative to a limited setof emotional syndromes (e.g., Anh relative major depression andan overarching category of anxiety disorder, Leventhal, Piper, etal., 2014). Hence, the extent of transdiagnostic relevance to vari-ous manifestations of emotional psychopathology (e.g., major de-pression vs. panic disorder vs. social anxiety disorder vs. PTSD) isnot entirely clear. Furthermore, besides a few examples (e.g.,emotion regulation; Brandt et al., 2012), there has been limitedinvestigation of Anh, AS, and DT relative to other emotionalconstructs in the smoking literature. Such research would clarifythe “catchment area” of potential types of patients and areas of theliterature that could benefit from the transdiagnostic frameworkput forth here. The application of statistical approaches, such asmediation, to quantify the extent of covariation between emotionaldisorders and smoking that is accounted for by transdiagnosticemotional vulnerability factors is warranted. Such data could clar-ify the relative importance of the three factors identified here andwhether additional variance indirectly linking smoking and emo-tional disorder symptoms is unaccounted for and may perhapsreflect the influence of other (possibly transdiagnostic) processesoutside Anh, AS, and DT in emotion–smoking relations. Forexample, in a recent study of treatment-seeking smokers, emo-tional disorders were predictive of higher levels of nicotine depen-dence, greater perceived barriers to cessation, and greater severityof problematic symptoms while quitting in past attempts (Zvolen-sky, Farris, Leventhal, & Schmidt, 2014). Each of these relationswas accounted for by the indirect effect of AS, suggesting that thisconstruct may partially account for the link between emotionaldisorders and various clinically relevant smoking processes.
Targeting multiple transdiagnostic vulnerability factors usinga single treatment framework. Though some research for apply-ing psychosocial treatment strategies that target Anh, AS, and DT
to enhance smoking cessation have been used (e.g., R. A. Brownet al., 2008), the majority of this literature is preliminary and lacksdefinitive randomized controlled trials. Furthermore, this work haslargely been unintegrated, which could reflect, in part, the commonemphasis on a single manifest disorder (e.g., Anh treatment isconsidered more often in populations with depression than thosewith a primary anxiety concern). Accordingly, efforts to targetmultiple transdiagnostic vulnerabilities within a common treat-ment framework are needed, as such a framework could be appli-cable to a large diagnostically heterogeneous population of smok-ers with emotional problems.
Limited conceptualization of transdiagnostic emotional vul-nerabilities as dynamic factors over time and that reciprocallyrelate with smoking. The majority of smoking research hasexamined Anh, AS, and DT as static traits. However, as notedabove, each of these factors is somewhat malleable in response tocertain factors, including smoking. For instance, there is evidencethat these factors may be temporarily altered in acute abstinenceamong regular smokers (Powell et al., 2002, 2004), and some datasuggesting that the shape of trajectories of transdiagnostic emo-tional vulnerabilities during a cessation attempt may demarcatesmoking relapse risk (AS, Assayag et al., 2012; Anh, Cook et al.,2012). Hence, additional work is needed to examine within-personvariation across multiple stages of the smoking uptake or cessationprocess as well as in response to relevant factors, such as stress orintervention. Such work, which lends itself to ecological momen-tary assessment methods (Shiffman, 2009), is likely to refine theprecision of theoretical models, enhance knowledge of treatmentmechanisms, and identify which stages of smoking uptake andcessation processes may require particular prevention and cessa-tion interventions tailored to Anh, AS, and DT levels.
Sparse research on developmental context and early risk.There is limited work on how transdiagnostic factors increase riskof (and may result from) smoking initiation and progression inyouths. Adolescence is a critical time for the development ofneural pathways underlying emotional processing and risk taking(Dahl, 2004). Hence, it is likely that this period may be associatedwith significant and clinically relevant malleability in Anh, AS,and DT; changes in smoking behavior; and the coupling of theseprocesses. Not only can studying relations of Anh, AS, and DT tosmoking in adolescents be used to identify youths at risk in needof intervention, studying such relations is critical for informingtargets for preventive interventions aimed to offset the risk ofsmoking due to emotional disorder and preventing emotional dis-order risk impacted by smoking. To date, we are aware of nosmoking prevention intervention that specifically targets any of thethree transdiagnostic factors.
Poor understanding of moderating factors. Almost allsmoking research on transdiagnostic emotional vulnerabilities hasused a “main effect approach” with the goal of isolating a bivariaterelation between Anh, AS, and DT to smoking processes as theyapply to general populations and contexts. However, demographiccharacteristics such as gender, age, ethnicity, and socioeconomicstatus have been shown to impact the relation of emotional disor-ders to smoking and other health behaviors and outcomes (Gavin,Rue, & Takeuchi, 2010; Husky, Mazure, Paliwal, & McKee,2008). Such factors may mark important sociocultural or biolog-ical processes, such as cultural differences in the experience orexpression of emotional distress and psychopathology (Hunter &
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24 LEVENTHAL AND ZVOLENSKY
Schmidt, 2010), that could influence how emotional vulnerabilitiescouple with smoking. Indeed, one study found suggestive evidencethat low DT was associated with greater likelihood of being asmoker (vs. nonsmoker) in African Americans, but the DT-smoking association was attenuated in Whites (Dahne et al., 2014).Other factors, such as additional medical or psychiatric comorbid-ity, which may heighten emotion disturbance and limit alternativecoping mechanisms, could ultimately enhance the link betweenvulnerabilities and smoking. Identifying moderators of the relationof Anh, AS, and DT to smoking could also inform the identifica-tion of individuals and contexts in which smoking interventionsfocused on vulnerabilities may be most effective.
Modeling variability in transdiagnostic factors in the smok-ing literature. Much research on transdiagnostic vulnerabilityfactors in smoking has utilized observed raw score variables andhas modeled linear relations of quantitative levels of Anh, AS, andDT to smoking. This traditional approach is based upon twoassumptions that may not always be upheld: (a) observed scoresare accurate reflections of latent traits, and (b) each successiveincrease in Anh, AS, or DT is associated with a proportionalincrease in a smoking variable. Scaling methods based on itemresponse theory (IRT) that map particular items (and responsecategories within items) to different points upon a latent severitydimension might result in more accurate reflections of the latenttraits of Anh, AS, and DT (Muthén & Lehman, 1985). Certainitems may map differently onto latent dimensions across disparatesettings and populations (e.g., males vs. females) and hence re-quire unique modeling strategies. Techniques to assess differentialitem functioning using IRT can address this phenomenon (Muthén& Lehman, 1985), which may be particularly relevant for model-ing how variation in transdiagnostic constructs may changethroughout the smoking trajectory. Perhaps in later (vs. earlier)stages of tobacco dependence (e.g., relapse vs. early progression)certain manifestations of Anh, AS, or DT may be more or lessdiscriminatory of underlying latent constructs. IRT has yet to beapplied to the emotional vulnerability and smoking literature.
Taxometric analysis, which involves identifying the existence ofmeaningful breaks in the distribution of continuous observations(Meehl, 2001a), may also be a useful application to transdiagnosticfactors in smoking. For instance, AS was shown to have sometaxonic properties (with dimensional variation within the a taxon),suggesting a qualitatively unique group of individuals with highAS (Bernstein et al., 2007). Thus identifying whether taxons ofindividuals with high levels of Anh, AS, and DT are at greater riskof smoking is warranted, as continuous variation in these transdi-agnostic factors may not proportionally relate to successive in-creases in smoking. Along similar lines, exploring nonlinear mod-els (e.g., quadratic) to the relation of transdiagnostic factors tosmoking may also be useful.
Limited information on biological mechanisms. The limitedwork that has been conducted on biological processes in transdi-agnostic vulnerabilities in smoking has focused on whether Anh,AS, and DT moderate the effects of nicotine administration andabstinence manipulations on behavioral outcomes (e.g., Leventhal,Munafò, et al., 2009, Leventhal, Waters, et al., 2019; Vujanovic &Zvolensky, 2009). Work incorporating pharmacological chal-lenges other than nicotine and positron emission tomography im-aging are likely to yield insights into other neuropharmacologicalpathways that may innervate with the nicotinic acetylcholine re-
ceptor circuits to underpin why transdiagnostic emotional vulner-abilities may be linked with smoking. Furthermore, other technol-ogies, including functional magnetic resonance imaging, may yieldinsight into the neuroanatomical substrates underlying the relationbetween emotional vulnerabilities and smoking. Finally, moleculargenetic research studies are needed. As evidence emerges thatlinks certain gene regions to risk of developing transdiagnosticvulnerabilities (e.g., corticotropin-releasing hormone receptorType 1 gene region and Anh; Bogdan, Santesso, Fagerness, Perlis,& Pizzagalli, 2011), the proteins coded for by such genes might beintegral in the relation between such vulnerabilities and smoking.
Integrative Theoretical Model Linking TransdiagnosticEmotional Vulnerabilities to Smoking
Model Overview
Though important gaps in the literature remain, we apply theexisting knowledge base to an integrative theoretical model toexplain how and why transdiagnostic emotional vulnerabilities arekey to the comorbidity between smoking and emotional disorders(see Figure 2). A central element of this model is that transdiag-nostic emotional vulnerabilities directly amplify expected and ac-tual experience of smoking’s three primary acute affect-modulatory effects, which transmit risk of progressing across thesmoking trajectory (i.e., experimentation, progression, mainte-nance, inability to make a cessation attempt, relapse followingcessation, and recurrence). On the basis of empirical findings andtheoretical notions reviewed above, we propose that Anh amplifiessmoking’s reward-enhancing (and pleasure-enhancing) effects, ASamplifies smoking’s anxiolytic effects, and poor DT amplifiessmoking’s distress-terminating effects. Given that these threeaffect-modulatory effects may collectively account for a signifi-cant portion of critical pathways underlying addiction motivation(Baker, Piper, McCarthy, Majeskie, & Fiore, 2004; Morissette etal., 2007; Watkins et al., 2000), we argue that it is plausible thatAnh, AS, and DT are key factors linking emotional disorders tosmoking.
We propose that the effects of Anh, AS, and DT on these threeaffect-modulatory effects may be manifested across two types ofchanges in acute tobacco use (i.e., tobacco administration andabstinence) and in two ways (e.g., actual in-the-moment experi-ence and anticipated effects). That is, we hypothesize that Anh, AS,and DT not only amplify smoking-induced reward, anxiolysis, anddistress termination, but also amplify the effects of smoking absti-nence on reward declinations, anxiogenesis, and distress exacerbation.We further propose that Anh, AS, and DT amplify the formation ofbeliefs that tobacco administration and abstinence produce affectenhancement and worsening, respectively.
Initiation and Progression of Smoking
We suspect that these processes could play out as follows. Never-smoking youths with elevated transdiagnostic emotional vulnerabili-ties may have stronger expectations that smoking produces affect-enhancing effects (Stone & Leventhal, 2014), based on their learninghistory in relation to other affect-modulatory behaviors (e.g., low-DTnever smokers may learn that certain foods help to alleviate distressdue to eating-induced stress reduction) or observational learning (e.g.,
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25EMOTIONAL VULNERABILITIES AND SMOKING
seeing and hearing from others’ experiences with smoking, tobaccoadvertising). Additionally, individuals with these vulnerabilities mayfind information and stimuli in their environment that promote ex-pectancies for affect modulation more personally salient (e.g., highAnh may be hyperattuned to learning opportunities for behaviors thatmight produce pleasure, high AS may be hyperattuned to learningopportunities for behaviors that might produce anxiolysis, low-DTindividuals may be hyperattuned to learning opportunities for behav-iors that might alleviate distress). Hence, they may be more likely todevelop expectancies for smoking-induced affect modulation prior toinitiation. Stronger expectations of smoking’s anticipated effects onemotional state along with additional tendencies toward pursuinghigh-potency and low-effort affect-modulatory behaviors and agents,such as nicotine, may heighten willingness to experiment with smok-ing. Once smoking is initiated, those with elevated transdiagnosticemotional vulnerabilities may experience stronger smoking-inducedaffect modulation, which is likely to enhance the reinforcing proper-ties of smoking, motivate further smoking behavior, and ultimatelyaccelerate progression from infrequent to regular smoking and possi-
ble nicotine dependence. During this process, any cognitive expecta-tions of smoking’s affect-modulatory effects may be strengthenedbased on actual experience. Furthermore, smoking expectancies mayserve to enhance actual emotion experienced from smoking (Juliano& Brandon, 2002; i.e., placebo/expectancy effects) and ultimatelypromote a positive feedback loop whereby cognitive anticipatory andemotional experiential processes of smoking’s effects bidirectionallyenhance one another over time. Such processes may further elevatethe reinforcing value of smoking and therefore promote progression toregular smoking for individuals with elevated vulnerabilities.
Maintenance of Regular Smoking
Once habitual smoking is established, many smokers are likelyto experience temporary states of deprivation prior to any interestin quitting smoking (e.g., smoking restrictions at work, waking upafter not smoking overnight). Smokers with elevated transdiagnos-tic emotional vulnerabilities may experience amplified exacerba-tions in affect disturbance after these temporary abstinence states
Figure 2. Integrative theoretical model identifying transdiagnostic emotional vulnerability factors as keyelements linking emotional symptoms and syndromes to stages of the smoking trajectory. Different transdiag-nostic emotional vulnerabilities are proposed to putatively amplify the impact of different types of smoking’saffect-modulatory effects on smoking behavior: (a) anhedonia (Anh) amplifies smoking-induced reward, (b)anxiety sensitivity (AS) amplifies smoking-induced anxiolysis, and (c) poor distress tolerance (DT) amplifiessmoking-induced distress reduction. PTSD � posttraumatic stress disorder; GAD � generalized anxietydisorder.
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26 LEVENTHAL AND ZVOLENSKY
(e.g., Cook et al., 2004). These experiences may motivate thequick resumption of smoking behavior to counteract these tempo-rary abstinence-provoked states of affect disturbance, which maybe an important maintaining factor for regular smoking. Further-more, actual experience with smoking-induced affect exacerbationmay be highly personally salient for individuals with elevatedvulnerabilities and therefore may promote the development ofstrong cognitive expectations that smoking abstinence worsensaffect (e.g., Abrams, Zvolensky, et al., 2011). Simply believingthat abstinence worsens affect may directly enhance any actualemotion disturbance experienced during abstinence (Hendricks &Leventhal, 2013; i.e., placebo/expectancy effects). Hence, cogni-tive anticipatory and experiential processes involving abstinence-provoked affect disturbance may bidirectionally enhance one an-other over time, further maintaining smoking behavior. Overall, astrong drive to experience smoking-induced affect enhancementand avoid abstinence-induced affect exacerbation may be impor-tant factors that maintain regular smoking in those with elevatedtransdiagnostic emotional vulnerabilities.
Cessation, Relapse, and Recurrence
Due to heightened anticipated and actual experiences that ab-stinence may exacerbate affect, smokers with elevated transdiag-nostic emotional vulnerabilities may perceive greater barriers tocessation and avoid quitting altogether (e.g., Kraemer et al., 2013).Emotionally vulnerable smokers who overcome such barriers andultimately make cessation attempts may experience strong affectdisturbance upon quitting, which may motivate lapses back tosmoking. Such lapses are likely to produce particularly strongsmoking-induced affect enhancement for those with elevatedtransdiagnostic emotional vulnerabilities (e.g., Perkins et al.,2010). The strong reinforcement (i.e., affect-enhancing) experi-ence of lapses is likely to motivate additional lapses, as well asfurther reinforce cognitive expectancies regarding smoking’saffect-modulatory effects. Ultimately, the lapse process is likely toeventually promote a full-blown relapse back to precessationsmoking level and recurrence and worsening of nicotine depen-dence. Relapse propensity is a key indicator of loss of control oversmoking, and abstinence-induced worsening of affect reflectswithdrawal. This model and empirical review illustrates that Anh,AS, and DT amplify both of these phenomena, which are coreelements of tobacco use disorder (American Psychiatric Associa-tion, 2013). Accordingly, we can infer that transdiagnostic emo-tional vulnerabilities play key roles in nicotine dependence risk.
We further hypothesize that during the smoking dependence pro-cess, individuals with elevated transdiagnostic emotional vulnerabil-ities may experience a worsening of Anh, AS, and DT as a result oftheir smoking. As noted in the sections above, experiencing smoking-induced affect modulation may reinforce maladaptive responses toemotional cues and worsen transdiagnostic emotional vulnerabilitiesprocesses. For instance, poor-DT smokers may avoid experiencing anatural habituation to distressing states due to smoking-induced es-cape of distress and may therefore not learn to strengthen their DTskills. High-Anh smokers may exhibit a narrowing in their repertoireof nonsmoking reinforcers, which may lead to less nonsmokingpositive reinforcement and heightened Anh. High-AS smokers mayexperience physiological effects from smoking (e.g., smoking-induced cardiovascular symptoms), which could reinforce AS-related
fears of anxiety-related sensations. These are some examples of manytypes of mechanisms whereby smoking might worsen transdiagnosticvulnerability processes. As a result, a positive feedback loop inbetween transdiagnostic emotional vulnerabilities and smokingbehavior may develop (as well as a further heightening ofmanifest emotional symptomatology produced by worseningAnh, AS, and DT given that these factors putatively underlieemotional pathology risk). Such a feedback loop may producevicious cycles that may link smoking and various manifestemotional disorders, with transdiagnostic vulnerability factorsplaying a key intermediate role (see Figure 1). Finally, giventhe possibility that multiple transdiagnostic vulnerability fac-tors may operate through independent, overlapping, and possi-bly interactive pathways to and from smoking (e.g., Zvolensky,Stewart, et al., 2009), each of the above-mentioned mechanismsmay have cumulative impact and account for multimorbidity ofseveral emotional symptoms and syndromes with smoking.
Conclusion
We are hopeful that the framework put forth here will stimulateexciting new work that meaningfully advances understanding ofthe comorbidity between emotional disorders and cigarette smok-ing. On the basis of this review, we conclude that Anh, AS, DT (a)are distinct from other emotion constructs, manifest symptomatol-ogy, and each other; (b) are aptly represented as overarchingvulnerability factors that give rise to a variety of different types ofemotional symptomatology; (c) are malleable (can be changed andtherefore targeted in treatment); (d) drive movement across mul-tiple stages of the smoking trajectory (i.e., initiation, escalation/progression, maintenance, cessation/relapse); (e) collectively am-plify the anticipated and actual affect-modulatory (and reinforcing)properties of smoking in independent ways to drive smokingbehavior; (f) are exacerbated by smoking in some cases; and (g)appear to be nonoverlapping contributors to certain smoking pro-cesses (e.g., relapse risk).
To the extent the conceptualization proposed here is accurate, aprimary clinical implication is that an integrated, transdiagnostic ap-proach for smoking intervention (and mental health promotion) thatspecifically assesses and targets these processes may be warranted forthe individuals with one or more emotional comorbidities. First andforemost, the current review suggests that it would behoove smokingcessation practitioners not to solely assess manifest emotional symp-tomatology. Rather, assessment of transdiagnostic emotional vulner-abilities, including Anh, AS, and DT, may provide clinically impor-tant information for prognosticating which patients may be likely toexperience certain treatment barriers (e.g., nicotine withdrawal, ciga-rette craving, avoidance of quitting, treatment dropout) and be at highrisk for relapse at certain stages of the cessation process (e.g., all threefactors have been linked to early lapse, Anh has been linked tolong-term relapse). Such information could inform the nature andtiming of cessation treatments and could suggest that patients withconcomitant emotional vulnerabilities would at the very least requiremore intensive intervention than the typical patient. Given that someof evidence reviewed above indicates that certain vulnerabilities mayconfer incremental nonoverlapping sources of smoking relapse risk,patients with elevations on multiple transdiagnostic emotional vulner-abilities may require particular clinical attention. Furthermore, thisreview points toward an eventual transdiagnostic treatment model that
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27EMOTIONAL VULNERABILITIES AND SMOKING
may be useful for the overall population of smokers with one ormultiple emotional comorbidities. Such a transdiagnostic treatmentmay ultimately be more efficient and cost-effective than diagnosis-specific treatments, given the increased expense of training in differ-ent protocols for each type of comorbidity. For example, a set ofdistinct therapeutic tactics could be used to target specific emotionalvulnerability processes within a common treatment framework (e.g.,behavioral exercises will incorporate exposure to smoking-related cues following quit day to enhance tolerance of high-anxiety and distress states without smoking, as well as BA tocounter the Anh and behavioral and social withdrawal associ-ated with depression that may motivate smoking). Because thetreatment literature for targeting transdiagnostic factors is stillemerging, future work is sorely needed to develop such inte-grated protocols, evaluate their efficacy, and explore their rel-evance to smoking prevention and cessation.
Although the current framework focuses on only three transdi-agnostic vulnerability factors and emotion–smoking comorbidity,we believe that the “big picture” elements of this framework canserve as a prototype for other related research agendas. Theseconcepts may potentially generalize to smoking research on othertransdiagnostic emotional vulnerabilities (e.g., emotional accep-tance). Furthermore, one could envision these transdiagnostic con-cepts being applied to (a) understanding the comorbidity betweenemotional disorder and use, abuse, and addiction to substancesother than tobacco; (b) elucidating the underlying elements linkingemotional disorders to other behaviors that influence health andare emotionally determined (e.g., physical activity, eating); and (c)identifying transdiagnostic vulnerabilities that span emotional andnonemotional disorders—Anh, for instance, is implicated in psy-chotic disorders (Horan, Kring, & Blanchard, 2006)—and theextent to which they account for broad comorbidities with smokingand other behaviors and conditions. Ultimately, theoreticallyguided work focusing on transdiagnostic psychopathologic vulner-abilities may be a key paradigm for advancing clinical and scien-tific efforts dedicated to reducing the public health burden asso-ciated with emotion–smoking co-occurrence and possibly otherimportant comorbidities.
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31EMOTIONAL VULNERABILITIES AND SMOKING
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Received January 7, 2014Revision received August 16, 2014
Accepted August 20, 2014 �
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37EMOTIONAL VULNERABILITIES AND SMOKING